Abstract
Stimulation of adenylate cyclase by dopamine in homogenates of the striatum was unaltered in rats which had received either a single or a series of 10 electroconvulsive shocks. However, stimulation by the selective D 1 dopamine receptor agonist SKF 38393 was significantly increased in homogenates of striatum from rats which had received chronic electroconvulsive shock, compared to those which received sham treatment. In homogenates of the limbic forebrain, stimulation by both 100 μM dopamine and by 4 μM SKF 38393 was significantly increased after chronic electroconvulsive shock. The activity of D 2 receptors, as measured by inhibition of forskolin-stimulated adenylate cyclase, in the presence of the d 1 receptor antagonist SCH 23390, was unaltered by chronic electroconvulsive shock in either area of the brain. The selective effect of chronic electroconvulsive shock in increasing the activity of D 1 receptors may account both for the increase, in dopamine-mediated behaviour, seen after chronic electroconvulsive shock and for the antiparkinsonian effects of this treatment.
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