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Abstract –Adenosine 3′,5′‐cyclic monophosphate (cyclic AMP) levels increase about 5‐fold in the cerebral cortex and 2‐fold in the cerebellum following electroconvulsive shock (ECS). The peak levels of cyclic AMP occur at 45 s after ECS in the cerebral cortex, and at 15 s in the cerebellum. In the cerebral cortex, ECS produces twice the cyclic AMP accumulation as does decapitation in a comparable time period; however, the relative effect of a number of neurotropic agents on the cyclic AMP accumulation is essentially the same, whether stimulated by decapitation or by ECS. In the cerebellum, the levels of guanosine 3′,5′‐cyclic monophosphate (cyclic GMP) also increase following ECS. The cyclic GMP levels are greatest at 60 s after ECS during the postictal depression. An association between elevated cerebellar cyclic GMP and depression seems unlikely, since CNS depressants either lowered or had no effect on cyclic GMP levels. From these results, cyclic nucleotide profiles following treatments such as ECS or decapitation may be useful in elucidating the molecular events involved in seizures, brain injury and ischemia.
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Lust et al. (1976) studied this question.
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