Abstract
Treatment of rats with electroconvulsive shock once daily for 10–12 days increased the density of α 1-adrenoceptors labeled by [ 3H]prazosin in homogenates of frontal cerebral cortex. A single treatment did not affect [ 3H]prazosin binding. Repeated treatment with electroconvulsive shock did not appear to affect α 1-adrenoceptor binding in the hippocampus or hypothalamus. Treatment of rats with reserpine also increased [ 3H]prazosin binding in the frontal cortex. In contrast to electroconvulsive shock, three weeks administration of tricyclic antidepressant drugs, monoamine oxidase inhibitors, or atypical antidepressant drugs did not significantly affect [ 3H]prazosin binding sites in the frontal cortex. The affinities of antidepressant drugs for α 1-adrenoceptors ranged from about 50 nM for tricyclic and atypical antidepressants to about 100 μM for monoamine oxidase inhibitors. The high affinities of the tricyclic and atypical antidepressant drugs for α 1-adrenoceptors could contribute to clinical differences between these classes of drugs and monoamine oxidase inhibitors. Furthermore, the electroconvulsive shock-induced increase in α 1-adrenoceptors could contribute to differences in clinical effects between this treatment and antidepressant drugs.
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