Neurogenic influences of bilateral adrenalectomy on monoamine oxidase.
Bilateral adrenalectomy (10 days) increased the monoamine oxidase activity of the rat heart, vas deferens, spleen, superior cervical ganglion, and hypothalamus but not that of the rest of the brain, kidney, and liver. Experiments were made to determine whether the increased activity was due to neurogenic influences and whether the enhanced activity of monoamine oxidase was intra- or extraneuronally located. Ganglionic blockade with chlorisondamine failed to alter the rise in cardiac monoamine oxidase. Likewise, superior cervical ganglion monoamine oxidase was unaffected by surgical denervation. 6-Hydroxydopamine abolished the increase in monoamine oxidase activity of the vas deferens, spleen, and superior cervical ganglion but failed to alter that of the kidney, hypothalamus, and the rest of the brain. Cardiac monoamine oxidase was reduced markedly by 6-hydroxydopamine, but the remaining activity was still significantly elevated over the respective control values. The data suggest that the increase in organ monoamine oxidase is predominantly of neuronal origin and that this increase is not due to transsynaptic induction.
Neurogenic influences of bilateral adrenalectomy on monoamine oxidase. Bilateral adrenalectomy (10 days) increased the monoamine oxidase activity of the rat heart, vas deferens, spleen, superior cervical ganglion, and hypothalamus but not that of the rest of the brain, kidney, and liver. Experiments were made to determine whether the increased activity was due to neurogenic influences and whether the enhanced activity of monoamine oxidase was intra- or extraneuronally located. Ganglionic blockade with chlorisondamine failed to alter the rise in cardiac monoamine oxidase. Likewise, superior cervical ganglion monoamine oxidase was unaffected by surgical denervation. 6-Hydroxydopamine abolished the increase in monoamine oxidase activity of the vas deferens, spleen, and superior cervical ganglion but failed to alter that of the kidney, hypothalamus, and the rest of the brain. Cardiac monoamine oxidase was reduced markedly by 6-hydroxydopamine, but the remaining activity was still significantly elevated over the respective control values. The data suggest that the increase in organ monoamine oxidase is predominantly of neuronal origin and that this increase is not due to transsynaptic induction.