| pubmed-article:6123960 | pubmed:abstractText | The effects of chronic administration of the nonselective monoamine oxidase (MAO) inhibitor, phenelzine, and two selective inhibitors, clorgyline, and pargyline on adrenergic receptor binding and MAO activity were studied in the rat brain. Chronic but not acute administration of both phenelzine and the MAO-A inhibitor, clorgyline, resulted in significant decreases in cortical beta-adrenoreceptor binding ([3H]dihydroalprenolol) of 47 and 24% respectively. In contrast pargyline, which only partially inhibited MAO-A, caused only a nonsignificant (7%) change in rat cortical beta-receptor binding. In a more detailed study, chronic administration of clorgyline also caused changes in alpha-adrenergic receptor binding: by day 3 of treatment, significant changes were already observable in alpha-2-adrenergic receptor binding ([3H]clonidine), although changes in alpha-1 ([3H]WB4101)- and beta ([3H]dihydroalprenolol)-cortical receptor binding were not present until day 10. After 21 days of clorgyline treatment, the Bmax's of alpha-2-, alpha-1- and beta-adrenergic cortical receptors were reduced by 62, 36 and 34% respectively. In brainstem, alpha-2- and beta-receptors were reduced by 60 and 74%. The magnitude of these changes and particularly the rapidity of the alpha-2 changes suggest that clorgyline-induced alpha-2 autoreceptor changes may precede and contribute to the changes in postsynpatic alpha-1- and beta-receptors. These sequential alterations in adrenergic receptors may be pertinent to the efficacy and delay in onset of the clinical changes which follow treatment with these antidepressants. | lld:pubmed |
