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Authors:Michael Numan Pages: 163 - 190 Abstract: Behavioral and Cognitive Neuroscience Reviews, Volume 5, Issue 4, Page 163-190, December 2006. A theoretical neural model is developed, along with supportive evidence, to explain how the medial preoptic area (MPOA) of the hypothalamus can regulate maternal responsiveness toward infant-related stimuli. It is proposed that efferents from a hormone-primed MPOA (a) depress a central aversion system (composed of neural circuits between the amygdala, medial hypothalamus, and midbrain) so that novel infant stimuli do not activate defensive or avoidance behavior and (b) excite the mesolimbic dopamine system so that active, voluntary maternal responses are promoted. The effects of oxytocin and maternal experience are included in the model, and the specificity of MPOA effects are discussed. The model may be relevant to the mechanisms through which other hypothalamic nuclei regulate other basic motivational states. In addition, aspects of the model may define a core neural circuitry for maternal behavior in mammals. Citation: Behavioral and Cognitive Neuroscience Reviews PubDate: 2016-05-18T01:08:32Z DOI: 10.1177/1534582306288790 Issue No:Vol. 5, No. 4 (2016)
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Authors:James W. Grau, Eric D. Crown, Adam R. Ferguson, Stephanie N. Washburn, Michelle A. Hook, Rajesh C. Miranda Pages: 191 - 239 Abstract: Behavioral and Cognitive Neuroscience Reviews, Volume 5, Issue 4, Page 191-239, December 2006. Using spinally transected rats, research has shown that neurons within the L4-S2 spinal cord are sensitive to response-outcome (instrumental) relations. This learning depends on a form of N-methyl-D-aspartate (NMDA)-mediated plasticity. Instrumental training enables subsequent learning, and this effect has been linked to the expression of brain-derived neurotrophic factor. Rats given uncontrollable stimulation later exhibit impaired instrumental learning, and this deficit lasts up to 48 hr. The induction of the deficit can be blocked by prior training with controllable shock, the concurrent presentation of a tonic stimulus that induces antinociception, or pretreatment with an NMDA or gamma-aminobutyric acid-A antagonist. The expression of the deficit depends on a kappa opioid. Uncontrollable stimulation enhances mechanical reactivity (allodynia), and treatments that induce allodynia (e.g., inflammation) inhibit learning. In intact animals, descending serotonergic neurons exert a protective effect that blocks the adverse consequences of uncontrollable stimulation. Uncontrollable, but not controllable, stimulation impairs the recovery of function after a contusion injury. Citation: Behavioral and Cognitive Neuroscience Reviews PubDate: 2016-05-18T01:08:33Z DOI: 10.1177/1534582306289738 Issue No:Vol. 5, No. 4 (2016)
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Pages: 240 - 240 Abstract: Behavioral and Cognitive Neuroscience Reviews, Volume 5, Issue 4, Page 240-240, December 2006.
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