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Transient cerebral ischemia results in selective neuronal cell death. The mechanisms underlying this selective vulnerability to ischemia are only beginning to be elucidated. We studied the effect of ischemia on α 1 -adrenergic receptor binding by measuring [ 3 H]prazosin binding in gerbil forebrain membranes after 10 min of bilateral carotid occlusion. Binding was reduced from 62 ± 3 to 33 ± 4 fmol/mg protein. Binding in the same membranes to β 2 -adrenergic receptors were also decreased, but not to the extent of that to β 1 -adrenergic receptors. Binding to muscarinic cholinergic ([ 3 H]quinuclydil benzilate) and β 1 -adrenergic receptors were only slightly depressed. Surprisingly, the protein content was significantly increased in the membrane fraction studied from ischemic forebrain (68 ± 4 mg/g wet weight) compared with sham operated controls (57 ± 4). The dramatic decrease in α 1 -adrenergic receptor binding during ischemia is consistent with receptor binding studies of membranes pretreated with phospholipase A 2 in vitro. It is not clear what effect this change in α 1 -adrenergic receptor binding has on subsequent selective neuronal death. The recent demonstration that catecholamines and locus ceruleus neurons influence the loss of CA 1 neurons in the hippocampus suggests that it may play an important modulatory role.

Rapid Reduction in [3H]Prazosin Binding to Gerbil Forebrain Membranes during Bilateral Common Carotid Artery Occlusion

Rapid Reduction in [³H]Prazosin Binding to Gerbil Forebrain Membranes during Bilateral Common Carotid Artery Occlusion