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Neuroembryology and Aging
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ISSN (Print) 1661-3406 - ISSN (Online) 1661-3414
Published by Karger

[122 journals]

Contents Vol. 5, 2008
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  Abstract:
  Neuroembryol Aging 2008;5:I–III
Subject Index Vol. 5, 2008
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  Neuroembryol Aging 2008;5:192
Author Index Vol. 5, 2008
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  Abstract:
  Neuroembryol Aging 2008;5:191
The Griffoniasimplicifolia I Isolectin B4 and Tomato Lectin Recognize
Astrocytes instead of Microglia in Adult Hamster Retina
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  Abstract: Two lectins, Griffonia simplicifolia I isolectin B4 (GS-I lectin) and Lycopersicon esculentum (LE) lectin, reported to be specific microglia markers in a number of animals including rodents, were used to stain hamster retinas. In the adult hamster retina, both of them failed to stain microglia but instead labeled astrocytes (in addition to endothelial cells). GS-I lectin-positive astrocytes were mainly located at peripheral regions of the retina but were variable in number and staining intensity, while LE lectin stained most astrocytes as judged by co-localization with anti-glial fibrillary acidic protein staining. To see whether astrocytes (and/or microglia) would be labeled by the lectins during postnatal retinal development, retinas from newborns all the way to adults were studied. Starting from P0, GS-I lectin selectively labeled astrocytes located adjacent to and peripheral to the tips of developing blood vessels, suggesting a functional association of glycoproteins containing α-D-galactose (the terminal sugar residue with binding affinity to GS-I) with the migration of the astrocytic front during development. The GS-I lectin staining on this population of astrocytes became reduced as the astrocytic front reached the retinal periphery, so that in the adult only astrocytes in the periphery became positive for GS-I. In contrast, LE lectin stained most astrocytes in the developing retina, starting from P2 and with maximum staining intensity achieved around P14, which continued unchanged to adulthood. During early postnatal retinal development, both lectins could label microglia, but the staining was abolished well before the retina became mature. GS-I could label microglia until P18, and the stained cells were mainly confined to the retinal periphery where blood vessels were absent, suggesting that expression of the terminal α-D-galactose residue is regulated by interaction with the developing vasculature (and/or astrocytes). LE could mark microglia till P6, but the labeling was weaker compared with GS-I. The results indicate that at least in the hamster, GS-I and LE lectin may be a more selective marker for retinal astrocytes than microglia. It would be interesting to see whether some other animals will exhibit a similar picture, and whether the expression of the sugar residues (specific for GS-I and LE lectin binding) on astrocytes instead of microglia will confer any functional consequences uniquely different from those animals with specific microglia binding.
  Neuroembryol Aging 2008;5:166–181
Expression of Dab2, a Tumor Suppressor, in the Human Fetal Hippocampus and
Neocortex
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  Abstract: Dab2, first identified as a tumor suppressor in ovarian cancerous cells and tissues, is an adaptor protein involved in several signal transduction pathways. Our previous studies of mouse embryos have shown that Dab2 is expressed in the early developing central nervous system and that knockdown of the protein expression perturbs the normal development of the neural tube. In this study, we investigated Dab2 expression in the human fetal hippocampus and temporal, sensory, visual, motor and frontal cortices from 12 to 32 weeks of gestation with a specific immunohistochemical staining method. The hippocampus showed the strongest Dab2 expression among all the brain regions examined. Within the hippocampus, Dab2 expression was first detected at 12–14 weeks in all cellular layers with varying intensities, and the highest level of expression was observed in the pyramidal layer at 26–28 weeks. In the temporal cortex, Dab2 was also expressed in all cellular layers at 12–14 weeks, and its expression peaked at 18–20 weeks and then became weaker at 26–32 weeks. The expression pattern was different in the sensory cortex: the expression was the strongest at 12–14 weeks and then gradually reduced with age. In the visual cortex, Dab2 expression was mainly localized in the marginal zone, upper cortical plate and subcortical layers, whereas the motor and frontal cortices exhibited only low levels of Dab2 expression mostly in the subcortical layers. Our results demonstrated a specific spatiotemporal pattern of Dab2 expression in the human fetal hippocampus and neocortex, implicating roles of Dab2 in the early development of the human brain.
  Neuroembryol Aging 2008;5:182–190
Effects of Soluble Amyloid βProtein (Aβ25–35) on Delayed Rectifier
Potassium Current in CA3 Neurons of Rat Hippocampal Slices
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  Abstract: The aim of this study was toinvestigate the effects of soluble amyloid βprotein (Aβ), with the amino acid sequence 25–35 (Aβ25–35), on delayed rectifier potassium current (Ik) in CA3 neurons of rat hippocampal slices using blind whole-cell patch-clamp recording techniques. We also studied the neurotoxic mechanism of soluble Aβ25–35 in Alzheimer’s disease. Results showed thatsoluble Aβ25–35 significantly suppressed Ik in CA3 neurons of rat hippocampal slices in time-dependent and voltage-dependent manners. Soluble Aβ25–35 significantly shifted the steady-state activation curve of Ik to more negative potentials. Before and after application of Aβ25–35, the half-activation potentials of Ik were 5.88 ± 0.67 and –2.81 ± 0.76 mV, respectively (n = 8; p < 0.05), but the slope factor was not significantly changed. The results suggest that the inhibitory effect of soluble Aβ25–35 on Ik may be one of the mechanisms of neurotoxicity, which may play an important role in the pathogenesis of Alzheimer’s disease.
  Neuroembryol Aging 2008;5:151–155
Study of Neuronal Apoptosis and Changes in Expression of the Proteins
Related to the Mitochondrial Pathway after Aβ1–42 Injection in the Rat
Hippocampus
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  Abstract: The objective was to study neuronal apoptosis and changes in the proteins related to the mitochondrial pathway in the hippocampus of a rat model of Alzheimer’s disease (AD) and discuss its significance in AD. Thirty-six Sprague-Dawley rats were divided into 3 groups: a normal group, a control group and an AD group. AD was established by injecting β-amyloid1–42 (Aβ1–42) into the hippocampus. Learning and memory ability was estimated with a Y maze at different times. The apoptotic neurons were detected by the TdT-mediated X-dUTP nick end labeling (TUNEL) method. Cytochrome C and caspase-9 protein expression in the hippocampus was detected by Western blot. The results showed that there was obvious impairment of learning and memory in rats of the AD group after Aβ1–42 injection. The apoptotic neurons in the hippocampus of the rats in the AD group were significantly increased compared with the normal group and the control group (p < 0.01), and the expression of cytochrome C and caspase-9 in hippocampus in AD group was significantly increased too (p < 0.01). The results suggest that the mitochondrial pathway is one of the important neuronic apoptotic pathways induced by Aβ1–42 in the hippocampus, and may play an important role in the pathogenesis of AD.
  Neuroembryol Aging 2008;5:156–160
Effect of Chronic Hypoxic Hypercapnia on the Expression of Bcl-2 and Bax
Genes and Apoptosis in Rat Hippocampal Neurons
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  Abstract: The objective of this paper is to explore the effect of chronic hypoxic hypercapnia on the apoptosis of rat neural cells in the hippocampus, as well as the relationship between apoptosis and Bcl-2 and Bax gene expression. In this study, 50 male Sprague-Dawley rats were randomly divided into 5 groups: a normal control group, and 4 hypoxic hypercapnia groups which received hypoxic hypercapnia treatment for 1, 2 , 3 and 4 weeks. The in situ apoptosis in the hippocampus was detected by TUNEL staining. The expression of bcl-2 and bax mRNA in the hippocampus was examined by RT-PCR. Results showed that the apoptosis index (AI) and expression of Bax mRNA increased with the duration of hypoxic hypercapnia, and that the expression of Bcl-2 mRNA increased at the beginning but then declined. There was a significant positive correlation between AI and the expression of Bax mRNA (r = 0.814, p < 0.01), and there was a significant negative correlation between AI and the ratio of Bcl-2 mRNA/Bax mRNA (r = –0.405, p < 0.01). The results suggest that apoptosis can be induced by chronic hypoxic hypercapnia in the rat hippocampus. The ratio of Bcl-2/Bax declined gradually, which accelerates the occurrence of apoptosis.
  Neuroembryol Aging 2008;5:161–165
Correlation between nNOS Expression and Erectile Dysfunction in
Experimental Diabetes Mellitus Rats of Different Ages
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  Abstract: Objective: To assess the correlation between neuronal nitric oxide synthase (nNOS) expression in the brain, lumbosacral spinal cord, sympathetic trunk, prostate and penis, and erectile dysfunction (ED) associated with diabetes mellitus (DM). Methods: DM was induced in adult male Sprague-Dawley rats by injecting streptozotocin. After 1, 2, 3 and 4 months, apomorphine was injected to test the penile reflex. The animals were then sacrificed, and the corpora cavernosa were isolated for a diastolic function test. In addition, the cortex of the brain, lumbosacral spinal cord, thoracic and lumbar sympathetic trunk, and root of the penis and prostate of each animal were subjected to a nNOS catalytic activity assay. Results: The times of penile reflex decreased gradually with the prolongation of DM. Acetylcholine-induced corpus cavernosum relaxation also markedly decreased in DM rats. On the other hand, in DM rats nNOS expression was elevated in the temporal cortex, hippocampus and hypothalamus, but was reduced in the spinal cord, sympathetic trunk and prostate. Statistics showed that nNOS expression in the brain correlated negatively with penis reflex and corpus cavernosum relaxation, while nNOS expression in the spinal cord, sympathetic trunk, penis and prostate had a positive correlation with penis reflex and corpus cavernosum relaxation. Conclusion: The expression of nNOS in the central and peripheral nervous systems correlated with diabetic ED and was a cause of diabetic ED.
  Neuroembryol Aging 2008;5:144–150
N-Methyl-D-Aspartate Receptors Mediate Excitotoxicity in Amyloid
Beta-Induced Synaptic Pathology of Alzheimer’s Disease
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  Abstract: Mounting evidence suggests that cognitive impairment begins with subtle alterations of synaptic efficacy prior to frank neuronal degeneration, and synaptic dysfunction may be induced by diffusible oligomeric assemblies of amyloid beta peptide (Aβ). The mechanisms underlying Aβ neurotoxicity are complex but might involve N-methyl-D-aspartate receptor (NMDAR). This review focuses on the action of NMDAR and its subunits in Aβ-induced synaptic dysfunction. The localized apoptotic mechanism that contributes to synaptic dysfunction in Alzheimer’s disease will also be discussed.
  Neuroembryol Aging 2008;5:134–143