Hayakawa H, Yokota N, Yamawaki S
Department of Psychiatry and Neuroscience, Kure National Hospital, Hiroshima, Japan.
Yakubutsu Seishin Kodo. 1990 Jun;10(2):281-8.
Effect of electroconvulsive shock (ECS) on central serotonin (5-HT) receptor function was studied in order to elucidate its antidepressive mechanism. Repeated ECS treatment, but not imipramine treatment, increased the density of [3H]8-hydroxy-2-(di-n-propylamino)tetraline ( [3H]8-OH-DPAT) binding in hippocampus, and enhanced 5-HT metabolism in all regions except hippocampus. Parachloroamphetamine (PCA), a neurotoxin of 5-HT neuron, did not affect the up-regulation of [3H]8-OH-DPAT binding (5-HT1A receptor) induced by ECS. These results suggest that presynaptic 5-HT terminal does not modulate the up-regulation of 5-HT1A receptor induced by ECS. In addition, 5-HT1A-receptor-mediated behavior (forepaw treading) was enhanced by repeated ECS treatment, but unchanged by imipramine treatment. The effect of ECS on 5-HT1A function is not parallel with that of imipramine, thus it is difficult to explain 5-HT1A receptor mainly contributes to the antidepressive effect of ECS. The above results suggested that the up-regulation of 5-HT1A receptor induced by repeated ECS treatment did not directly relate to presynaptic 5-HT function and other receptors might modify the effects of ECS.
