Brain-Pituitary-Adrenal Interrelationships
DOI: 10.1159/000394216
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Brain and Pituitary-Adrenal Interactions Studies on Central Monoamine Neurons

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Cited by 23 publications
(9 citation statements)
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“…In this report, we confirm the sensitivity of CA central neurones to ADX [11,12,21,22,42,43,48]. However, the better anatomical resolution as well as the use of a sensitive index in order to characterize the activity of the CA neurones revealed clear-cut differential effects among the three major brain stem CA groups.…”
Section: Discussionsupporting
confidence: 72%
“…In this report, we confirm the sensitivity of CA central neurones to ADX [11,12,21,22,42,43,48]. However, the better anatomical resolution as well as the use of a sensitive index in order to characterize the activity of the CA neurones revealed clear-cut differential effects among the three major brain stem CA groups.…”
Section: Discussionsupporting
confidence: 72%
“…The fact that the modification of plasma levels of P-EI induced by disruption of the VB was only temporary is in line with previous reports, including, for example, the tran sient enhancement of the ACTH response to stress seen in VB-lesioned rats, in demonstrating that an interference with catecholaminergic transmission does not result in perma nent deficits in adenohypophyseal secretion [7,46,48], Al though there may be a redundancy in control of [3-EI re lease, a supersensitivity to norepinephrine derived from un destroyed fibers may account for the recovery in P-EI secre tion. In fact, a 10-fold supersensitivity to the suppressive ef fect of norepinephrine upon CRF release was seen in rats treated 2 weeks previously with 6-hydroxydopamine [13].…”
Section: Discussionsupporting
confidence: 91%
“…As reviewed elsewhere, there is compelling evidence for the existence of a norepinephrinergic mechanism operating at a hypothal amic site which suppresses adenohypophyseal secretion of ACTH into plasma both tonicaliy and in response to stress [2, 7-9, 13, 36, 37, 46). Furthermore, we have recently ob served that, in contrast to lesions of the VB, selective des truction of the locus ceruleus, the primary source of the dor sal bundle, fails to modify plasma levels of P-EI [22], whilst the VB has similarly been identified as the norepinephriner gic system modulating ACTH release [7,8,9,36,46]. Our findings concerning P-EI are in good correspondence with those with ACTH in view of the coexistence and concomit ant outflow of adenohypophyseal P-EI and ACTH upon challenge by corticotrophic releasing factor (CRF) in vitro.…”
Section: Discussionmentioning
confidence: 99%
“…Roth et al (1982) described increased adrenaline and noradrenaline concentration in the hypothalamus and hippocampus of rats after swim¬ ming in cold water dailv for 21 days. Because of the known inhibitory action of the ventral noradrenergic bundle in the rat, extensively innervating the hypothalamus, on the release of the corticotrophinreleasing hormone (Fuxe et al 1973;Weiner & Ganong 1978;Rose et al 1976; Moore & Bloom 1979;Gann et al 1978;Ganong 1980;Jones et al 1980) it is conceivaKe that suppression of ACTH release under conditions of prolonged stress may account for the decrease in plasma cortisol levels.…”
Section: Discussionmentioning
confidence: 99%