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Journal Cover Neuron
  [SJR: 11.464]   [H-I: 372]   [175 followers]  Follow
    
   Full-text available via subscription Subscription journal
   ISSN (Print) 0896-6273 - ISSN (Online) 1097-4199
   Published by Elsevier Homepage  [3043 journals]
  • Exciting Times Ahead
    • Authors: Mariela Zirlinger
      First page: 247
      Abstract: Publication date: 11 October 2017
      Source:Neuron, Volume 96, Issue 2
      Author(s): Mariela Zirlinger


      PubDate: 2017-10-14T00:55:04Z
      DOI: 10.1016/j.neuron.2017.09.060
       
  • Mapping Brain Activity onto Molecularly Defined Cells
    • Authors: Alexander Jones; Leon G. Reijmers
      Pages: 248 - 249
      Abstract: Publication date: 11 October 2017
      Source:Neuron, Volume 96, Issue 2
      Author(s): Alexander Jones, Leon G. Reijmers
      The brain processes information and generates behavior by employing a wide array of different cell types. In this issue of Neuron, Wu et al. (2017) report a novel method that enables the efficient identification of molecularly defined cells that participate in a specific brain function.
      Teaser The brain processes information and generates behavior by employing a wide array of different cell types. In this issue of Neuron, Wu et al. (2017) report a novel method that enables the efficient identification of molecularly defined cells that participate in a specific brain function.

      PubDate: 2017-10-14T00:55:04Z
      DOI: 10.1016/j.neuron.2017.09.054
       
  • Obsessing about Uncertainty'
    • Authors: Jacqueline Scholl; Matthew F.S. Rushworth
      Pages: 250 - 252
      Abstract: Publication date: 11 October 2017
      Source:Neuron, Volume 96, Issue 2
      Author(s): Jacqueline Scholl, Matthew F.S. Rushworth
      A striking observation in obsessive-compulsive disorder is that patients know that their obsessions and compulsions are excessive, but their symptoms nevertheless persist. Drawing on computational models from basic neuroscience, Vaghi and colleagues (2017) suggest a quantitative account of this clinical finding.
      Teaser A striking observation in obsessive-compulsive disorder is that patients know that their obsessions and compulsions are excessive, but their symptoms nevertheless persist. Drawing on computational models from basic neuroscience, Vaghi and colleagues suggest a quantitative account of this clinical finding.

      PubDate: 2017-10-14T00:55:04Z
      DOI: 10.1016/j.neuron.2017.09.045
       
  • A Corticostriatal Balancing Act Supports Skill Learning
    • Authors: Victoria L. Corbit; Susanne E. Ahmari; Aryn H. Gittis
      Pages: 253 - 255
      Abstract: Publication date: 11 October 2017
      Source:Neuron, Volume 96, Issue 2
      Author(s): Victoria L. Corbit, Susanne E. Ahmari, Aryn H. Gittis
      In this issue of Neuron, Kupferschmidt et al. (2017) reveal the shifting dynamics of functionally defined corticostriatal pathways during skill learning in mice using fiber photometry. They show different time courses in plasticity of associative and sensorimotor circuits across learning that involve changes at both the synaptic and cortical level.
      Teaser In this issue of Neuron, Kupferschmidt et al. reveal the shifting dynamics of functionally defined corticostriatal pathways during skill learning in mice using fiber photometry. They show different time courses in plasticity of associative and sensorimotor circuits across learning that involve changes at both the synaptic and cortical level.

      PubDate: 2017-10-14T00:55:04Z
      DOI: 10.1016/j.neuron.2017.09.046
       
  • Implicit and Explicit Learning Mechanisms Meet in Monkey Prefrontal Cortex
    • Authors: Matthew V. Chafee; David A. Crowe
      Pages: 256 - 258
      Abstract: Publication date: 11 October 2017
      Source:Neuron, Volume 96, Issue 2
      Author(s): Matthew V. Chafee, David A. Crowe
      In this issue, Loonis et al. (2017) provide the first description of unique synchrony patterns differentiating implicit and explicit forms of learning in monkey prefrontal networks. Their results have broad implications for how prefrontal networks integrate the two learning mechanisms to control behavior.
      Teaser In this issue, Loonis et al. provide the first description of unique synchrony patterns differentiating implicit and explicit forms of learning in monkey prefrontal networks. Their results have broad implications for how prefrontal networks integrate the two learning mechanisms to control behavior.

      PubDate: 2017-10-14T00:55:04Z
      DOI: 10.1016/j.neuron.2017.09.049
       
  • Nuclear Pore Protein Meets Transcription Factor in Neural Fate
    • Authors: Taro Kitazawa; Filippo M. Rijli
      Pages: 259 - 261
      Abstract: Publication date: 11 October 2017
      Source:Neuron, Volume 96, Issue 2
      Author(s): Taro Kitazawa, Filippo M. Rijli
      How nuclear architecture contributes to transcriptional regulation in neural progenitor cells (NeuPCs) is poorly understood. A study by Toda et al. (2017) now shows that the nuclear pore protein Nup153 associates with the Sox2 transcription factor in the regulation of NeuPC maintenance and neural fate.
      Teaser How nuclear architecture contributes to transcriptional regulation in neural progenitor cells (NeuPCs) is poorly understood. A study by Toda et al. (2017) now shows that the nuclear pore protein Nup153 associates with the Sox2 transcription factor in the regulation of NeuPC maintenance and neural fate.

      PubDate: 2017-10-14T00:55:04Z
      DOI: 10.1016/j.neuron.2017.09.059
       
  • Hazards to Early Development: The Biological Embedding of Early Life
           Adversity
    • Authors: Charles A. Nelson
      Pages: 262 - 266
      Abstract: Publication date: 11 October 2017
      Source:Neuron, Volume 96, Issue 2
      Author(s): Charles A. Nelson
      The number of children under 18 years of age has increased worldwide over the past decade. This growth spurt is due, in part, to remarkable progress in child survival. Alas, surviving early hazards, like prematurity or infectious disease, does not guarantee that children’s development will not be compromised by other hazards as they grow older. Throughout the world, children continue to be confronted with a large number of biological and psychosocial challenges that greatly limit their developmental potential. The focus of this article is how such adverse experiences impact the developing brain.
      Teaser In this NeuroView, Nelson discusses the major hazards that impede healthy development, focusing in particular on neglect and on children exposed to multiple forms of psychological and biological adversity.

      PubDate: 2017-10-14T00:55:04Z
      DOI: 10.1016/j.neuron.2017.09.027
       
  • Striatal Local Circuitry: A New Framework for Lateral Inhibition
    • Authors: Dennis A. Burke; Horacio G. Rotstein; Veronica A. Alvarez
      Pages: 267 - 284
      Abstract: Publication date: 11 October 2017
      Source:Neuron, Volume 96, Issue 2
      Author(s): Dennis A. Burke, Horacio G. Rotstein, Veronica A. Alvarez
      This Perspective will examine the organization of intrastriatal circuitry, review recent findings in this area, and discuss how the pattern of connectivity between striatal neurons might give rise to the behaviorally observed synergism between the direct/indirect pathway neurons. The emphasis of this Perspective is on the underappreciated role of lateral inhibition between striatal projection cells in controlling neuronal firing and shaping the output of this circuit. We review some classic studies in combination with more recent anatomical and functional findings to lay out a framework for an updated model of the intrastriatal lateral inhibition, where we explore its contribution to the formation of functional units of processing and the integration and filtering of inputs to generate motor patterns and learned behaviors.
      Teaser Striatum integrates cortical and limbic information to assist in the selection of appropriate behaviors. Burke et al. review recent findings implicating local striatal circuitry in this computation and hypothesize a framework wherein lateral inhibition between projection neurons facilitates action selection.

      PubDate: 2017-10-14T00:55:04Z
      DOI: 10.1016/j.neuron.2017.09.019
       
  • Lost in Transportation: Nucleocytoplasmic Transport Defects in ALS and
           Other Neurodegenerative Diseases
    • Authors: Hong Joo Kim; J. Paul Taylor
      Pages: 285 - 297
      Abstract: Publication date: 11 October 2017
      Source:Neuron, Volume 96, Issue 2
      Author(s): Hong Joo Kim, J. Paul Taylor
      Amyotrophic lateral sclerosis (ALS) is a progressive, fatal neurodegenerative disease characterized by degeneration of upper and lower motor neurons in the brain and spinal cord. The hallmark pathological feature in most cases of ALS is nuclear depletion and cytoplasmic accumulation of the protein TDP-43 in degenerating neurons. Consistent with this pattern of intracellular protein redistribution, impaired nucleocytoplasmic trafficking has emerged as a mechanism contributing to ALS pathology. Dysfunction in nucleocytoplasmic transport is also an emerging theme in physiological aging and other related neurodegenerative diseases, such as Huntington’s and Alzheimer’s diseases. Here we review transport through the nuclear pore complex, pointing out vulnerabilities that may underlie ALS and potentially contribute to this and other age-related neurodegenerative diseases.
      Teaser Kim and Taylor provide an overview of transport through the nuclear pore complex, and they review the evidence suggesting that defects in nucleocytoplasmic transport contribute to ALS and perhaps other age-related neurodegenerative diseases.

      PubDate: 2017-10-14T00:55:04Z
      DOI: 10.1016/j.neuron.2017.07.029
       
  • Diagnosing the Neural Circuitry of Reading
    • Authors: Brian A. Wandell; Rosemary K. Le
      Pages: 298 - 311
      Abstract: Publication date: 11 October 2017
      Source:Neuron, Volume 96, Issue 2
      Author(s): Brian A. Wandell, Rosemary K. Le
      We summarize the current state of knowledge of the brain’s reading circuits, and then we describe opportunities to use quantitative and reproducible methods for diagnosing these circuits. Neural circuit diagnostics—by which we mean identifying the locations and responses in an individual that differ significantly from measurements in good readers—can help parents and educators select the best remediation strategy. A sustained effort to develop and share diagnostic methods can support the societal goal of improving literacy.
      Teaser Wandell and Le summarize the current knowledge of the brain’s reading circuits. They describe methods for identifying brain locations and responses in a poor reader that differ from typical good readers. Precise diagnoses can help parents and educators select remediation strategies.

      PubDate: 2017-10-14T00:55:04Z
      DOI: 10.1016/j.neuron.2017.08.007
       
  • Detecting Activated Cell Populations Using Single-Cell RNA-Seq
    • Authors: Ye Emily Wu; Lin Pan; Yanning Zuo; Xinmin Li; Weizhe Hong
      Pages: 313 - 329.e6
      Abstract: Publication date: 11 October 2017
      Source:Neuron, Volume 96, Issue 2
      Author(s): Ye Emily Wu, Lin Pan, Yanning Zuo, Xinmin Li, Weizhe Hong
      Single-cell RNA sequencing offers a promising opportunity for probing cell types mediating specific behavioral functions and the underlying molecular programs. However, this has been hampered by a long-standing issue in transcriptional profiling of dissociated cells, specifically the transcriptional perturbations that are artificially induced during conventional whole-cell dissociation procedures. Here, we develop Act-seq, which minimizes artificially induced transcriptional perturbations and allows for faithful detection of both baseline transcriptional profiles and acute transcriptional changes elicited by behavior/experience-driven activity. Using Act-seq, we provide the first detailed molecular taxonomy of distinct cell types in the amygdala. We further show that Act-seq robustly detects seizure-induced acute gene expression changes in multiple cell types, revealing cell-type-specific activation profiles. Furthermore, we find that acute stress preferentially activates neuronal subpopulations that express the neuropeptide gene Cck. Act-seq opens the way for linking physiological stimuli with acute transcriptional dynamics in specific cell types in diverse complex tissues.
      Teaser Wu et al. develop Act-seq, which minimizes artificially induced transcriptional changes during single-cell dissociation and thus enables faithful characterization of baseline transcriptional profiles and detection of specific cell populations activated by physiological stimuli using single-cell sequencing.

      PubDate: 2017-10-14T00:55:04Z
      DOI: 10.1016/j.neuron.2017.09.026
       
  • Functional Convergence at the Retinogeniculate Synapse
    • Authors: Elizabeth Y. Litvina; Chinfei Chen
      Pages: 330 - 338.e5
      Abstract: Publication date: 11 October 2017
      Source:Neuron, Volume 96, Issue 2
      Author(s): Elizabeth Y. Litvina, Chinfei Chen
      Precise connectivity between retinal ganglion cells (RGCs) and thalamocortical (TC) relay neurons is thought to be essential for the transmission of visual information. Consistent with this view, electrophysiological measurements have previously estimated that 1–3 RGCs converge onto a mouse geniculate TC neuron. Recent advances in connectomics and rabies tracing have yielded much higher estimates of retinogeniculate convergence, although not all identified contacts may be functional. Here we use optogenetics and a computational simulation to determine the number of functionally relevant retinogeniculate inputs onto TC neurons in mice. We find an average of ten RGCs converging onto a mature TC neuron, in contrast to >30 inputs before developmental refinement. However, only 30% of retinogeniculate inputs exceed the threshold for dominating postsynaptic activity. These results signify a greater role for the thalamus in visual processing and provide a functional perspective of anatomical connectivity data.
      Teaser Litvina and Chen address a controversial disconnect between functional and recent connectomic characterizations of retinogeniculate convergence. Few strong among many converging inputs dominate retinogeniculate transmission. Heterogeneity of synaptic strengths demonstrates potential complexity of visual thalamic function.

      PubDate: 2017-10-14T00:55:04Z
      DOI: 10.1016/j.neuron.2017.09.037
       
  • Posterior Cingulate Neurons Dynamically Signal Decisions to Disengage
           during Foraging
    • Authors: David L. Barack; Steve W.C. Chang; Michael L. Platt
      Pages: 339 - 347.e5
      Abstract: Publication date: 11 October 2017
      Source:Neuron, Volume 96, Issue 2
      Author(s): David L. Barack, Steve W.C. Chang, Michael L. Platt
      Foraging for resources is a fundamental behavior balancing systematic search and strategic disengagement. The foraging behavior of primates is especially complex and requires long-term memory, value comparison, strategic planning, and decision-making. Here we provide evidence from two different foraging tasks that neurons in primate posterior cingulate cortex (PCC) signal decision salience during foraging to motivate disengagement from the current strategy. In our foraging tasks, salience refers to the difference between decision thresholds and the net harvested reward. Salience signals were stronger in poor foraging contexts than rich ones, suggesting low harvest rates recruit mechanisms in PCC that regulate strategic disengagement and exploration during foraging.
      Teaser Barack et al. report that foraging salience motivated strategic disengagement in two distinct tasks. Posterior cingulate neurons preferentially signaled salience and forecast divergent choices when reward rates were low, suggesting a role in the strategic control of behavior.

      PubDate: 2017-10-14T00:55:04Z
      DOI: 10.1016/j.neuron.2017.09.048
       
  • Amyloid Beta Peptides Block New Synapse Assembly by Nogo Receptor-Mediated
           Inhibition of T-Type Calcium Channels
    • Authors: Yanjun Zhao; Sivaprakash Sivaji; Michael C. Chiang; Haadi Ali; Monica Zukowski; Sareen Ali; Bryan Kennedy; Alex Sklyar; Alice Cheng; Zihan Guo; Alexander K. Reed; Ravindra Kodali; Jennifer Borowski; Georgia Frost; Patrick Beukema; Zachary P. Wills
      Pages: 355 - 372.e6
      Abstract: Publication date: 11 October 2017
      Source:Neuron, Volume 96, Issue 2
      Author(s): Yanjun Zhao, Sivaprakash Sivaji, Michael C. Chiang, Haadi Ali, Monica Zukowski, Sareen Ali, Bryan Kennedy, Alex Sklyar, Alice Cheng, Zihan Guo, Alexander K. Reed, Ravindra Kodali, Jennifer Borowski, Georgia Frost, Patrick Beukema, Zachary P. Wills
      Compelling evidence links amyloid beta (Aβ) peptide accumulation in the brains of Alzheimer’s disease (AD) patients with the emergence of learning and memory deficits, yet a clear understanding of the events that drive this synaptic pathology are lacking. We present evidence that neurons exposed to Aβ are unable to form new synapses, resulting in learning deficits in vivo. We demonstrate the Nogo receptor family (NgR1–3) acts as Aβ receptors mediating an inhibition of synapse assembly, plasticity, and learning. Live imaging studies reveal Aβ activates NgRs on the dendritic shaft of neurons, triggering an inhibition of calcium signaling. We define T-type calcium channels as a target of Aβ-NgR signaling, mediating Aβ’s inhibitory effects on calcium, synapse assembly, plasticity, and learning. These studies highlight deficits in new synapse assembly as a potential initiator of cognitive pathology in AD, and pinpoint calcium dysregulation mediated by NgRs and T-type channels as key components. Video
      Teaser Amyloid beta peptides inhibit learning, but how they do so is unclear. Zhao et al. demonstrate Aβ blocks learning by inhibiting synapse assembly via the NgR family. Aβ-NgR signaling inhibits synaptogenesis by blocking T-type calcium channels.

      PubDate: 2017-10-14T00:55:04Z
      DOI: 10.1016/j.neuron.2017.09.041
       
  • Paclitaxel Reduces Axonal Bclw to Initiate IP3R1-Dependent Axon
           Degeneration
    • Authors: Sarah E. Pease-Raissi; Maria F. Pazyra-Murphy; Yihang Li; Franziska Wachter; Yusuke Fukuda; Sara J. Fenstermacher; Lauren A. Barclay; Gregory H. Bird; Loren D. Walensky; Rosalind A. Segal
      Pages: 373 - 386.e6
      Abstract: Publication date: 11 October 2017
      Source:Neuron, Volume 96, Issue 2
      Author(s): Sarah E. Pease-Raissi, Maria F. Pazyra-Murphy, Yihang Li, Franziska Wachter, Yusuke Fukuda, Sara J. Fenstermacher, Lauren A. Barclay, Gregory H. Bird, Loren D. Walensky, Rosalind A. Segal
      Chemotherapy-induced peripheral neuropathy (CIPN) is a debilitating side effect of many cancer treatments. The hallmark of CIPN is degeneration of long axons required for transmission of sensory information; axonal degeneration causes impaired tactile sensation and persistent pain. Currently the molecular mechanisms of CIPN are not understood, and there are no available treatments. Here we show that the chemotherapeutic agent paclitaxel triggers CIPN by altering IP3 receptor phosphorylation and intracellular calcium flux, and activating calcium-dependent calpain proteases. Concomitantly paclitaxel impairs axonal trafficking of RNA-granules and reduces synthesis of Bclw (bcl2l2), a Bcl2 family member that binds IP3R1 and restrains axon degeneration. Surprisingly, Bclw or a stapled peptide corresponding to the Bclw BH4 domain interact with axonal IP3R1 and prevent paclitaxel-induced degeneration, while Bcl2 and BclxL cannot do so. Together these data identify a Bclw-IP3R1-dependent cascade that causes axon degeneration and suggest that Bclw-mimetics could provide effective therapy to prevent CIPN.
      Teaser Pease-Raissi et al. show that the anti-apoptotic Bcl2 family protein Bclw plays a unique role in preventing IP3R1-dependent axon degeneration and that the chemotherapeutic agent paclitaxel diminishes trafficking and translation of bclw, thereby removing the brakes on this degenerative cascade.

      PubDate: 2017-10-14T00:55:04Z
      DOI: 10.1016/j.neuron.2017.09.034
       
  • Loss of CLOCK Results in Dysfunction of Brain Circuits Underlying Focal
           Epilepsy
    • Authors: Peijun Li; Xiaoqin Fu; Nathan A. Smith; Julie Ziobro; Julian Curiel; Milagros J. Tenga; Brandon Martin; Samuel Freedman; Christian A. Cea-Del Rio; Livio Oboti; Tammy N. Tsuchida; Chima Oluigbo; Amanda Yaun; Suresh N. Magge; Brent O’Neill; Amy Kao; Tesfaye G. Zelleke; Dewi T. Depositario-Cabacar; Svetlana Ghimbovschi; Susan Knoblach; Chen-Ying Ho; Joshua G. Corbin; Howard P. Goodkin; Stefano Vicini; Molly M. Huntsman; William D. Gaillard; Gregorio Valdez; Judy S. Liu
      Pages: 387 - 401.e6
      Abstract: Publication date: 11 October 2017
      Source:Neuron, Volume 96, Issue 2
      Author(s): Peijun Li, Xiaoqin Fu, Nathan A. Smith, Julie Ziobro, Julian Curiel, Milagros J. Tenga, Brandon Martin, Samuel Freedman, Christian A. Cea-Del Rio, Livio Oboti, Tammy N. Tsuchida, Chima Oluigbo, Amanda Yaun, Suresh N. Magge, Brent O’Neill, Amy Kao, Tesfaye G. Zelleke, Dewi T. Depositario-Cabacar, Svetlana Ghimbovschi, Susan Knoblach, Chen-Ying Ho, Joshua G. Corbin, Howard P. Goodkin, Stefano Vicini, Molly M. Huntsman, William D. Gaillard, Gregorio Valdez, Judy S. Liu
      Because molecular mechanisms underlying refractory focal epilepsy are poorly defined, we performed transcriptome analysis on human epileptogenic tissue. Compared with controls, expression of Circadian Locomotor Output Cycles Kaput (CLOCK) is decreased in epileptogenic tissue. To define the function of CLOCK, we generated and tested the Emx-Cre; Clock flox/flox and PV-Cre; Clock flox/flox mouse lines with targeted deletions of the Clock gene in excitatory and parvalbumin (PV)-expressing inhibitory neurons, respectively. The Emx-Cre; Clock flox/flox mouse line alone has decreased seizure thresholds, but no laminar or dendritic defects in the cortex. However, excitatory neurons from the Emx-Cre; Clock flox/flox mouse have spontaneous epileptiform discharges. Both neurons from Emx-Cre; Clock flox/flox mouse and human epileptogenic tissue exhibit decreased spontaneous inhibitory postsynaptic currents. Finally, video-EEG of Emx-Cre; Clock flox/flox mice reveals epileptiform discharges during sleep and also seizures arising from sleep. Altogether, these data show that disruption of CLOCK alters cortical circuits and may lead to generation of focal epilepsy.
      Teaser Li, Fu, et al. find that expression of the circadian transcription factor CLOCK is decreased in the “seizure focus” from patients with intractable epilepsy and that CLOCK loss of function in cortical excitatory neurons is sufficient for epileptogenesis in mouse.

      PubDate: 2017-10-14T00:55:04Z
      DOI: 10.1016/j.neuron.2017.09.044
       
  • Role of the Astroglial Glutamate Exchanger xCT in Ventral Hippocampus in
           Resilience to Stress
    • Authors: Carla Nasca; Benedetta Bigio; Danielle Zelli; Paolo de Angelis; Timothy Lau; Masahiro Okamoto; Hideyo Soya; Jason Ni; Lars Brichta; Paul Greengard; Rachael L. Neve; Francis S. Lee; Bruce S. McEwen
      Pages: 402 - 413.e5
      Abstract: Publication date: 11 October 2017
      Source:Neuron, Volume 96, Issue 2
      Author(s): Carla Nasca, Benedetta Bigio, Danielle Zelli, Paolo de Angelis, Timothy Lau, Masahiro Okamoto, Hideyo Soya, Jason Ni, Lars Brichta, Paul Greengard, Rachael L. Neve, Francis S. Lee, Bruce S. McEwen
      We demonstrate that stress differentially regulates glutamate homeostasis in the dorsal and ventral hippocampus and identify a role for the astroglial xCT in ventral dentate gyrus (vDG) in stress and antidepressant responses. We provide an RNA-seq roadmap for the stress-sensitive vDG. The transcription factor REST binds to xCT promoter in co-occupancy with the epigenetic marker H3K27ac to regulate expression of xCT, which is also reduced in a genetic mouse model of inherent susceptibility to depressive-like behavior. Pharmacologically, modulating histone acetylation with acetyl-L-carnitine (LAC) or acetyl-N-cysteine (NAC) rapidly increases xCT and activates a network with mGlu2 receptors to prime an enhanced glutamate homeostasis that promotes both pro-resilient and antidepressant-like responses. Pharmacological xCT blockage counteracts NAC prophylactic effects. GFAP+-Cre-dependent overexpression of xCT in vDG mimics pharmacological actions in promoting resilience. This work establishes a mechanism by which vDG protection leads to stress resilience and antidepressant responses via epigenetic programming of an xCT-mGlu2 network.
      Teaser Nasca et al. demonstrate that stress differentially regulates glutamate homeostasis in the dorsal and ventral hippocampus and identify a mechanism by which buffering histone acetylation protects the stress-sensitive ventral dentate gyrus to promote resilience and antidepressant responses via epigenetic programming of an xCT-mGlu2 gene network.

      PubDate: 2017-10-14T00:55:04Z
      DOI: 10.1016/j.neuron.2017.09.020
       
  • The Anterior Insular Cortex→Central Amygdala Glutamatergic Pathway Is
           Critical to Relapse after Contingency Management
    • Authors: Marco Venniro; Daniele Caprioli; Michelle Zhang; Leslie R. Whitaker; Shiliang Zhang; Brandon L. Warren; Carlo Cifani; Nathan J. Marchant; Ofer Yizhar; Jennifer M. Bossert; Cristiano Chiamulera; Marisela Morales; Yavin Shaham
      Pages: 414 - 427.e8
      Abstract: Publication date: 11 October 2017
      Source:Neuron, Volume 96, Issue 2
      Author(s): Marco Venniro, Daniele Caprioli, Michelle Zhang, Leslie R. Whitaker, Shiliang Zhang, Brandon L. Warren, Carlo Cifani, Nathan J. Marchant, Ofer Yizhar, Jennifer M. Bossert, Cristiano Chiamulera, Marisela Morales, Yavin Shaham
      Despite decades of research on neurobiological mechanisms of psychostimulant addiction, the only effective treatment for many addicts is contingency management, a behavioral treatment that uses alternative non-drug reward to maintain abstinence. However, when contingency management is discontinued, most addicts relapse to drug use. The brain mechanisms underlying relapse after cessation of contingency management are largely unknown, and, until recently, an animal model of this human condition did not exist. Here we used a novel rat model, in which the availability of a mutually exclusive palatable food maintains prolonged voluntary abstinence from intravenous methamphetamine self-administration, to demonstrate that the activation of monosynaptic glutamatergic projections from anterior insular cortex to central amygdala is critical to relapse after the cessation of contingency management. We identified the anterior insular cortex-to-central amygdala projection as a new addiction- and motivation-related projection and a potential target for relapse prevention.
      Teaser Venniro et al. demonstrate that the monosynaptic glutamatergic projection from the anterior insular cortex to central amygdala is critical to relapse to methamphetamine seeking after choice-based voluntary abstinence, a rat model of the human condition of relapse after cessation of contingency management.

      PubDate: 2017-10-14T00:55:04Z
      DOI: 10.1016/j.neuron.2017.09.024
       
  • Astrocyte-Secreted Glypican 4 Regulates Release of Neuronal Pentraxin 1
           from Axons to Induce Functional Synapse Formation
    • Authors: Isabella Farhy-Tselnicker; Adriana C.M. van Casteren; Aletheia Lee; Veronica T. Chang; A. Radu Aricescu; Nicola J. Allen
      Pages: 428 - 445.e13
      Abstract: Publication date: 11 October 2017
      Source:Neuron, Volume 96, Issue 2
      Author(s): Isabella Farhy-Tselnicker, Adriana C.M. van Casteren, Aletheia Lee, Veronica T. Chang, A. Radu Aricescu, Nicola J. Allen
      The generation of precise synaptic connections between developing neurons is critical to the formation of functional neural circuits. Astrocyte-secreted glypican 4 induces formation of active excitatory synapses by recruiting AMPA glutamate receptors to the postsynaptic cell surface. We now identify the molecular mechanism of how glypican 4 exerts its effect. Glypican 4 induces release of the AMPA receptor clustering factor neuronal pentraxin 1 from presynaptic terminals by signaling through presynaptic protein tyrosine phosphatase receptor δ. Pentraxin then accumulates AMPA receptors on the postsynaptic terminal forming functional synapses. Our findings reveal a signaling pathway that regulates synaptic activity during central nervous system development and demonstrates a role for astrocytes as organizers of active synaptic connections by coordinating both pre and post synaptic neurons. As mutations in glypicans are associated with neurological disorders, such as autism and schizophrenia, this signaling cascade offers new avenues to modulate synaptic function in disease.
      Teaser Astrocytes are important regulators of synapse formation. Farhy-Tselnicker et al. identify the molecular pathway of active neuronal synapse formation induced by astrocyte-secreted glypican 4. These data functionally link astrocytes to signaling cascades activated in both pre- and postsynaptic neurons.

      PubDate: 2017-10-14T00:55:04Z
      DOI: 10.1016/j.neuron.2017.09.053
       
  • Dynamics of Gut-Brain Communication Underlying Hunger
    • Authors: Lisa R. Beutler; Yiming Chen; Jamie S. Ahn; Yen-Chu Lin; Rachel A. Essner; Zachary A. Knight
      Pages: 461 - 475.e5
      Abstract: Publication date: 11 October 2017
      Source:Neuron, Volume 96, Issue 2
      Author(s): Lisa R. Beutler, Yiming Chen, Jamie S. Ahn, Yen-Chu Lin, Rachel A. Essner, Zachary A. Knight
      Communication between the gut and brain is critical for homeostasis, but how this communication is represented in the dynamics of feeding circuits is unknown. Here we describe nutritional regulation of key neurons that control hunger in vivo. We show that intragastric nutrient infusion rapidly and durably inhibits hunger-promoting AgRP neurons in awake, behaving mice. This inhibition is proportional to the number of calories infused but surprisingly independent of macronutrient identity or nutritional state. We show that three gastrointestinal signals—serotonin, CCK, and PYY—are necessary or sufficient for these effects. In contrast, the hormone leptin has no acute effect on dynamics of these circuits or their sensory regulation but instead induces a slow modulation that develops over hours and is required for inhibition of feeding. These findings reveal how layers of visceral signals operating on distinct timescales converge on hypothalamic feeding circuits to generate a central representation of energy balance.
      Teaser Beutler et al. reveal how nutritional signals regulate the hypothalamic hunger circuit. They show that intragastric nutrients inhibit AgRP neurons rapidly in a way dependent solely on calorie content, whereas the satiety hormone leptin only acts on timescale of hours.

      PubDate: 2017-10-14T00:55:04Z
      DOI: 10.1016/j.neuron.2017.09.043
       
  • Parallel, but Dissociable, Processing in Discrete Corticostriatal Inputs
           Encodes Skill Learning
    • Authors: David A. Kupferschmidt; Konrad Juczewski; Guohong Cui; Kari A. Johnson; David M. Lovinger
      Pages: 476 - 489.e5
      Abstract: Publication date: 11 October 2017
      Source:Neuron, Volume 96, Issue 2
      Author(s): David A. Kupferschmidt, Konrad Juczewski, Guohong Cui, Kari A. Johnson, David M. Lovinger
      Changes in cortical and striatal function underlie the transition from novel actions to refined motor skills. How discrete, anatomically defined corticostriatal projections function in vivo to encode skill learning remains unclear. Using novel fiber photometry approaches to assess real-time activity of associative inputs from medial prefrontal cortex to dorsomedial striatum and sensorimotor inputs from motor cortex to dorsolateral striatum, we show that associative and sensorimotor inputs co-engage early in action learning and disengage in a dissociable manner as actions are refined. Disengagement of associative, but not sensorimotor, inputs predicts individual differences in subsequent skill learning. Divergent somatic and presynaptic engagement in both projections during early action learning suggests potential learning-related in vivo modulation of presynaptic corticostriatal function. These findings reveal parallel processing within associative and sensorimotor circuits that challenges and refines existing views of corticostriatal function and expose neuronal projection- and compartment-specific activity dynamics that encode and predict action learning.
      Teaser Kupferschmidt et al. probe real-time activity dynamics of associative and sensorimotor cortical projections to striatum during skill learning. They reveal substantive co-engagement and dissociable disengagement of the two pathways across learning and find that associative pathway disengagement predicts subsequent skill learning.

      PubDate: 2017-10-14T00:55:04Z
      DOI: 10.1016/j.neuron.2017.09.040
       
  • Increased Prevalence of Calcium Transients across the Dendritic Arbor
           during Place Field Formation
    • Authors: Mark E.J. Sheffield; Michael D. Adoff; Daniel A. Dombeck
      Pages: 490 - 504.e5
      Abstract: Publication date: 11 October 2017
      Source:Neuron, Volume 96, Issue 2
      Author(s): Mark E.J. Sheffield, Michael D. Adoff, Daniel A. Dombeck
      Hippocampal place cell ensembles form a cognitive map of space during exposure to novel environments. However, surprisingly little evidence exists to support the idea that synaptic plasticity in place cells is involved in forming new place fields. Here we used high-resolution functional imaging to determine the signaling patterns in CA1 soma, dendrites, and axons associated with place field formation when mice are exposed to novel virtual environments. We found that putative local dendritic spikes often occur prior to somatic place field firing. Subsequently, the first occurrence of somatic place field firing was associated with widespread regenerative dendritic events, which decreased in prevalence with increased novel environment experience. This transient increase in regenerative events was likely facilitated by a reduction in dendritic inhibition. Since regenerative dendritic events can provide the depolarization necessary for Hebbian potentiation, these results suggest that activity-dependent synaptic plasticity underlies the formation of many CA1 place fields.
      Teaser Sheffield et al. reveal microscopic plasticity-related events occurring in hippocampal neurons that likely underlie spatial memory formation when animals encounter new environments.

      PubDate: 2017-10-14T00:55:04Z
      DOI: 10.1016/j.neuron.2017.09.029
       
  • Pyramidal Cell-Interneuron Circuit Architecture and Dynamics in
           Hippocampal Networks
    • Authors: Daniel Fine English; Sam McKenzie; Talfan Evans; Kanghwan Kim; Euisik Yoon; György Buzsáki
      Pages: 505 - 520.e7
      Abstract: Publication date: 11 October 2017
      Source:Neuron, Volume 96, Issue 2
      Author(s): Daniel Fine English, Sam McKenzie, Talfan Evans, Kanghwan Kim, Euisik Yoon, György Buzsáki
      Excitatory control of inhibitory neurons is poorly understood due to the difficulty of studying synaptic connectivity in vivo. We inferred such connectivity through analysis of spike timing and validated this inference using juxtacellular and optogenetic control of presynaptic spikes in behaving mice. We observed that neighboring CA1 neurons had stronger connections and that superficial pyramidal cells projected more to deep interneurons. Connection probability and strength were skewed, with a minority of highly connected hubs. Divergent presynaptic connections led to synchrony between interneurons. Synchrony of convergent presynaptic inputs boosted postsynaptic drive. Presynaptic firing frequency was read out by postsynaptic neurons through short-term depression and facilitation, with individual pyramidal cells and interneurons displaying a diversity of spike transmission filters. Additionally, spike transmission was strongly modulated by prior spike timing of the postsynaptic cell. These results bridge anatomical structure with physiological function.
      Teaser English, McKenzie, et al. identify, validate, and quantify monosynaptic connections between pyramidal cells and interneurons, using the spike timing of pre- and postsynaptic neurons in vivo. Their large-scale method uncovers a backbone of connectivity rules in the hippocampus CA1 circuit.

      PubDate: 2017-10-14T00:55:04Z
      DOI: 10.1016/j.neuron.2017.09.033
       
  • A Meta-Analysis Suggests Different Neural Correlates for Implicit and
           Explicit Learning
    • Authors: Roman F. Loonis; Scott L. Brincat; Evan G. Antzoulatos; Earl K. Miller
      Pages: 521 - 534.e7
      Abstract: Publication date: 11 October 2017
      Source:Neuron, Volume 96, Issue 2
      Author(s): Roman F. Loonis, Scott L. Brincat, Evan G. Antzoulatos, Earl K. Miller
      A meta-analysis of non-human primates performing three different tasks (Object-Match, Category-Match, and Category-Saccade associations) revealed signatures of explicit and implicit learning. Performance improved equally following correct and error trials in the Match (explicit) tasks, but it improved more after correct trials in the Saccade (implicit) task, a signature of explicit versus implicit learning. Likewise, error-related negativity, a marker for error processing, was greater in the Match (explicit) tasks. All tasks showed an increase in alpha/beta (10–30 Hz) synchrony after correct choices. However, only the implicit task showed an increase in theta (3–7 Hz) synchrony after correct choices that decreased with learning. In contrast, in the explicit tasks, alpha/beta synchrony increased with learning and decreased thereafter. Our results suggest that explicit versus implicit learning engages different neural mechanisms that rely on different patterns of oscillatory synchrony.
      Teaser Loonis et al. find that explicit and implicit learning use feedback about correct choices versus errors differently. Implicit learning relies more on theta synchrony (3–7 Hz) while explicit learning relies on alpha/beta synchrony (10–30 Hz).

      PubDate: 2017-10-14T00:55:04Z
      DOI: 10.1016/j.neuron.2017.09.032
       
  • Revealing a Role for NMDA Receptors in Regulating STN Inputs following the
           Loss of Dopamine
    • Authors: Aphroditi A. Mamaligas; Christopher P. Ford
      Pages: 1227 - 1229
      Abstract: Publication date: 13 September 2017
      Source:Neuron, Volume 95, Issue 6
      Author(s): Aphroditi A. Mamaligas, Christopher P. Ford
      In this issue of Neuron, Chu et al. (2017) show that dopamine depletion using a 6-OHDA model causes a decrease in hyperdirect inputs from the motor cortex directly to the STN and that rescuing this loss alleviates Parkinsonian symptoms.
      Teaser In this issue of Neuron, Chu et al. (2017) show that dopamine depletion using a 6-OHDA model causes a decrease in hyperdirect inputs from the motor cortex directly to the STN and that rescuing this loss alleviates Parkinsonian symptoms.

      PubDate: 2017-09-18T08:09:07Z
      DOI: 10.1016/j.neuron.2017.08.041
       
  • Smells Familiar: Pheromone-Induced Neurotransmitter Switching Mediates
           Social Discrimination
    • Authors: Michael Gliksberg; Gil Levkowitz
      Pages: 1229 - 1231
      Abstract: Publication date: 13 September 2017
      Source:Neuron, Volume 95, Issue 6
      Author(s): Michael Gliksberg, Gil Levkowitz
      Social discrimination is regulated by a variety of sensory inputs. In this issue of Neuron, Dulcis et al. (2017) show that chemosensory-mediated kin preference in Xenopus is determined by changes in neurotransmitter composition, which are regulated by specific microRNAs.
      Teaser Social discrimination is regulated by a variety of sensory inputs. In this issue of Neuron, Dulcis et al. show that chemosensory-mediated kin preference in Xenopus is determined by changes in neurotransmitter composition, which are regulated by specific microRNAs.

      PubDate: 2017-09-18T08:09:07Z
      DOI: 10.1016/j.neuron.2017.08.044
       
  • Resolving CNS mRNA Heterogeneity: Examining mRNA Alternative
           Polyadenylation at a Cell-Type-Specific Level
    • Authors: Martine Therrien; Myriam Heiman
      Pages: 1232 - 1233
      Abstract: Publication date: 13 September 2017
      Source:Neuron, Volume 95, Issue 6
      Author(s): Martine Therrien, Myriam Heiman
      Alternative polyadenylation often regulates mRNA isoform usage. In this issue of Neuron, Hwang et al. (2017) describe a powerful new cell-type-specific methodology, cTag-PAPERCLIP, which can be used to study alternative polyadenylation in the CNS.
      Teaser Alternative polyadenylation often regulates mRNA isoform usage. In this issue of Neuron, Hwang et al. (2017) describe a powerful new cell-type-specific methodology, cTag-PAPERCLIP, which can be used to study alternative polyadenylation in the CNS.

      PubDate: 2017-09-18T08:09:07Z
      DOI: 10.1016/j.neuron.2017.08.045
       
  • Movement Coding at the Mesoscale in Posterior Parietal Cortex
    • Authors: Jonathan R. Whitlock
      Pages: 1234 - 1236
      Abstract: Publication date: 13 September 2017
      Source:Neuron, Volume 95, Issue 6
      Author(s): Jonathan R. Whitlock
      Neural correlates of movement planning have been studied most commonly using signals isolated from single cells. However, in this issue of Neuron, Wilber et al. (2017) show that movement trajectories are encoded and replayed in the collective activity of thousands of cells at a time in the posterior parietal cortex.
      Teaser Neural correlates of movement planning have been studied most commonly using signals isolated from single-cells. However, in this issue of Neuron, Wilber et al. (2017) show that movement trajectories are encoded and replayed in the collective activity of thousands of cells at a time in the posterior parietal cortex.

      PubDate: 2017-09-18T08:09:07Z
      DOI: 10.1016/j.neuron.2017.08.042
       
  • “Beginning with the Smallest Intake”: Children’s Brain Development
           and the Role of Neuroscience in Global Environmental Health
    • Authors: Kam Sripada
      Pages: 1242 - 1245
      Abstract: Publication date: 13 September 2017
      Source:Neuron, Volume 95, Issue 6
      Author(s): Kam Sripada
      Early exposure to environmental toxins like lead, air pollution, and arsenic can have long-lasting and irreversible consequences for children’s neurodevelopment, especially in the developing world. Though the number of pollutants increases each year, some neuroscientists are forging partnerships to improve measurement, raise awareness, and promote global health.
      Teaser Early exposure to environmental toxins like lead, air pollution, and arsenic can have long-lasting and irreversible consequences for children’s neurodevelopment, especially in the developing world. Though the number of pollutants increases each year, some neuroscientists are forging partnerships to improve measurement, raise awareness, and promote global health.

      PubDate: 2017-09-18T08:09:07Z
      DOI: 10.1016/j.neuron.2017.08.009
       
  • Neuroimmunology of Traumatic Brain Injury: Time for a Paradigm Shift
    • Authors: Yasir N. Jassam; Saef Izzy; Michael Whalen; Dorian B. McGavern; Joseph El Khoury
      Pages: 1246 - 1265
      Abstract: Publication date: 13 September 2017
      Source:Neuron, Volume 95, Issue 6
      Author(s): Yasir N. Jassam, Saef Izzy, Michael Whalen, Dorian B. McGavern, Joseph El Khoury
      Traumatic brain injury (TBI) is a leading cause of morbidity and disability, with a considerable socioeconomic burden. Heterogeneity of pathoanatomical subtypes and diversity in the pathogenesis and extent of injury contribute to differences in the course and outcome of TBI. Following the primary injury, extensive and lasting damage is sustained through a complex cascade of events referred to as “secondary injury.” Neuroinflammation is proposed as an important manipulable aspect of secondary injury in animal and human studies. Because neuroinflammation can be detrimental or beneficial, before developing immunomodulatory therapies, it is necessary to better understand the timing and complexity of the immune responses that follow TBI. With a rapidly increasing body of literature, there is a need for a clear summary of TBI neuroimmunology. This review presents our current understanding of the immune response to TBI in a chronological and compartment-based manner, highlighting early changes in gene expression and initial signaling pathways that lead to activation of innate and adaptive immunity. Based on recent advances in our understanding of innate immune cell activation, we propose a new paradigm to study innate immune cells following TBI that moves away from the existing M1/M2 classification of activation states toward a stimulus- and disease-specific understanding of polarization state based on transcriptomic and proteomic profiling.
      Teaser Jassam et al. review advances in the role of neuroinflammation in traumatic brain injury (TBI) in a chronological and compartment-based manner. The authors propose a new paradigm that moves away from the existing M1/M2 approach to classify microglia in TBI toward a proteomics- and transcriptomics-based approach.

      PubDate: 2017-09-18T08:09:07Z
      DOI: 10.1016/j.neuron.2017.07.010
       
  • Whole-Cell Recording of Neuronal Membrane Potential during Behavior
    • Authors: Carl C.H. Petersen
      Pages: 1266 - 1281
      Abstract: Publication date: 13 September 2017
      Source:Neuron, Volume 95, Issue 6
      Author(s): Carl C.H. Petersen
      Neuronal membrane potential is of fundamental importance for the mechanistic understanding of brain function. This review discusses progress in whole-cell patch-clamp recordings for low-noise measurement of neuronal membrane potential in awake behaving animals. Whole-cell recordings can be combined with two-photon microscopy to target fluorescently labeled neurons, revealing cell-type-specific membrane potential dynamics of retrogradely or genetically labeled neurons. Dual whole-cell recordings reveal behavioral modulation of membrane potential synchrony and properties of synaptic transmission in vivo. Optogenetic manipulations are also readily integrated with whole-cell recordings, providing detailed information about the effect of specific perturbations on the membrane potential of diverse types of neurons. Exciting developments for future behavioral experiments include dendritic whole-cell recordings and imaging, and use of the whole-cell recording pipette for single-cell delivery of drugs and DNA, as well as RNA expression profiling. Whole-cell recordings therefore offer unique opportunities for investigating the neuronal circuits and synaptic mechanisms driving membrane potential dynamics during behavior.
      Teaser In this Primer, Petersen discusses current and future applications of the whole-cell patch-clamp recording technique for studying the cellular and synaptic circuit mechanisms driving neuronal membrane potential dynamics in awake behaving animals.

      PubDate: 2017-09-18T08:09:07Z
      DOI: 10.1016/j.neuron.2017.06.049
       
  • RAN Translation Regulated by Muscleblind Proteins in Myotonic Dystrophy
           Type 2
    • Authors: Tao Zu; John D. Cleary; Yuanjing Liu; Monica Bañez-Coronel; Jodi L. Bubenik; Fatma Ayhan; Tetsuo Ashizawa; Guangbin Xia; H. Brent Clark; Anthony T. Yachnis; Maurice S. Swanson; Laura P.W. Ranum
      Pages: 1292 - 1305.e5
      Abstract: Publication date: 13 September 2017
      Source:Neuron, Volume 95, Issue 6
      Author(s): Tao Zu, John D. Cleary, Yuanjing Liu, Monica Bañez-Coronel, Jodi L. Bubenik, Fatma Ayhan, Tetsuo Ashizawa, Guangbin Xia, H. Brent Clark, Anthony T. Yachnis, Maurice S. Swanson, Laura P.W. Ranum
      Several microsatellite-expansion diseases are characterized by the accumulation of RNA foci and RAN proteins, raising the possibility of a mechanistic connection. We explored this question using myotonic dystrophy type 2, a multisystemic disease thought to be primarily caused by RNA gain-of-function effects. We demonstrate that the DM2 CCTG⋅CAGG expansion expresses sense and antisense tetrapeptide poly-(LPAC) and poly-(QAGR) RAN proteins, respectively. In DM2 autopsy brains, LPAC is found in neurons, astrocytes, and glia in gray matter, and antisense QAGR proteins accumulate within white matter. LPAC and QAGR proteins are toxic to cells independent of RNA gain of function. RNA foci and nuclear sequestration of CCUG transcripts by MBNL1 is inversely correlated with LPAC expression. These data suggest a model that involves nuclear retention of expansion RNAs by RNA-binding proteins (RBPs) and an acute phase in which expansion RNAs exceed RBP sequestration capacity, are exported to the cytoplasm, and undergo RAN translation. Video
      Teaser Zu et al. show that the DM2 CCTG⋅CAGG expansion expresses sense and antisense poly-(LPAC) and poly-(QAGR) RAN proteins. Nuclear sequestration of CCUG transcripts by MBNL1 reduces poly-(LPAC) RAN proteins, and sequestration failure leads to upregulation of RAN proteins.

      PubDate: 2017-09-18T08:09:07Z
      DOI: 10.1016/j.neuron.2017.08.039
       
  • Loss of Hyperdirect Pathway Cortico-Subthalamic Inputs Following
           Degeneration of Midbrain Dopamine Neurons
    • Authors: Hong-Yuan Chu; Eileen L. McIver; Ryan F. Kovaleski; Jeremy F. Atherton; Mark D. Bevan
      Pages: 1306 - 1318.e5
      Abstract: Publication date: 13 September 2017
      Source:Neuron, Volume 95, Issue 6
      Author(s): Hong-Yuan Chu, Eileen L. McIver, Ryan F. Kovaleski, Jeremy F. Atherton, Mark D. Bevan
      The motor symptoms of Parkinson’s disease (PD) are linked to abnormally correlated and coherent activity in the cortex and subthalamic nucleus (STN). However, in parkinsonian mice we found that cortico-STN transmission strength had diminished by 50%–75% through loss of axo-dendritic and axo-spinous synapses, was incapable of long-term potentiation, and less effectively patterned STN activity. Optogenetic, chemogenetic, genetic, and pharmacological interrogation suggested that downregulation of cortico-STN transmission in PD mice was triggered by increased striato-pallidal transmission, leading to disinhibition of the STN and increased activation of STN NMDA receptors. Knockdown of STN NMDA receptors, which also suppresses proliferation of GABAergic pallido-STN inputs in PD mice, reduced loss of cortico-STN transmission and patterning and improved motor function. Together, the data suggest that loss of dopamine triggers a maladaptive shift in the balance of synaptic excitation and inhibition in the STN, which contributes to parkinsonian activity and motor dysfunction.
      Teaser Chu et al. report that, following loss of dopamine, activation of subthalamic nucleus (STN) NMDA receptors triggers a maladaptive reduction in cortico-STN transmission.

      PubDate: 2017-09-18T08:09:07Z
      DOI: 10.1016/j.neuron.2017.08.038
       
  • cTag-PAPERCLIP Reveals Alternative Polyadenylation Promotes Cell-Type
           Specific Protein Diversity and Shifts Araf Isoforms with Microglia
           Activation
    • Authors: Hun-Way Hwang; Yuhki Saito; Christopher Y. Park; Nathalie E. Blachère; Yoko Tajima; John J. Fak; Ilana Zucker-Scharff; Robert B. Darnell
      Pages: 1334 - 1349.e5
      Abstract: Publication date: 13 September 2017
      Source:Neuron, Volume 95, Issue 6
      Author(s): Hun-Way Hwang, Yuhki Saito, Christopher Y. Park, Nathalie E. Blachère, Yoko Tajima, John J. Fak, Ilana Zucker-Scharff, Robert B. Darnell
      Alternative polyadenylation (APA) is increasingly recognized to regulate gene expression across different cell types, but obtaining APA maps from individual cell types typically requires prior purification, a stressful procedure that can itself alter cellular states. Here, we describe a new platform, cTag-PAPERCLIP, that generates APA profiles from single cell populations in intact tissues; cTag-PAPERCLIP requires no tissue dissociation and preserves transcripts in native states. Applying cTag-PAPERCLIP to profile four major cell types in the mouse brain revealed common APA preferences between excitatory and inhibitory neurons distinct from astrocytes and microglia, regulated in part by neuron-specific RNA-binding proteins NOVA2 and PTBP2. We further identified a role of APA in switching Araf protein isoforms during microglia activation, impacting production of downstream inflammatory cytokines. Our results demonstrate the broad applicability of cTag-PAPERCLIP and a previously undiscovered role of APA in contributing to protein diversity between different cell types and cellular states within the brain.
      Teaser Hwang et al. develop cTag-PAPERCLIP to profile mRNA 3′ ends in individual cell types from intact tissues in vivo. They use cTag-PAPERCLIP to show that mRNA alternative polyadenylation contributes to protein diversity between different cell types and cellular states within the brain.

      PubDate: 2017-09-18T08:09:07Z
      DOI: 10.1016/j.neuron.2017.08.024
       
  • A Fully Automated Approach to Spike Sorting
    • Authors: Jason E. Chung; Jeremy F. Magland; Alex H. Barnett; Vanessa M. Tolosa; Angela C. Tooker; Kye Y. Lee; Kedar G. Shah; Sarah H. Felix; Loren M. Frank; Leslie F. Greengard
      Pages: 1381 - 1394.e6
      Abstract: Publication date: 13 September 2017
      Source:Neuron, Volume 95, Issue 6
      Author(s): Jason E. Chung, Jeremy F. Magland, Alex H. Barnett, Vanessa M. Tolosa, Angela C. Tooker, Kye Y. Lee, Kedar G. Shah, Sarah H. Felix, Loren M. Frank, Leslie F. Greengard
      Understanding the detailed dynamics of neuronal networks will require the simultaneous measurement of spike trains from hundreds of neurons (or more). Currently, approaches to extracting spike times and labels from raw data are time consuming, lack standardization, and involve manual intervention, making it difficult to maintain data provenance and assess the quality of scientific results. Here, we describe an automated clustering approach and associated software package that addresses these problems and provides novel cluster quality metrics. We show that our approach has accuracy comparable to or exceeding that achieved using manual or semi-manual techniques with desktop central processing unit (CPU) runtimes faster than acquisition time for up to hundreds of electrodes. Moreover, a single choice of parameters in the algorithm is effective for a variety of electrode geometries and across multiple brain regions. This algorithm has the potential to enable reproducible and automated spike sorting of larger scale recordings than is currently possible.
      Teaser Chung, Magland, et al. present MountainSort, a new fully automatic spike sorting package with a powerful GUI. MountainSort has accuracy comparable to current methods and runtimes faster than real time, enabling automatic and reproducible spike sorting for high-density extracellular recordings.

      PubDate: 2017-09-18T08:09:07Z
      DOI: 10.1016/j.neuron.2017.08.030
       
  • Dopamine Neurons Respond to Errors in the Prediction of Sensory Features
           of Expected Rewards
    • Authors: Yuji K. Takahashi; Hannah M. Batchelor; Bing Liu; Akash Khanna; Marisela Morales; Geoffrey Schoenbaum
      Pages: 1395 - 1405.e3
      Abstract: Publication date: 13 September 2017
      Source:Neuron, Volume 95, Issue 6
      Author(s): Yuji K. Takahashi, Hannah M. Batchelor, Bing Liu, Akash Khanna, Marisela Morales, Geoffrey Schoenbaum
      Midbrain dopamine neurons have been proposed to signal prediction errors as defined in model-free reinforcement learning algorithms. While these algorithms have been extremely powerful in interpreting dopamine activity, these models do not register any error unless there is a difference between the value of what is predicted and what is received. Yet learning often occurs in response to changes in the unique features that characterize what is received, sometimes with no change in its value at all. Here, we show that classic error-signaling dopamine neurons also respond to changes in value-neutral sensory features of an expected reward. This suggests that dopamine neurons have access to a wider variety of information than contemplated by the models currently used to interpret their activity and that, while their firing may conform to predictions of these models in some cases, they are not restricted to signaling errors in the prediction of value.
      Teaser In the current study, Takahashi et al. show that dopamine neurons signal errors in predicting the sensory features of reward independent of value. These data indicate a broader role for dopaminergic errors in learning than currently proposed.

      PubDate: 2017-09-18T08:09:07Z
      DOI: 10.1016/j.neuron.2017.08.025
       
  • A Sensorimotor Circuit in Mouse Cortex for Visual Flow Predictions
    • Authors: Marcus Leinweber; Daniel R. Ward; Jan M. Sobczak; Alexander Attinger; Georg B. Keller
      Pages: 1420 - 1432.e5
      Abstract: Publication date: 13 September 2017
      Source:Neuron, Volume 95, Issue 6
      Author(s): Marcus Leinweber, Daniel R. Ward, Jan M. Sobczak, Alexander Attinger, Georg B. Keller
      The cortex is organized as a hierarchical processing structure. Feedback from higher levels of the hierarchy, known as top-down signals, have been shown to be involved in attentional and contextual modulation of sensory responses. Here we argue that top-down input to the primary visual cortex (V1) from A24b and the adjacent secondary motor cortex (M2) signals a prediction of visual flow based on motor output. A24b/M2 sends a dense and topographically organized projection to V1 that targets most neurons in layer 2/3. By imaging the activity of A24b/M2 axons in V1 of mice learning to navigate a 2D virtual environment, we found that their activity was strongly correlated with locomotion and resulting visual flow feedback in an experience-dependent manner. When mice were trained to navigate a left-right inverted virtual environment, correlations of neural activity with behavior reversed to match visual flow. These findings are consistent with a predictive coding interpretation of visual processing.
      Teaser Top-down input to visual cortex from prefrontal areas is involved in attentional and contextual modulation of sensory responses. Leinweber et al. argue that, in the mouse, top-down input to V1 from A24b/M2 carries a prediction of visual flow given movement.

      PubDate: 2017-09-18T08:09:07Z
      DOI: 10.1016/j.neuron.2017.08.036
       
  • Ligand-Selective Wnt Receptor Complexes in CNS Blood Vessels: RECK and
           GPR124 Plugged In
    • Authors: Harald J. Junge
      Pages: 983 - 985
      Abstract: Publication date: 30 August 2017
      Source:Neuron, Volume 95, Issue 5
      Author(s): Harald J. Junge
      CNS angiogenesis and blood-brain barrier integrity are controlled by the canonical Wnt pathway. In this issue of Neuron, Cho et al. (2017) use advanced mouse genetics and biochemical experiments to unravel the ligand-specific association of membrane proteins GPR124 and RECK with Wnt receptor complexes.
      Teaser CNS angiogenesis and blood-brain barrier integrity are controlled by the canonical Wnt pathway. In this issue of Neuron, Cho et al. (2017) use advanced mouse genetics and biochemical experiments to unravel the ligand-specific association of membrane proteins GPR124 and RECK with Wnt receptor complexes.

      PubDate: 2017-08-31T08:35:03Z
      DOI: 10.1016/j.neuron.2017.08.026
       
  • To Fight or Not to Fight
    • Authors: Talmo D. Pereira; Mala Murthy
      Pages: 986 - 988
      Abstract: Publication date: 30 August 2017
      Source:Neuron, Volume 95, Issue 5
      Author(s): Talmo D. Pereira, Mala Murthy
      In this issue of Neuron, Watanabe et al. (2017) uncover how octopamine, an invertebrate norepinephrine analog, modulates the neural pathways that bias Drosophila males toward aggression.
      Teaser In this issue of Neuron, Watanabe et al. uncover how octopamine, an invertebrate norepinephrine analog, modulates the neural pathways that bias Drosophila males toward aggression.

      PubDate: 2017-08-31T08:35:03Z
      DOI: 10.1016/j.neuron.2017.08.029
       
  • Synapse-Specific Encoding of Fear Memory in the Amygdala
    • Authors: Stephen Maren
      Pages: 988 - 990
      Abstract: Publication date: 30 August 2017
      Source:Neuron, Volume 95, Issue 5
      Author(s): Stephen Maren
      Input specificity is a fundamental property of long-term potentiation (LTP), but it is not known if learning is mediated by synapse-specific plasticity. Kim and Cho (2017) now show that fear conditioning is mediated by synapse-specific LTP in the amygdala, allowing animals to discriminate stimuli that predict threat from those that do not.
      Teaser Input specificity is a fundamental property of long-term potentiation (LTP), but it is not known if learning is mediated by synapse-specific plasticity. Kim and Cho (2017) now show that fear conditioning is mediated by synapse-specific LTP in the amygdala, allowing animals to discriminate stimuli that predict threat from those that do not.

      PubDate: 2017-08-31T08:35:03Z
      DOI: 10.1016/j.neuron.2017.08.020
       
  • Differential Regulation of Evoked and Spontaneous Release by Presynaptic
           NMDA Receptors
    • Authors: Therése Abrahamsson; Christina You Chien Chou; Si Ying Li; Adamo Mancino; Rui Ponte Costa; Jennifer Anne Brock; Erin Nuro; Katherine Anne Buchanan; Dale Elgar; Arne Vladimir Blackman; Adam Tudor-Jones; Julia Oyrer; William Todd Farmer; Keith Kazuo Murai; Per Jesper Sjöström
      Abstract: Publication date: Available online 12 October 2017
      Source:Neuron
      Author(s): Therése Abrahamsson, Christina You Chien Chou, Si Ying Li, Adamo Mancino, Rui Ponte Costa, Jennifer Anne Brock, Erin Nuro, Katherine Anne Buchanan, Dale Elgar, Arne Vladimir Blackman, Adam Tudor-Jones, Julia Oyrer, William Todd Farmer, Keith Kazuo Murai, Per Jesper Sjöström
      Presynaptic NMDA receptors (preNMDARs) control synaptic release, but it is not well understood how. Rab3-interacting molecules (RIMs) provide scaffolding at presynaptic active zones and are involved in vesicle priming. Moreover, c-Jun N-terminal kinase (JNK) has been implicated in regulation of spontaneous release. We demonstrate that, at connected layer 5 pyramidal cell pairs of developing mouse visual cortex, Mg2+-sensitive preNMDAR signaling upregulates replenishment of the readily releasable vesicle pool during high-frequency firing. In conditional RIM1αβ deletion mice, preNMDAR upregulation of vesicle replenishment was abolished, yet preNMDAR control of spontaneous release was unaffected. Conversely, JNK2 blockade prevented Mg2+-insensitive preNMDAR signaling from regulating spontaneous release, but preNMDAR control of evoked release remained intact. We thus discovered that preNMDARs signal differentially to control evoked and spontaneous release by independent and non-overlapping mechanisms. Our findings suggest that preNMDARs may sometimes signal metabotropically and support the emerging principle that evoked and spontaneous release are distinct processes.
      Teaser A long-standing question has been how presynaptic NMDA receptors influence high-frequency evoked neurotransmission but spontaneous release at low rates. Providing resolution, Abrahamsson et al. show that these receptors regulate evoked and spontaneous release via distinct RIM1αβ- and JNK2-dependent mechanisms, respectively.

      PubDate: 2017-10-14T00:55:04Z
      DOI: 10.1016/j.neuron.2017.09.030
       
  • Compulsivity Reveals a Novel Dissociation between Action and Confidence
    • Authors: Matilde M. Vaghi; Fabrice Luyckx; Akeem Sule; Naomi A. Fineberg; Trevor W. Robbins; Benedetto De Martino
      Abstract: Publication date: Available online 28 September 2017
      Source:Neuron
      Author(s): Matilde M. Vaghi, Fabrice Luyckx, Akeem Sule, Naomi A. Fineberg, Trevor W. Robbins, Benedetto De Martino
      Confidence and actions are normally tightly interwoven—if I am sure that it is going to rain, I will take an umbrella—therefore, it is difficult to understand their interplay. Stimulated by the ego-dystonic nature of obsessive-compulsive disorder (OCD), where compulsive actions are recognized as disproportionate, we hypothesized that action and confidence might be independently updated during learning. Participants completed a predictive-inference task designed to identify how action and confidence evolve in response to surprising changes in the environment. While OCD patients (like controls) correctly updated their confidence according to changes in the environment, their actions (unlike those of controls) mostly disregarded this knowledge. Therefore, OCD patients develop an accurate, internal model of the environment but fail to use it to guide behavior. Results demonstrated a novel dissociation between confidence and action, suggesting a cognitive architecture whereby confidence estimates can accurately track the statistic of the environment independently from performance.
      Teaser Vaghi, Luyckx et al. provide evidences of a novel dissociation between confidence and action in OCD patients with confidence accessing information that is not used to guide action.

      PubDate: 2017-09-30T03:20:09Z
      DOI: 10.1016/j.neuron.2017.09.006
       
  • Active Mechanisms of Vibration Encoding and Frequency Filtering in Central
           Mechanosensory Neurons
    • Authors: Anthony W. Azevedo; Rachel I. Wilson
      Abstract: Publication date: Available online 21 September 2017
      Source:Neuron
      Author(s): Anthony W. Azevedo, Rachel I. Wilson
      To better understand biophysical mechanisms of mechanosensory processing, we investigated two cell types in the Drosophila brain (A2 and B1 cells) that are postsynaptic to antennal vibration receptors. A2 cells receive excitatory synaptic currents in response to both directions of movement: thus, twice per vibration cycle. The membrane acts as a low-pass filter, so that voltage and spiking mainly track the vibration envelope rather than individual cycles. By contrast, B1 cells are excited by only forward or backward movement, meaning they are sensitive to vibration phase. They receive oscillatory synaptic currents at the stimulus frequency, and they bandpass filter these inputs to favor specific frequencies. Different cells prefer different frequencies, due to differences in their voltage-gated conductances. Both Na+ and K+ conductances suppress low-frequency synaptic inputs, so cells with larger voltage-gated conductances prefer higher frequencies. These results illustrate how membrane properties and voltage-gated conductances can extract distinct stimulus features into parallel channels.
      Teaser Azevedo and Wilson show that coarse and fine features of mechanical vibrations are encoded in parallel channels in the Drosophila brain. The “fine-feature” cells exploit the kinetic properties of voltage-gated ion channels to extract specific frequencies from their synaptic inputs.

      PubDate: 2017-09-24T08:12:10Z
      DOI: 10.1016/j.neuron.2017.09.004
       
  • Earl K. Miller
    • Abstract: Publication date: 13 September 2017
      Source:Neuron, Volume 95, Issue 6
      Earl Miller studies the neural basis of high-level cognitive functions. In an interview with Neuron, he discusses the need for a holistic approach to figure out the brain, how ideas don’t happen in a vacuum, and the challenge of convincing the public that science produces facts; he also shares an open invitation to see Pavlov’s Dogz.
      Teaser Earl Miller studies the neural basis of high-level cognitive functions. In an interview with Neuron, he discusses the need for a holistic approach to figure out the brain, how ideas don’t happen in a vacuum, and the challenge of convincing the public that science produces facts; he also shares an open invitation to see Pavlov’s Dogz.

      PubDate: 2017-09-18T08:09:07Z
       
  • David Rowitch
    • Abstract: Publication date: 13 September 2017
      Source:Neuron, Volume 95, Issue 6
      David Rowitch is a physician-scientist studying developmental genetics of glia in health and disease. In an interview with Neuron, he talks about the importance of single-cell and whole-genome sequencing and the need for raw data sharing and tissue banks encompassing human brain development and disease, and encourages active crosstalk between basic scientists and clinicians.
      Teaser David Rowitch is a physician-scientist studying developmental genetics of glia in health and disease. In an interview with Neuron, he talks about the importance of single-cell and whole-genome sequencing and the need for raw data sharing and tissue banks encompassing human brain development and disease, and encourages active crosstalk between basic scientists and clinicians.

      PubDate: 2017-09-18T08:09:07Z
       
  • Laminar Organization of Encoding and Memory Reactivation in the Parietal
           Cortex
    • Authors: Aaron Wilber; Ivan Skelin Wei Bruce McNaughton
      Abstract: Publication date: 13 September 2017
      Source:Neuron, Volume 95, Issue 6
      Author(s): Aaron A. Wilber, Ivan Skelin, Wei Wu, Bruce L. McNaughton
      Egocentric neural coding has been observed in parietal cortex (PC), but its topographical and laminar organization is not well characterized. We used multi-site recording to look for evidence of local clustering and laminar consistency of linear and angular velocity encoding in multi-neuronal spiking activity (MUA) and in the high-frequency (300–900 Hz) component of the local field potential (HF-LFP), believed to reflect local spiking activity. Rats were trained to run many trials on a large circular platform, either to LED-cued goal locations or as a spatial sequence from memory. Tuning to specific self-motion states was observed and exhibited distinct cortical depth-invariant coding properties. These patterns of collective local and laminar activation during behavior were reactivated in compressed form during post-experience sleep and temporally coupled to cortical delta waves and hippocampal sharp-wave ripples. Thus, PC neuron motion encoding is consistent across cortical laminae, and this consistency is maintained during memory reactivation.
      Teaser Wilber, Skelin, et al. use multi-site recordings to demonstrate tuning across large populations of cells organized into modules encoding specific movements in parietal cortex. Activity patterns were shown to reactivate during post-experience sleep and were temporally coupled to hippocampal reactivation.

      PubDate: 2017-09-18T08:09:07Z
       
  • Stable Positioning of Unc13 Restricts Synaptic Vesicle Fusion to Defined
           Release Sites to Promote Synchronous Neurotransmission
    • Authors: Suneel Reddy-Alla; Mathias A. Böhme; Eric Reynolds; Christina Beis; Andreas T. Grasskamp; Malou M. Mampell; Marta Maglione; Meida Jusyte; Ulises Rey; Husam Babikir; Anthony W. McCarthy; Christine Quentin; Tanja Matkovic; Dominique Dufour Bergeron; Zeeshan Mushtaq; Fabian Göttfert; David Owald; Thorsten Mielke; Stefan W. Hell; Stephan J. Sigrist; Alexander M. Walter
      Abstract: Publication date: Available online 31 August 2017
      Source:Neuron
      Author(s): Suneel Reddy-Alla, Mathias A. Böhme, Eric Reynolds, Christina Beis, Andreas T. Grasskamp, Malou M. Mampell, Marta Maglione, Meida Jusyte, Ulises Rey, Husam Babikir, Anthony W. McCarthy, Christine Quentin, Tanja Matkovic, Dominique Dufour Bergeron, Zeeshan Mushtaq, Fabian Göttfert, David Owald, Thorsten Mielke, Stefan W. Hell, Stephan J. Sigrist, Alexander M. Walter
      Neural information processing depends on precisely timed, Ca2+-activated synaptic vesicle exocytosis from release sites within active zones (AZs), but molecular details are unknown. Here, we identify that the (M)Unc13-family member Unc13A generates release sites and show the physiological relevance of their restrictive AZ targeting. Super-resolution and intravital imaging of Drosophila neuromuscular junctions revealed that (unlike the other release factors Unc18 and Syntaxin-1A) Unc13A was stably and precisely positioned at AZs. Local Unc13A levels predicted single AZ activity. Different Unc13A portions selectively affected release site number, position, and functionality. An N-terminal fragment stably localized to AZs, displaced endogenous Unc13A, and reduced the number of release sites, while a C-terminal fragment generated excessive sites at atypical locations, resulting in reduced and delayed evoked transmission that displayed excessive facilitation. Thus, release site generation by the Unc13A C terminus and their specific AZ localization via the N terminus ensure efficient transmission and prevent ectopic, temporally imprecise release.
      Teaser Neurotransmission relies on synaptic vesicle release from unique sites. Reddy-Alla et al. now identify a function of Unc13A in release site generation and stable positioning with sub-active zone precision to ensure well-defined Ca2+ channel distances and adequate release probability.

      PubDate: 2017-09-07T12:12:02Z
      DOI: 10.1016/j.neuron.2017.08.016
       
  • Connexin 43-Mediated Astroglial Metabolic Networks Contribute to the
           Regulation of the Sleep-Wake Cycle
    • Authors: Jerome Clasadonte; Eliana Scemes; Zhongya Wang; Detlev Boison; Philip G. Haydon
      Abstract: Publication date: Available online 31 August 2017
      Source:Neuron
      Author(s): Jerome Clasadonte, Eliana Scemes, Zhongya Wang, Detlev Boison, Philip G. Haydon
      Astrocytes produce and supply metabolic substrates to neurons through gap junction-mediated astroglial networks. However, the role of astroglial metabolic networks in behavior is unclear. Here, we demonstrate that perturbation of astroglial networks impairs the sleep-wake cycle. Using a conditional Cre-Lox system in mice, we show that knockout of the gap junction subunit connexin 43 in astrocytes throughout the brain causes excessive sleepiness and fragmented wakefulness during the nocturnal active phase. This astrocyte-specific genetic manipulation silenced the wake-promoting orexin neurons located in the lateral hypothalamic area (LHA) by impairing glucose and lactate trafficking through astrocytic networks. This global wakefulness instability was mimicked with viral delivery of Cre recombinase to astrocytes in the LHA and rescued by in vivo injections of lactate. Our findings propose a novel regulatory mechanism critical for maintaining normal daily cycle of wakefulness and involving astrocyte-neuron metabolic interactions.
      Teaser Astrocytes supply energy metabolites to neurons, but how this influences behavior is unclear. Clasadonte et al. demonstrate that delivery of lactate from astrocytes to neurons is required for normal orexinergic neuronal activity and hence daily cycles of wakefulness.

      PubDate: 2017-09-07T12:12:02Z
      DOI: 10.1016/j.neuron.2017.08.022
       
  • Neurotransmitter Switching Regulated by miRNAs Controls Changes in Social
           Preference
    • Authors: Davide Dulcis; Giordano Lippi; Christiana J. Stark; Long H. Do; Darwin K. Berg; Nicholas C. Spitzer
      Abstract: Publication date: Available online 31 August 2017
      Source:Neuron
      Author(s): Davide Dulcis, Giordano Lippi, Christiana J. Stark, Long H. Do, Darwin K. Berg, Nicholas C. Spitzer
      Changes in social preference of amphibian larvae result from sustained exposure to kinship odorants. To understand the molecular and cellular mechanisms of this neuroplasticity, we investigated the effects of olfactory system activation on neurotransmitter (NT) expression in accessory olfactory bulb (AOB) interneurons during development. We show that protracted exposure to kin or non-kin odorants changes the number of dopamine (DA)- or gamma aminobutyric acid (GABA)-expressing neurons, with corresponding changes in attraction/aversion behavior. Changing the relative number of dopaminergic and GABAergic AOB interneurons or locally introducing DA or GABA receptor antagonists alters kinship preference. We then isolate AOB microRNAs (miRs) differentially regulated across these conditions. Inhibition of miR-375 and miR-200b reveals that they target Pax6 and Bcl11b to regulate the dopaminergic and GABAergic phenotypes. The results illuminate the role of NT switching governing experience-dependent social preference.
      Teaser Acquisition of social preference for siblings versus non-siblings is dynamic, but the developmental regulatory mechanisms have been unclear. Dulcis et al. found that sustained exposure to olfactory cues converts non-kin aversion to attraction via neurotransmitter switching coordinated by microRNAs.

      PubDate: 2017-09-07T12:12:02Z
      DOI: 10.1016/j.neuron.2017.08.023
       
  • In Vivo Magnetic Recording of Neuronal Activity
    • Authors: Laure Caruso; Thomas Wunderle; Christopher Murphy Lewis; Joao Valadeiro; Vincent Trauchessec; Josué Trejo Rosillo; José Pedro Amaral; Jianguang Ni; Patrick Jendritza; Claude Fermon; Susana Cardoso; Paulo Peixeiro Freitas; Pascal Fries; Myriam Pannetier-Lecoeur
      Abstract: Publication date: Available online 30 August 2017
      Source:Neuron
      Author(s): Laure Caruso, Thomas Wunderle, Christopher Murphy Lewis, Joao Valadeiro, Vincent Trauchessec, Josué Trejo Rosillo, José Pedro Amaral, Jianguang Ni, Patrick Jendritza, Claude Fermon, Susana Cardoso, Paulo Peixeiro Freitas, Pascal Fries, Myriam Pannetier-Lecoeur
      Neuronal activity generates ionic flows and thereby both magnetic fields and electric potential differences, i.e., voltages. Voltage measurements are widely used but suffer from isolating and smearing properties of tissue between source and sensor, are blind to ionic flow direction, and reflect the difference between two electrodes, complicating interpretation. Magnetic field measurements could overcome these limitations but have been essentially limited to magnetoencephalography (MEG), using centimeter-sized, helium-cooled extracranial sensors. Here, we report on in vivo magnetic recordings of neuronal activity from visual cortex of cats with magnetrodes, specially developed needle-shaped probes carrying micron-sized, non-cooled magnetic sensors based on spin electronics. Event-related magnetic fields inside the neuropil were on the order of several nanoteslas, informing MEG source models and efforts for magnetic field measurements through MRI. Though the signal-to-noise ratio is still inferior to electrophysiology, this proof of concept demonstrates the potential to exploit the fundamental advantages of magnetophysiology.
      Teaser Caruso et al. report in vivo, intra-cortical recordings of magnetic fields that reflect neuronal activity, using magnetrodes, i.e., micron size magnetic sensors based on spin electronics.

      PubDate: 2017-08-31T08:35:03Z
      DOI: 10.1016/j.neuron.2017.08.012
       
 
 
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