Repeated electroconvulsive shock prevents increased neocortical beta 1-adrenoceptor binding after DSP-4 treatment in rats.
Repeated electroconvulsive shock (ECS) was administered to rats previously injected with DSP-4 (N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine hydrochloride), a noradrenergic neurotoxin. The normal increase in neocortical beta 1-adrenoceptor binding caused by noradrenaline depletion was effectively prevented by ECS. This finding suggests that the plasticity of the beta 1-adrenoceptor may be partially independent of endogenous noradrenaline concentration. Additionally, functional noradrenergic neurons are not necessarily a critical requirement for the antidepressant effect of electroconvulsive treatment in humans.
D000818:Animals; D001596:Benzylamines / Q000494:pharmacology*; D002540:Cerebral Cortex / Q000187:drug effects / Q000378:metabolism*; D004082:Dihydroalprenolol; D004597:Electroshock; D008297:Male; D009498:Neurotoxins / Q000494:pharmacology*; D051381:Rats; D011943:Receptors, Adrenergic, beta / Q000187:drug effects / Q000378:metabolism*
D001596:Benzylamines; D009498:Neurotoxins; D011943:Receptors, Adrenergic, beta; D004082:Dihydroalprenolol; C012102:DSP 4