Regulation of dihydropyridine calcium antagonist binding sites in the rat hippocampus following neurochemical lesions.
The effects of catecholaminergic, cholinergic, serotonergic, and glutaminergic terminal destruction and neurotransmitter depletion on [3H]nitrendipine binding to rat brain membranes were determined using the neurotoxins 6-hydroxydopamine, 5,7-dihydroxytryptamine, and kainic acid and the neurotransmitter-depleting agent reserpine. Following intracisternal injection of 6-hydroxydopamine there were time-dependent increases (14-23%) in the density but not change in the affinity of hippocampal [3H]nitrendipine binding sites. 6-Hydroxydopamine significantly increased [3H]nitrendipine binding in the hippocampus 4 and 10 days following injection. However, no significant change in binding was observed at 16 and 26 days. [3H]Nitrendipine binding in the cerebral cortex, striatum, cerebellum, and brain stem was unaffected by 6-hydroxydopamine. Neither 5,7-dihydroxytryptamine nor kainic acid affected [3H]nitrendipine binding in the hippocampus and cerebral cortex. Acute and chronic reserpinization also did not affect [3H]nitrendipine binding in the hippocampus and cerebral cortex. These results indicate that dihydropyridine calcium antagonist bindings sites in rat brain are subject to brain region-specific regulation following neurochemical lesions and may be present in their largest densities on postsynaptic membranes.
D000320:Adrenergic Fibers / Q000502:physiology; D000818:Animals; D015220:Calcium Channels; D002395:Catecholamines / Q000502:physiology; D002799:Cholinergic Fibers / Q000502:physiology; D005973:Glutamine / Q000502:physiology; D006624:Hippocampus / Q000032:analysis* / Q000187:drug effects; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D011978:Receptors, Nicotinic / Q000032:analysis*; D012701:Serotonin / Q000502:physiology; D009435:Synaptic Transmission
D015220:Calcium Channels; D002395:Catecholamines; D011978:Receptors, Nicotinic; D005973:Glutamine; D012701:Serotonin