| Summary: | The aim of this study has been to elucidate the neural pathways involved in the regulation of adrenal ornithine decarboxylase (ODC) activity. Administration of the dopamine-receptor agonists apomorphine (APM) and piribedil (PBD) to rats led to an increase in ODC activity of both the adrenal medulla and cortex. These effects were blocked by giving the animals the dopaminergic antagonist haloperidol. The APM-induced increase in adrenomedullary ODC activity was largely prevented by denervation of the adrenal, transection of the spinal cord, and transection of the mesencephalon-diencephalon. Section of ventral spinal roots reduced the induction to varying extents, depending on the number of roots cut and their location between T(,4) and T(,12). The inducing effect of APM on adrenocortical ODC was abolished by hypophysectomy. Splanchnicotomy, rhizotomy and bilateral adrenal demedullation each attenuated the action of the drug. In contrast to this, section of the spinal cord or surgical isolation of the hypothalamus (preparation of "hypothalamic island") potentiated its effect. Impairment of serotonergic nerve function by systemic administration of p-chlorophenylalanine and intraventricular injection of 5,6'-dihydroxytryptamine or electrolytic potentiated the effect of APM in the adrenal medulla, but reduced it in the cortex. These observations suggest that adrenal ODC activity is predominantly regulated by one or more central facilitatory dopaminergic pathways. The pathway for the regulation of the medullary enzyme involves nuclei in the diencephalon-telencephalon and ultimately acts through the sympathetic nervous sytem. The pathway for the cortex involves the hypothalamus and acts via the anterior pituitary gland. These pathways include serotonergic components, which have opposite net effects on the induction of ODC produced by APM: inhibitory for the medulla and facilitatory for the cortex.
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