Endogenous Ornithine Decarboxylase Research Articles

Neurotransmitter interaction in regulation of adrenocortical ornithine decarboxylase

Administration of the dopamine receptor agonists apomorphine (APM) and piribedil increases adrenocortical ornithine decarboxylase (ODC) activity. In this paper alterations in the sympathoadrenal system, and in the central dopaminergic and serotonergic systems have been produced to study the possible mechanism of action of APM on adrenocortical ODC. Unilateral splanchnicotomy, unilateral rhizotomy, and bilateral demedullation each attenuated the response of adrenocortical ODC to APM. Intracerebroventricular 6-hydroxydopamine and 5,6-dihydroxytryptamine, intraperitoneal p-chlorophenylalanine and electrolytic lesion of the medial raphe nucleus reduced the APM-induced increase. None of these treatments produced any changes in the endogenous ODC activity of the adrenal cortex. It is postulated that dopaminergic brain structures participate directly in the stimulatory effect on the hypophyseoadrenal system to increase adrenocortical ODC activity. An intact central serotonergic system seems to be necessary for APM to exert its effect on adrenocortical ODC activity, particularly the medial raphe nucleus.

Neuroendocrine control of adrenocortical ornithine decarboxylase activity.

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.