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• W2000552405 startingPage "2408" @default.
• W2000552405 abstract "Hippocampal inhibitory interneurons expressing glutamate decarboxylase-67 (GAD-67) considerably decline in number during old age. Studies in young adult animals further suggest that hippocampal GAD-67+ interneuron population is highly vulnerable to excitotoxic injury. However, the relative susceptibility of residual GAD-67+ interneurons in the aged hippocampus to excitotoxic injury is unknown. To elucidate this, using both adult and aged F344 rats, we performed stereological counting of GAD-67+ interneurons in different layers of the dentate gyrus and CA1 & CA3 sub-fields, at 3 months post-excitotoxic hippocampal injury inflicted through an intracerebroventricular administration of kainic acid (KA). Substantial reductions of GAD-67+ interneurons were found in all hippocampal layers and sub-fields after KA-induced injury in adult animals. Contrastingly, there was no significant change in GAD-67+ interneuron population in any of the hippocampal layers and sub-fields following similar injury in aged animals. Furthermore, the stability of GAD-67+ interneurons in aged rats after KA was not attributable to milder injury, as the overall extent of KA-induced hippocampal principal neuron loss was comparable between adult and aged rats. Interestingly, because of the age-related disparity in vulnerability of interneurons to injury, the surviving GAD-67+ interneuron population in the injured aged hippocampus remained comparable to that observed in the injured adult hippocampus despite enduring significant reductions in interneuron number with aging. Thus, unlike in the adult hippocampus, an excitotoxic injury to the aged hippocampus does not result in significantly decreased numbers of GAD-67+ interneurons. Persistence of GAD-67+ interneuron population in the injured aged hippocampus likely reflects an age-related change in the response of GAD-67+ interneurons to excitotoxic hippocampal injury. These results have implications towards understanding mechanisms underlying the evolution of initial precipitating injury into temporal lobe epilepsy in the elderly population." @default.
• W2000552405 created "2016-06-24" @default.
• W2000552405 creator A5050478696 @default.
• W2000552405 creator A5061746223 @default.
• W2000552405 creator A5069002539 @default.
• W2000552405 date "2009-08-01" @default.
• W2000552405 modified "2023-10-17" @default.
• W2000552405 title "Vulnerability of hippocampal GABA-ergic interneurons to kainate-induced excitotoxic injury during old age" @default.
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• W2000552405 doi "https://doi.org/10.1111/j.1582-4934.2009.00675.x" @default.
• W2000552405 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2855767" @default.
• W2000552405 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20141618" @default.
• W2000552405 hasPublicationYear "2009" @default.
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