Evidence for the Role of Adrenocortical Hormones in the Regulation of Noradrenaline and Dopamine Metabolism in Certain Brain Areas

Rastogi, R. P.; Singhal, Radhey L.

doi:10.1111/j.1476-5381.1978.tb07015.x

Cited by 64 publications

(21 citation statements)

References 28 publications

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“…In agreement with previous reports [6,37], no change in the CA content was observed following ADX. By con trast chronic ADX was followed by an increase of the ty rosine hydroxylation rate in the medullary CA groups, the amplitude and time course of which differed according to the nature of the group.…”

Section: Discussionsupporting

confidence: 82%

Differential Time Course Activation of the Brain Stem Catecholaminergic Groups following Chronic Adrenalectomy

1992

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The activity of the brain stem catecholaminergic (CA) cell groups of the ventrolateral (A₁C₁) and dorsomedial (A₂C₂) medulla that are known to contain primarily noradrenergic neurones (A₁ and A₂) and a smaller proportion of adrenergic cells (C₁ and C₂) as well as the noradrenergic group locus ceruleus (LC) in the dorsal pons was determined at various times up to 16 days following surgical adrenalectomy. The activity of the CA cell groups was estimated by the rate of tyrosine hydroxylation in vivo that was assessed by measuring the 3, 4-dihydroxyphenylalanine (DOPA) accumulated 20 min following administration of DOPA decarboxylase inhibitor NSD 1015. In the medullary nuclei noradrenaline content was found around 40- up to 70-fold the adrenaline content. This result was taken as evidence that the noradrenergic cells are likely to provide the main contribution to the tyrosine hydroxylation rate that we measured. Endogenous DOPA content represented between 2 and 10% of the noradrenaline content. NSD 1015 induced an accumulation of DOPA that was linear for at least 20 min and reached at this time more than 10-fold the endogenous level. While no modification of the in vivo tyrosine hydroxylation rate was observed in the LC, a significant increase was found in both medullary groups following adrenalectomy. In the A₁C₁ group it was detected 8 days after surgery and was then maintained with a maximum that represented up to a 60% increase over the basal value. In the A₂C₂ group the activation was slightly delayed and less marked. Increase in ACTH level occurred much earlier: it was about 70% of the maximal level already 4 days following adrenalectomy. The tyrosine hydroxylase activity measured in vitro with saturating concentrations of substrate and cofactors, was not affected by adrenalectomy. Daily injection of dexamethasone prevented the increase in plasma ACTH as well as the increase of the in vivo tyrosine hydroxylation rate in the medullary CA groups triggered by adrenalectomy. This activation is thus likely to be mediated by type II glucoreceptors and does not seem to involve an increase of the tyrosine hydroxylase content but rather other regulatory processes of the hydroxylation step in vivo. While the brain stem CA neurons are known to participate in the control of the hypothalamo-pituitary axis, their delayed activation following adrenalectomy suggests that they are not directly involved in the early increase in plasma ACTH level triggered by the lack of circulating corticosteroids.

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Section: Discussionsupporting

confidence: 82%

Differential Time Course Activation of the Brain Stem Catecholaminergic Groups following Chronic Adrenalectomy

1992

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“…We then determined the effects of each type of lesion, and a combi nation of both lesions on the ACTH-corticosterone re sponse to ether stress. Finally, as corticosteroids have repeatedly been shown to strongly modulate several func tional parameters related to brain CA (NA synaptic trans mission [19], and brain receptors [20][21][22], tyrosine hy droxylase in CA brain stem nuclei [23], and NA turnover in discrete hypothalamic areas [ 19]), we investigated the possible modulatory effects of plasma adrenocorticoid levels on the influence of the CA pathways on the ACTH response to ether stress.…”

Section: Introductionmentioning

confidence: 99%

Effects of Discrete Lesions in the Ventral Noradrenergic Ascending Bundle on the Corticotropic Stress Response Depend on the Site of the Lesion and on the Plasma Levels of Adrenal Steroids

Gaillet¹,

Alonso

Borgne³

et al. 1993

Neuroendocrinology

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Stereotaxic deletion of selected areas of the ventral noradrenergic ascending bundle (VNAB-X) by discrete bilateral injections of 6-hydroxydopamine (6-OHDA; 4 µg in 0.2 µl saline) was used to explore the role of brain catechol-amines (CA) and their interaction with corticosteroid feedback in stress responses of the ACTH-corticosterone (CORT) axis. The stereotaxic coordinates used for 6-OHDA lesions and the optimization of postlesion delays were determined by (a) radioautographic labeling of the VNAB axons after tracer injections into the dorsal A2/C2, or the ventral Al/Cl medullary areas, (b) histofiuorescence and immunocytochemical location of interrupted CA pathways versus the postlesional scar, and (c) postlesional noradrenaline and adrenaline concentrations in whole hypothalami and paraventricular nuclei (PVN) punch samples. Two sites of 6-OHDA lesions were selected; both led to striking falls in PVN concentrations of both CA. The more dorsal lesion (dVNAB-X) was the same as that of our earlier studies and interrupted pathways originating predominantly in the A2/C2 area; the second more ventral lesion (vVNAB-X) interrupted axons stemming preferentially from the A1/C1 area. Both VNAB lesions inhibited the ether stress-induced ACTH and CORT surges in rats with intact adrenals. But the blockade (overall poststress release, amplitude and swiftness of hormonal responses) by dVNAB-X was greater than by vVNAB-X. The basal ACTH level in adrenalectomized rats (ADX) was elevated 20-fold and ether stress induced a 4-fold ACTH surge. As in sham-ADX rats, vVNAB-X in ADX rats induced only moderate inhibition of the ACTH response versus ADX + sham-vVNAB-X controls. On the other hand ADX + dVNAB-X rats showed a greatly amplified ACTH stress response over the ADX-sham dVNAB-X controls. This amplification was reversed by oral CORT supplementation. The data suggest that the CA pathways of the VNAB participating, directly or indirectly, in the poststress corticotropic activation may include subsets of CA axons of different origins, whose functional roles in stress are modulated in opposite directions by the plasma corticosteroid level.

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“…Evidence suggests that both dopamin ergic [1][2][3]18] and serotonergic [2,18,41,43] activity re duces lordosis. Complementary evidence indicates that adrenalectomy facilitates and glucocorticoids inhibit the activity of MAO, an enzyme that metabolizes and inacti vates both dopamine and serotonin [33,38,40], Thus, adrenalectomy may decrease and corticosterone increase serotonergic and dopaminergic activity, thereby respecti vely increasing and decreasing lordosis. Some examination of sites of action of serotonergic suppression of lordosis has been conducted [19,41,43].…”

Section: Discussionmentioning

confidence: 99%

“…Finally, there is a possibility that the locus of the suppression of lordosis by corticosterone could relate to sites in which se rotonergic activity is believed to suppress this behavior [19,41,43]. This is based upon the suggestion [11,12] that the reg ulation of monoamine oxidase (MAO) activity by corticos terone [33,38,40], which in turn influences serotonin activity by controlling its degradation, may mediate the effects of the hormone on lordosis. Accordingly, the present study may shed some light on the mechanism subserving the modula tion of lordosis behavior by corticosterone.…”

mentioning

confidence: 99%

Alteration of Estrogen-Induced Lordosis through Central Administration of Corticosterone in Adrenalectomized-Ovariectomized Rats

Catanzaro

1987

Neuroendocrinology

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Corticosterone was administered through various modes into several brain regions of estrogen-treated adrenalectomized-ovariectomized female rats. Daily administration of 20 µg corticosterone dissolved in propylene glycol through intracerebral cannulae effectively inhibited female sexual receptivity at each of four sites: third ventricle, ventromedial hypothalamus, preoptic area, and septum. Similar administration of lesser daily doses failed to inhibit receptivity. Implantation of pure crystalline corticosterone also had no effect on receptivity at any site. Beeswax pellets chronically releasing low doses of corticosterone significantly inhibited receptivity when implanted in the medial hypothalamus and preoptic area, with similar nonsignificant trends in the lateral septum and medial forebrain bundle, but had no effect in the dorsal hippocampus or the amygdala. The effective sites are similar to those in which estrogen activity is known to induce receptivity and those in which serotonergic activity is believed to inhibit receptivity, but do not entirely correspond to sites in the brain showing the greatest uptake of corticosterone.

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Evidence for the Role of Adrenocortical Hormones in the Regulation of Noradrenaline and Dopamine Metabolism in Certain Brain Areas

Cited by 64 publications

References 28 publications

Differential Time Course Activation of the Brain Stem Catecholaminergic Groups following Chronic Adrenalectomy

Differential Time Course Activation of the Brain Stem Catecholaminergic Groups following Chronic Adrenalectomy

Effects of Discrete Lesions in the Ventral Noradrenergic Ascending Bundle on the Corticotropic Stress Response Depend on the Site of the Lesion and on the Plasma Levels of Adrenal Steroids

Alteration of Estrogen-Induced Lordosis through Central Administration of Corticosterone in Adrenalectomized-Ovariectomized Rats

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