Alterations in the γ‐Aminobutyric Acid‐Gated Chloride Channel Following Transient Forebrain Ischemia in the Gerbil

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Abstract
The role of inhibitory neurotransmission in selective neuronal degeneration after transient forebrain ischemia was studied by binding of t‐[35S]butylbicyclophosphorothionate ([35S]TBPS) to the γ‐aminobutyric acid (GABA)‐gated chloride channel and measurement of GABAA receptor function in Mongolian gerbil brain. [35S]TBPS binding to the hippocampus, striatum, and cortex quantified by autoradiography and muscimol‐stimulated 36Cl‐ uptake in synaptoneurosomes of the same regions were examined 1, 4, and 29 days after a 5‐min bilateral carotid occlusion. [35S]TBPS binding was decreased in the pyramidal cell dendritic layers, stratum oriens, and stratum lacunosum‐moleculare of the CA1 hippocampus, 4 and 29 days after occlusion, and in the stratum radiatum 29 days after occlusion. [35S]TBPS binding sites in the lateral striatum decreased 47% 4 days after occlusion. At the same time, there was a corresponding decrease in muscimol‐stimulated 36CI‐ uptake in the striatal synaptoneurosomes. Muscimol‐stimulated 36Cl‐ uptake in the hippocampus decreased slightly 4 days after occlusion and more so after 29 days, although these decreases were not significant. No changes were observed in somatosensory cortex at any time point. These data suggest that a portion of GABAA receptors in areas sensitive to ischemic insult are associated with degenerating neurons, whereas other GABAA receptors are spared.