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Taken together, this seems to indicate that reelin modulates the expression of GABAergic Purkinje neurons and is dysregulated in schizophrenia Maloku et al. Most GABA-ir cells were localized dorsally. This finding suggests that distinct populations of neural progenitors might respond to GABA differently. GABA and endogenously produced adenosine can interact to produce a neuroprotective effect during white matter anoxia in the optic nerve. These findings suggest chronic tonic inhibition mediated by extrasynaptic GABA A receptors following stroke impairs the plasticity required for functional recovery Clarkson et al. It is possible that this period of high GABAergic neuron migration may be a period of vulnerability that leads to schizophrenic cortical deficits. International Union of Pharmacology. Studies using a heterozygous reeler mouse HRM which displays roughly half the reelin expression of controls exhibits similar behaviors and structural deficits to those found in schizophrenic patients. The Journal of Comparative Neurology.