Neuroscience
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Comparative Study
Synapse-to-synapse variation of calcium channel subtype contributions in large mossy fiber terminals of mouse hippocampus.
Both N- and P/Q-type voltage-dependent calcium channels are involved in fast transmitter release in the hippocampus, but are differentially regulated. Although variable contributions of voltage-dependent calcium channel subtypes to presynaptic Ca2+ influx have been suggested to give a neural network of great diversity, their presence has only been demonstrated in a culture system and has remained unclear in the brain. Here, the individual large mossy fiber presynaptic terminal was labeled with Ca2+/Sr2+-sensitive fluorescent dextrans in the hippocampal slice of the mouse. ⋯ On the other hand, these terminals were similar in the fractional contributions of P/Q-type voltage-dependent calcium channels. These results provide direct evidence that individual large mossy fiber synapses are differential in the contribution of N- and R-type voltage-dependent calcium channel subtypes to presynaptic Ca2+/Sr2+ influx. We suggest that the synapse-to-synapse variation of presynaptic voltage-dependent calcium channel subtype contributions may be one of the mechanisms amplifying diversity of the hippocampal network.
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Current evidence suggests that behavioral sensitization to the chronic administration of levodopa (L-DOPA) to dopamine-depleted animals involves a plasticity of GABA-mediated signaling in output regions of the basal ganglia. The purpose of this study was to compare in adult rats with a unilateral 6-hydroxydopamine (6-OHDA) lesion the effects of an acute or chronic (for 3 or 7 days) injection of L-DOPA on mRNA levels encoding for glutamic acid decarboxylase (GAD65 and GAD67) in the striatum and GABA(A) receptor alpha1, beta2 and gamma2 subunits in the substantia nigra, pars reticulata (SNr), by in situ hybridization histochemistry. In addition, immunostaining levels for the alpha1 subunit were examined in the SNr. ⋯ In addition, alpha1 immunostaining in the SNr was significantly decreased in rats injected for 7 days but not for 3 days or acutely with L-DOPA. Our results demonstrate that a chronic administration of L-DOPA results in a progressive increase in GAD and decrease in GABA(A) receptor expression in the striatum and SNr, respectively. They provide further evidence that behavioral sensitization and dyskinesia induced by a chronic administration of L-DOPA in an experimental model of Parkinson's disease is paralleled by a plasticity of GABA-mediated signaling in the SNr.
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Comparative Study
Neural correlates of social odor recognition and the representation of individual distinctive social odors within entorhinal cortex and ventral subiculum.
Recognition of individual conspecifics is important for social behavior and requires the formation of memories for individually distinctive social signals. Individual recognition is often mediated by olfactory cues in mammals, especially nocturnal rodents such as golden hamsters. In hamsters, this form of recognition requires main olfactory system input to the lateral entorhinal cortex (LEnt). ⋯ This study reveals cellular mechanisms in LEnt and VS that may mediate a natural form of recognition memory in hamsters. These neuronal responses were similar to those observed in rats and monkeys during performance in standard recognition memory tasks. Consequently, the present data extend our understanding of the cellular basis for recognition memory and suggest that individual recognition requires similar neural mechanisms as those employed in laboratory tests of recognition memory.
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Our previous studies have shown that intracerebral administration of endotoxin, lipopolysaccharide (LPS), induces selective white matter injury and hypomyelination in the neonatal rat brain and that the LPS-induced brain injury is associated with activation of microglia. To test the hypothesis that inhibition of microglial activation may protect against LPS-induced white matter injury, we examined roles of minocycline, a putative suppressor of microglial activation, on LPS-induced brain injury in the neonatal rat. A stereotactic intracerebral injection of LPS (1 mg/kg) was performed in postnatal day 5 Sprague-Dawley rats and control rats were injected with sterile saline. ⋯ The protective effect of minocycline was associated with suppressed microglial activation as indicated by the decreased number of activated microglial cells following LPS stimulation and with consequently decreased elevation of interleukin 1beta and tumor necrosis factor-alpha concentrations induced by LPS and a reduced number of inducible nitric oxide synthase expressing cells. Protection of minocycline was also linked with the reduction in LPS-induced oxidative stress, as indicated by 4-hydroxynonenal positive OLs. The overall results suggest that reduction in microglial activation may protect the neonatal brain from LPS-induced white matter injury and inhibition of microglial activation might be an effective approach for the therapeutic treatment of infection-induced white matter injury.
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Comparative Study
Increase in proliferation and gliogenesis but decrease of early neurogenesis in the rat forebrain shortly after transient global ischemia.
Regarding regenerative strategies early post-ischemic therapeutic interventions might have a great impact on further pathophysiological cascades. To understand the early post-ischemic events we analyzed proliferation and neurogenesis as early as on day 3 after transient global ischemia in rats. Evaluations were performed not only in the dorsal hippocampus, where post-ischemic cell death develops selectively in the cornu ammonis, subfield 1 area, but also in distant areas like the ventricle wall and the striatum. ⋯ Interestingly, in locally defined zones we found nestin- and glial fibrillary acidic protein-signals clearly separated. In sham-operated animals, nestin could be detected in both neurogenic zones only without co-labeling with glial markers. In conclusion, during the first days after global ischemia, cell death of cornu ammonis, subfield 1-neurons was accompanied by a massive overall proliferation and activation of microglia/macrophages, a reduction of pre-ischemia existing doublecortin-positive precursors in the dentate gyrus and a re-expression of nestin in glial fibrillary acidic protein-positive astrocytes.