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J Axelrod

Publications and source records attributed to J Axelrod.

359 records · Page 20Linked to original sources
PubMed1965

Adrenaline synthesis: control by the pituitary gland and adrenal glucocorticoids.

The activity of phenylethanolamine-N-methyl transferase, an enzyme that synthesizes adrenaline from noradrenaline in the adrenal medulla, is markedly depressed following hypophysectomy. Enzyme activity is restored to normal after administration of ACTH or the potent glucocorticoid, dexamethasone. Thus the biosynthesis of adrenaline in the adrenal medulla appears to be regulated by the pituitary-adrenocortical system.

Adrenal Glands↗
PubMedDate not supplied

Increase of corticotropin-releasing factor staining in rat paraventricular nucleus neurones by depletion of hypothalamic adrenaline.

In response to stress, adrenocorticotropic hormone (ACTH) is released by corticotrophs in the anterior pituitary under the control of several central and peripheral factors including corticotropin-releasing factor (CRF), which was recently isolated from the brain and sequenced. Immunocytochemical studies have shown that most of the CRF-containing cell bodies that project to the median eminence are present in the hypothalamic paraventricular nucleus (PVN). A dense PNMT(phenylethanolamine-N-methyltransferase)-containing fibre network was also observed in the same region--PNMT is the final enzyme in the biosynthesis of adrenaline and has been demonstrated in the brain. In the present study we found an association of adrenergic nerve fibres and CRF neurones by immunohistochemistry using antisera to PNMT and CRF. To examine the functional significance of the adrenergic projection to the PVN, we blocked the synthesis of adrenaline using a specific inhibitor of PNMT. The depletion of adrenaline resulted in an increase in CRF immunoreactivity. The present results suggest that, as well as catecholamines which regulate ACTH release at the anterior pituitary level via a beta 2-adrenergic receptor mechanism, central catecholamines (mainly adrenaline) also affect ACTH release through their action on CRF cells. Peripheral catecholamines seem to have a direct stimulatory effect on the pituitary corticotroph cells, whereas the present findings suggest that central adrenaline-containing neurones have an inhibitory role in the physiological response to stress.

Animals↗