Brain noradrenaline depletion prevents ECS-induced enhancement of serotonin- and dopamine-mediated behaviour.
When rats are given a series of electroconvulsive shocks (ECSs) over several days, they display enhanced behavioural responses to both serotonin- and dopamine-receptor agonists. Because these changes are seen when the ECS is given in ways closely mimicking the clinical administration of electroconvulsive therapy (ECT), it has been suggested that the changes in postsynaptic monoamine function may be involved in the antidepressant mechanisms of ECT. Ligand-binding studies have excluded the possibility that ECS alters the characteristics of either the serotonin or dopamine receptor; ECS may therefore be acting on neuronal systems which modulate monoamine neurotransmission. As repeated ECS has recently been reported to decrease both noradrenaline (NA)-sensitive adenylate cyclase and beta-adrenoreceptor binding, we have examined here whether changes in NA function are related to the effects of ECS on the serotonin- and dopamine-mediated behaviours. We demonstrate that although selective depletion of NA does not alter the drug-induced serotonin- and dopamine-mediated responses, it abolishes the ECS-induced enhancement of these behaviours.
D000818:Animals; D001058:Apomorphine / Q000494:pharmacology*; D001522:Behavior, Animal / Q000187:drug effects*; D001921:Brain / Q000187:drug effects / Q000378:metabolism; D004298:Dopamine / Q000378:metabolism; D004597:Electroshock; D006892:Hydroxydopamines / Q000494:pharmacology; D009043:Motor Activity / Q000187:drug effects; D009638:Norepinephrine / Q000172:deficiency*; D011804:Quinolines / Q000494:pharmacology*; D011814:Quipazine / Q000494:pharmacology*; D051381:Rats; D012701:Serotonin / Q000378:metabolism
D006892:Hydroxydopamines; D011804:Quinolines; D012701:Serotonin; D011814:Quipazine; D001058:Apomorphine; D004298:Dopamine; D009638:Norepinephrine