Effect of adrenocorticotropin administration on beta-adrenergic receptor adaptations in rat brain cerebral cortex.
It has been reported that adrenocorticotropin (ACTH) administration reduces the time necessary for observing the imipramine-induced decline in beta-adrenergic receptor binding and function in rat brain frontal cortex. This interaction was examined in the present study following the destruction of the dorsal noradrenergic bundle in an attempt to determine whether the hormone treatment influences pre- or postsynaptic activity to facilitate the receptor response. Lesioning completely prevented the decline in beta-receptor binding normally observed following treatment with the drug combination. In fact, the number of cerebral cortical beta-adrenergic receptor binding sites was significantly greater in lesioned animals receiving ACTH than in lesioned controls. Lesioning significantly increased the amount of cyclic AMP produced in response to a saturating concentration of norepinephrine, an effect that was not influenced by ACTH treatment. These findings suggest that ACTH administration modifies the norepinephrine-stimulated cyclic nucleotide system indirectly, perhaps through an action on presynaptic neurons, whereas the effect on receptor recognition site number may be due to a direct action on the postsynaptic cell.
D000324:Adrenocorticotropic Hormone / Q000494:pharmacology*; D000818:Animals; D002540:Cerebral Cortex / Q000378:metabolism*; D000242:Cyclic AMP / Q000378:metabolism; D004082:Dihydroalprenolol / Q000378:metabolism; D007099:Imipramine / Q000494:pharmacology; D008297:Male; D009638:Norepinephrine / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D011943:Receptors, Adrenergic, beta / Q000187:drug effects / Q000378:metabolism*
D011943:Receptors, Adrenergic, beta; D004082:Dihydroalprenolol; D000324:Adrenocorticotropic Hormone; D000242:Cyclic AMP; D007099:Imipramine; D009638:Norepinephrine