Abstract
The increase in activity of adrenocortical ornithine decarboxylase (ODC) elicited by the administration of apomorphine (APM) was studied in rats, four days after transection of the spinal cord or 24 h after various types of brain surgery: transection of the mesencephalon or of the diencephalon, or hypothalamic deafferentation (creation of a "hypothalamic island"). Section of the cord elevated endogenous adrenocortical ODC activity and potentiated the induction of the enzyme by APM. Incomplete sections of the brain at the level of the mesencephalon or diencephalon produced no change in either endogenous or induced ODC activity. In contrast to this, interruption of the mesencephalic-diencephalic connections by complete diencephalic transection produced profound decreases of endogenous ODC and of the response to APM. Deafferentation of the hypothalamus raised endogenous ODC concentrations of the adrenal cortex and potentiated the response to APM. The results strongly suggest that APM acts at the level of the diencephalon (hypothalamus) to increase adrenocortical ODC activity. Diencephalic-mesencephalic connections must be intact for this to occur. Peripheral and extrahypothalamic influences play a modulatory role in this effect.
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