Effect of adrenalectomy and administration of hypertonic saline on the content of aldehyde fuchsin-positive neurosecretory material and posterior lobe hormones in the median eminence and the neural lobe of rats

Böck, R.; Detzer, K.; Geiger, Ashley; Lang, R.; Östermann, E.; Sinner, G.

doi:10.1007/bf00206271

Cited by 12 publications

(9 citation statements)

References 21 publications

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“…Our results also show that ADX did not induce a significant change in NIL AVP and OXY contents when animals received water containing 0.9% NaCl after sur gery; this observation coincides with an earlier study showing that 14 days of ADX also did not change the NIL neuropep tides content [41].…”

Section: Discussionsupporting

confidence: 79%

Changes in the Hypothalamo-Corticotrope Axis after Bilateral Adrenalectomy: Evidence for a Median Eminence Site of Glucocorticoid Action

et al. 1991

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Bilateral adrenalectomy (ADX) leads to increased ACTH synthesis and secretion. It is thought that endogenous glucocorticoids exert a feedback mechanism at both pituitary and brain levels. The present study has been performed in order to determine the effect of ADX on the release of hypothalamic neuropeptides with corticotropin-releasing activity (CRA) and if there exists a median eminence site of glucocorticoid action to regulate hypothalamic-pituitary-adrenal (HPA) function. Adrenalectomized and sham-operated male rats were killed at different periods after surgery (2, 5, 7 and 14 days) and trunk blood was collected for ACTH and corticosterone (B) concentrations measurement. Brain (median eminence, ME; and medial basal hypothalamus, MBH) and pituitary (anterior lobe, AP; and neurointermediate lobe, ) tissues were dissected in order to evaluate either peptide content or in vitro hormone release. The results indicate that ADX blunted plasma B levels and increased AP ACTH content and secretion in a time-related fashion up to the 14th day. ADX significantly decreased both CRF and CRA contents in the ME at all periods studied; ME arginine-vasopressin (AVP) increased 7 and 14 days after ADX. MBH CRF decreased after ADX, but returned to sham value 2 weeks later; similarly, MBH AVP decreased at all periods after ADX. Removal of endogenous glucocorticoids did not vary neither oxytocin (OXY) content in the ME and MBH nor AVP and OXY contents in the . In our superfusion experiments, we found that ADX increased basal AVP release and did not change spontaneous CRF secretion from ME terminals. Dexamethasone (Dxm, 10 nM) diminished AVP but not CRF output by ME tissues from adrenalectomized rats. A direct relationship was found between ME CRF and 28 mlí KC1 (hK+)-induced CRF release by MEs from adrenalectomized rats. ME fragments from adrenalectomized rats were hyperresponsive to kH⁺ stimulation of AVP release. Dxm (10 nM) decreased the hK+ -evoked CRF and AVP release by MEs from adrenalectomized rats. ADX and dexamethasone treatment did not influence basal and hK⁺-elicited ME OXY release. Additionally, a rapid glucocorticoid inhibitory effect on ACTH secretion by isolated AP cells from both sham and adrenalectomized rats was found, and an in vitro corticotrope hyporesponse to 0.63 nM CRF and 9.25 nM AVP stimulation during several days after ADX. We conclude that ADX: (a) increases AP ACTH synthesis and secretion by activating the CRF and AVP neurosecretory systems; (b) induces a hypersecretion of ME AVP under basal and hK+-stimulated conditions; (c) induces an ME site of glucocorticoid action to inhibit CRF and AVP release; (d) decreases the corticotrope response to specific stimulation for several days, and (e) influences neither the hypothalamic-median eminence OXY nor AVP and OXY system. These results further suggest that the ME is an important site of glucocorticoid action to regulate HPA function.

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Section: Discussionsupporting

confidence: 79%

Changes in the Hypothalamo-Corticotrope Axis after Bilateral Adrenalectomy: Evidence for a Median Eminence Site of Glucocorticoid Action

et al. 1991

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“…Chronic osmostimulation has remarkably little if any ef fect on the amount of AVP in the outer zone of the M E after 7 days of salt-drinking despite the obvious depletion of im munoreactive AVP (and OXY) from the inner layer of the ME and the NL, confirming findings by Bock et al [1] and Mink et al [II]. The stronger immunoreactivity and in creased beading observed at 30 and 90 days of salt-loading support the notion of a neuronal AVP system independent of that projecting to the NL and that may be involved in salt regulation [II].…”

Section: Discussionsupporting

confidence: 78%

Immunohistochemical Investigation of the Magnocellular Peptidergic Hypothalamo-Neurohypophysial System of the Rat Chronically Stimulated by Long-Term Administration of Hypertonic Saline

Peña

et al. 1988

Neuroendocrinology

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The hypothalamic supraoptic (SON) and paraventricular nuclei (PVN), median eminences (ME) and neural lobes (NL) of normally hydrated control rats (group 1), and of rats drinking 2% NaCl for 7 (group 2), 30 (group 3) or 90 days (group 4) were investigated using immunohistochemistry for neurophysins (NP), arginine vasopressin (AVP) or oxytocin (OXY). Animals from the 3 experimental groups showed equivalent decreased levels of immunoreactive NP in the SON and PVN, but the greatest decrease was in the SON. Dendrites of SON and PVN neurons became loaded progressively with immunoreactive NP, AVP and OXY as salt loading proceeded. In rats of group 2, axons leaving the SON and PVN showed a marked depletion of immunoreactive material. The latter was found mainly at the periphery of widely spaced axonal swellings, clearly contrasting with the small and narrowly spaced beads of the neurosecretory axons of control rats. In rats of groups 3 and 4, axons leaving the SON and PVN resembled those of control rats. In the ME of the animals in all experimental groups, the same degree of decrease of immunoreactive NP was observed. In rats of group 3, bundles of axons containing immunoreactive AVP and OXY frequently projected through the ependymal lining of the ME into the third ventricle. In the NL of all experimental animals, a marked decrease occurred in the amount of immunoreactive NP, AVP and OXY. The decrease of immunoreactive AVP, however, was more pronounced in rats of group 2 than in those of groups 3 and 4. The NL of rats in group 4 were approximately 80% larger than those of control rats. Particularly striking in these hypertrophied NL were networks of expanded perivascular basal lamina and large intra-axonal vacuoles. The survival of rats to the long-term salt loading and the changes observed in the hypothalamo-neurohypophysial system indicate that these animals have developed adaptive mechanisms to the salt load.

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“…Indeed, the PVN-median eminence vasopressinergic pathway has been clearly shown to be influenced by stimuli of the corticotropic system (7)(8)(9)(10)(11) and the content of VP in the MBH, which contains the median eminence region, remained unchanged in Ahx rats, in distinction to the concomitant sharp decrease in the VP content of the neurointermediate lobe of the hypophysis. Furthermore, an electrically induced release of VP from the MBH in vitro was enhanced 13-fold when the tissue was taken from Ahx rats as compared with that when the tissue was taken from sham-operated rats.…”

Section: Stress-induced Vp Releasementioning

confidence: 94%

“…If not the neurohypophysis, then the source of VP found in plasma after foot shock stress in Ahx rats may be the median eminence region, a second major neurohemal contact zone of vasopressinergic neurons (7,8). Indeed, the PVN-median eminence vasopressinergic pathway has been clearly shown to be influenced by stimuli of the corticotropic system (7)(8)(9)(10)(11) and the content of VP in the MBH, which contains the median eminence region, remained unchanged in Ahx rats, in distinction to the concomitant sharp decrease in the VP content of the neurointermediate lobe of the hypophysis.…”

Section: Stress-induced Vp Releasementioning

confidence: 99%

“…Indeed, VP exists in a separate, probably parvocellular pathway which runs from the paraventricular nuclei (PVN) of the hypothalamus to the external layer of the median eminence and terminates in close proximity to the hypophysial portal circulation (7). VP has been found in the hypophysial portal blood (7); adrenalectomy increases the immunohistochemical staining for VP in the external layer of the median eminence (8), activates the synthesis of VP in the PVN-median eminence pathway (9, 10), and markedly enhances the electrically induced release of VP from the median eminence region in vitro (11), whereas almost no such changes were observed in the neurointermediate lobe of the hypophysis (NIL) (8,9,11). Although these lines of evidence suggest that under conditions, which activate more or less selectively the corticotropic system, VP like other hypothalamicreleasing factors, may be released from nerve terminals in the external layer of the median eminence, such a situation has not as yet been demonstrated in conscious animals.…”

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confidence: 98%

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Foot Shock Stress-Induced Release of Vasopressin in Adenohypophysectomized and Hypophysectomized Rats*

et al. 1985

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The effect of inescapable electric foot shock stress on vasopressin (VP) release was studied in conscious rats. In sham-operated animals, foot shock stress markedly increased plasma beta-endorphin-like immunoreactivity whereas plasma VP levels (RIA) remained unchanged. However, after selective ablation of the anterior lobe of the hypophysis, foot shock stress produced an 8-fold increase in plasma VP concentrations. Injection of hypertonic saline did not change plasma VP levels in adenohypophysectomized (Ahx) rats, while in sham-operated rats VP levels increased in response to this osmotic challenge. Neurointermediate lobes or medial basal hypothalami (MBH; containing the median eminence region) were superfused in vitro and stimulated electrically; as compared to sham operations, the evoked release of VP from the neurointermediate lobes was abolished, whereas that from the MBH was markedly (13-fold) enhanced when the tissues were taken from Ahx rats. The VP-like immunoreactivity released from the MBH of Ahx rats comigrated with synthetic arginine-VP on Sephadex G-15 column chromatography. Similarly, as found in Ahx rats, foot shock stress markedly raised plasma VP levels in totally hypophysectomized rats, whereas after selective ablation of the neurointermediate lobe of the hypophysis VP levels increased only slightly after stress. In conclusion, our data indicate that 1) foot shock stress induces the release of VP from some site other than the neurohypophysis, probably from the median eminence region, in Ahx rats; and 2) an increase in plasma osmolality is a powerful stimulus for the release of VP from the neurohypophysis but cannot release VP from the median eminence region. Thus, our results support the concept of a morphological and functional differentiation of the vasopressinergic neurosecretory system.

show abstract

Effect of adrenalectomy and administration of hypertonic saline on the content of aldehyde fuchsin-positive neurosecretory material and posterior lobe hormones in the median eminence and the neural lobe of rats

Cited by 12 publications

References 21 publications

Changes in the Hypothalamo-Corticotrope Axis after Bilateral Adrenalectomy: Evidence for a Median Eminence Site of Glucocorticoid Action

Changes in the Hypothalamo-Corticotrope Axis after Bilateral Adrenalectomy: Evidence for a Median Eminence Site of Glucocorticoid Action

Immunohistochemical Investigation of the Magnocellular Peptidergic Hypothalamo-Neurohypophysial System of the Rat Chronically Stimulated by Long-Term Administration of Hypertonic Saline

Foot Shock Stress-Induced Release of Vasopressin in Adenohypophysectomized and Hypophysectomized Rats*

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