The effects of electroconvulsive therapy and antidepressant drugs on monoamine receptors in rodent brain--similarities and differences.

Abstract

Repeated administration to rodents of electroconvulsive shock (ECS) produces changes in brain monoamine biochemistry and function, several of which are also seen after repeated administration of antidepressant drugs. Both repeated ECS and antidepressant drug administration decrease cortical beta-adrenoceptor density and attenuate the alpha 2-adrenoceptor-mediated sedation response to clonidine injection. Neither procedure alters phenylephrine-induced locomotor activity in mice, a measure of alpha 1-adrenoceptor function. Most antidepressant drugs decrease type 2 5-hydroxytryptamine (5-HT2) receptor density in frontal cortex and 5-HT2 receptor-mediated head-twitch behaviour in mice. In contrast, repeated ECS increases both 5-HT2 receptor density and the head-twitch response, making it difficult to propose any simple hypothesis linking changes in this receptor with antidepressant activity. The putative agonist for the 5-HT1A receptor 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) produces a hypothermic response in mice, apparently by acting as an agonist at presynaptic 5-HT1 receptors. Repeated administration of antidepressant drugs and lithium markedly attenuates this hypothermic response. Repeated ECS also attenuates this response, the attenuation lasting for at least 20 days after the last ECS. Repeated ECS, but not antidepressant drug administration, markedly enhances dopamine-mediated behaviour. While the similarities in action between ECS and antidepressant drugs may help explain the therapeutic action of electroconvulsive treatment, the differences may provide clues to the efficacy of this treatment in drug-resistant depressive illness.