PubMed · 7704728
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A D Rogol. 1994. Hypopituitarism.. https://pubmed.ncbi.nlm.nih.gov/7704728/
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The effects of emotional stressors on the release of arginine vasopressin (AVP) and oxytocin (OXT) within the rat hypothalamus and the origin and physiological significance of AVP released within the hypothalamic paraventricular nucleus (PVN) were investigated. First, adult male Wistar rats with a microdialysis probe aimed at the PVN or the supraoptic nucleus were exposed to either a dominant male rat (social defeat) or a novel cage. Release of AVP within the PVN was significantly increased in response to social defeat but not to novelty. In contrast to an activation of the hypothalamic-pituitary-adrenal (HPA) system, neither stressor stimulated the hypothalamic-neurohypophysial system (unchanged plasma AVP and OXT and unchanged release within the supraoptic nucleus [AVP] and the PVN [OXT]). Next, we demonstrated by simultaneous microdialysis of the suprachiasmatic nucleus and the PVN that AVP measured in PVN dialysates during social defeat was probably of intranuclear origin. Finally, a mixture of a V1 AVP and the alpha-helical corticotropin-releasing hormone (CRH) receptor antagonists administered via inverse microdialysis into the PVN caused a significant increase in the plasma adrenocorticotropic hormone (ACTH) concentration compared with vehicle-treated controls both under basal conditions and during social defeat, indicating inhibitory effects of intra-PVN-released AVP and/or CRH on HPA system activity. The antagonists failed to affect anxiety-related behavior of the animals as assessed with the elevated plus-maze. Taken together, our results show for the first time that AVP is released within the PVN in response to an emotional stressor. We hypothesize that this intranuclear release provides a negative tonus on ACTH secretion.
Double labeling of dispersed anterior pituitary cells revealed the coexistence of galanin immunoreactivity with adrenocorticotropic hormone (ACTH) as well as prolactin. However, only laser confocal microscopy showed three different areas of immunoreactivity within the corticotroph cytoplasm, two of them for ACTH and galanin separately and the third containing both immunoreactivities. To determine a possible relation between ACTH cells and galanin, 4-day cultures of anterior pituitary cells from female rats were examined by cell blot assay, and they showed ACTH release inhibition by 10(-6)M galanin. Furthermore, after 17 beta-estradiol treatment to maximize lactotroph galanin release in vitro, the cell blotting-assessed secretory level of corticotroph cells was very similar to that of cells in the presence of 10(-6)M galanin. In fact, immunoneutralization with galanin antiserum quenched the inhibitory effect of galanin on ACTH secretion. Our study suggests that locally produced galanin can modulate corticotropin release.
During lactation, the regulation of the activity of the hypothalamic-pituitary-adrenal (HPA) axis is modified in that tonically elevated glucocorticoid secretion is observed together with blunted ACTH secretion following exposure to various stressors. Although decreased CRF mRNA levels have been reported in neurons of the paraventricular nucleus (PVN) which control ACTH secretion, the mechanisms underlying stress hyporesponsiveness during lactation are still largely unknown. In addition, lactation is associated with inhibition of reproductive functions and the involvement of the PVN neurons in this inhibition is unclear. In these studies, we tested the hypothesis that the effects of stimulatory noradrenergic afferents to the hypothalamic PVN are decreased during lactation, maintaining stress hyporesponsiveness. We also determined whether PVN noradrenergic afferents could modulate suckling-induced luteinizing hormone (LH) suppression. Virgin and lactating females, on day 2 of lactation, received either sham (SHAM) or 6-hydroxydopamine (6OH-DA) lesions over the PVN. Suppression of plasma LH secretion following a suckling test was determined on day 9 in ovariectomized females and plasma ACTH and corticosterone (B) responses to swim stress were determined on day 11 of lactation. In virgin females, 6OH-DA lesion caused a significant reduction in the ACTH and B responses to swim stress. In SHAM lactating females, plasma ACTH response to stress was blunted compared to SHAM virgins, but 6-OHDA lesion did not reduce ACTH levels further. Lesions in lactating females reduced basal LH secretion, although not significantly, but suckling did not further inhibit LH secretion as observed in SHAM lactating females. In all lesioned groups, PVN tyrosine hydroxylase (TH) immunoreactivity was reduced compared to SHAM rats. These results suggest that brainstem (nor)adrenergic inputs to the PVN act to facilitate ACTH stress response in virgin rats, while in lactating rats this facilitation is absent. In addition, (nor)adrenergic cells projecting to the PVN might also participate in the modulation of GnRH and LH secretion during suckling.