Changes in noradrenergic neuroendocrine responses following repeated seizures and the mechanism of action of ECT.

To investigate the mechanism of action of ECT in depression, functional changes in central noradrenergic systems, resulting from a series of electroshock- or photic-induced seizures have been evaluated in baboons. The plasma growth hormone (GH) response to IV infusion of an alpha 2-noradrenergic agonist clonidine (0.02 mg/kg) or a beta 2-adrenergic antagonist, ICI 118,551 (0.02 mg/kg) has been measured before, during and up to 15 days after the series of seizures. Electroshock (ECS) or sham ECS was given with standard clinical premedication (atropine, methohexital, suxamethonium and oxygen ventilation) seven times over 15 days. Plasma GH responses were unchanged 24 h after one or seven ECS. An enhanced GH response occurred 7 and 15 days after the seventh ECS. Sham ECS (seven times in 15 days) produced no changes in GH response to clonidine. The plasma GH response to ICI 118,551 was apparently decreased 1 and 7 days after the seventh ECS. Photic seizures were induced seven times in 15 days in baboons which were primed with a subconvulsant dose of D,L-allylglycine (180 mg/kg), but were otherwise drug-free. Plasma GH responses to clonidine were enhanced 1 and 7 days after the seventh photically induced seizure. It is concluded that in the primate there is an enhancement of a central alpha 2-noradrenergic response during 1-15 days after a sequence of generalised seizures. The time course of this enhancement appears to be influenced by drugs given directly before the seizures.