Mapping study of noradrenergic stimulation of vasopressin release

Leibowitz, Sarah F.; Eidelman, Dov; Suh, Jin Suck; Díaz, Sonia Pértega; Sladek, Celia D.

doi:10.1016/0014-4886(90)90042-q

Cited by 46 publications

(23 citation statements)

References 49 publications

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“…The SON is the main target for the noradrenergic system arising from the brainstem (Cunningham and Sawchenko, 1988, Sawchenko and Swanson, 1981). During states of heightened neurosecretory activity, noradrenaline, via the α 1 -adrenoreceptor, plays a critical excitatory role in the release of OT and VP from magnocellular neurons (Armstrong, et al, 1986, Leibowitz, et al, 1990, Willoughby, et al, 1987). Within the SON, the majority of adrenergic varicosities are found ventral to the magnocellular cell bodies in the dendritic zone (McNeill and Sladek, 1980, Swanson, et al, 1981).…”

Section: Discussionmentioning

confidence: 99%

Neuronal activity and axonal sprouting differentially regulate CNTF and CNTF receptor complex in the rat supraoptic nucleus

Askvig¹,

Leiphon²,

Watt³

2012

Experimental Neurology

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We demonstrated previously that the hypothalamic supraoptic nucleus (SON) undergoes a robust axonal sprouting response following unilateral transection of the hypothalamo-neurohypophysial tract. Concomitant with this response is an increase in ciliary neurotrophic factor (CNTF) and CNTF receptor alpha (CNTFRα) expression in the contralateral non-uninjured SON from which the axonal outgrowth occurs. While these findings suggest that CNTF may act as a growth factor in support of neuronal plasticity in the SON, it remained to be determined if the observed increase in neurotrophin expression was related to the sprouting response per se or more generally to the increased neurosecretory activity associated with the post-lesion response. Therefore we used immunocytochemistry and Western blot analysis to examine the expression of CNTF and the components of the CNTF receptor complex in sprouting versus osmotically-stimulated SON. Western blot analysis revealed a significant increase in CNTF, CNTFRα, and gp130, but not LIFRβ, protein levels in the sprouting SON at 10 days post lesion in the absence of neuronal loss. In contrast, osmotic stimulation of neurosecretory activity in the absence of injury resulted in a significant decrease in CNTF protein levels with no change in CNTFRα, gp130, or LIFRβ protein levels. Immunocytochemical analysis further demonstrated gp130 localization on magnocellular neurons and astrocytes while the LIFRβ receptor was found only on astrocytes in the SON. These results are consistent with the hypothesis that increased CNTF and CNTFR complex in the sprouting, metabolically active SON are related directly to the sprouting response and not the increase in neurosecretory activity.

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Section: Discussionmentioning

confidence: 99%

Neuronal activity and axonal sprouting differentially regulate CNTF and CNTF receptor complex in the rat supraoptic nucleus

Askvig¹,

Leiphon²,

Watt³

2012

Experimental Neurology

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“…Candidate ligands for stress activation of IL-6 neurons include noradrenaline and IL-1␤, molecules capable of activating HNS neurons (3,21) and known to induce c-Fos and activate the MAPK pathway (17,34). Blockade of either ligand through intracerebroventricular injections of a ␤-adrenergic blocker or IL-1 receptor antagonist attenuates the plasma IL-6 response to psychological stress (14,30), providing strong evidence for endogenous roles of noradrenaline and IL-1␤ in the central regulation of stress-induced IL-6.…”

Section: Discussionmentioning

confidence: 99%

Stress activation of IL-6 neurons in the hypothalamus

Jankord

Zhang

Flak

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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An emerging literature attests to the ability of psychological stress to alter the inflammatory cytokine environment of the body. While the ability of stress to cause cytokine release is well established, the neural pathways involved in this control have yet to be identified. This study tests the hypothesis that IL-6 neurons of the hypothalamo-neurohypophyseal system (HNS), a neural pathway proposed to secrete IL-6 into the circulation, are activated in response to psychological stress. Colocalization studies confirm robust expression of IL-6 in cell bodies and fibers of vasopressin (but not oxytocin) neurons of the paraventricular (PVN) and supraoptic nucleus (SON) of the rat hypothalamus. In response to restraint, there was a greater increase in c-Fos expression in SON IL-6-positive (IL-6ϩ) neurons. In addition, both psychogenic (restraint) or systemic stress (hypoxia) lead to phosphorylated ERK induction only in IL-6ϩ magnocellular neurons, indicating selective activation of the MAPK signaling pathway in the IL-6 subset of magnocellular neurons. Finally, restraint upregulated IL-6 mRNA expression in both the PVN and SON, which was accompanied by a four-fold increase in circulating IL-6. The data indicate that noninflammatory stressors selectively activate IL-6 magnocellular neurons, upregulate IL-6 gene expression in the PVN and SON, and increase plasma IL-6. In summary, results show that IL-6 neurons of the HNS are a recruited component of the response to psychological stress. cytokine; magnocellular; supraoptic nucleus; paraventricular nucleus; hypothalamo-neurohypophyseal system STRESS CAUSES THE RELEASE of proinflammatory cytokines. The impact of stress on the inflammatory environment is a key mechanism by which stress negatively affects health (18). Inflammation is a contributing factor in a variety of human diseases (10) and is implicated in the progression of metabolic disorders (4), cardiovascular disease (2), depression (27), and autoimmune disease (9), all disorders that are stress sensitive.The acute-phase response to psychological stress is quite similar to the acute-phase response to infection, even when the perceived stressor poses no immediate threat to homeostasis. Like infection, stress increases proinflammatory cytokines (31), body temperature (22), activation of the hypothalamopituitary-adrenocortical (HPA) axis, and production of acutephase proteins in the liver (13). Although the magnitude of change in individual factors may vary, there is a large overlap between responses to stress and infection. With infection, IL-1␤, IL-6, and TNF-␣ are the primary mediators of the systemic acute-phase response and are derived from immune cells. In contrast, immune cells collected after psychological stress in humans do not show increased in vitro cytokine production (31), despite the fact that there are increases in the circulating concentration of IL-1␤ and IL-6. In particular, IL-6 production from immune cells collected in vivo then stimulated in vitro does not increase following stress exposure (31...

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“…PVN parvocellular neurones exposed to NE exhibit both inhibitory and excitatory effects, with α 1 ‐AR activation increasing action potential discharge, excitatory post‐synaptic potential (EPSP) frequency and, in some cases, direct depolarisation of neuronal membranes, whereas α 2 ‐AR activation decreases action potential discharge . Functionally, increased NE in the PVN increases AVP, CRH and oxytocin secretion …”

Section: Introductionmentioning

confidence: 99%

Activation of alpha‐1 adrenergic receptors increases cytosolic calcium in neurones of the paraventricular nucleus of the hypothalamus

Milanick

Polo‐Parada

Dantzler

et al. 2019

J Neuroendocrinology

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Norepinephrine (NE) activates adrenergic receptors (ARs) in the hypothalamic paraventricular nucleus (PVN) to increase excitatory currents, depolarise neurones and, ultimately, augment neuro‐sympathetic and endocrine output. Such cellular events are known to potentiate intracellular calcium ([Ca2+]i); however, the role of NE with respect to modulating [Ca2+]i in PVN neurones and the mechanisms by which this may occur remain unclear. We evaluated the effects of NE on [Ca2+]i of acutely isolated PVN neurones using Fura‐2 imaging. NE induced a slow increase in [Ca2+]i compared to artificial cerebrospinal fluid vehicle. NE‐induced Ca2+ elevations were mimicked by the α1‐AR agonist phenylephrine (PE) but not by α2‐AR agonist clonidine (CLON). NE and PE but not CLON also increased the overall number of neurones that increase [Ca2+]i (ie, responders). Elimination of extracellular Ca2+ or intracellular endoplasmic reticulum Ca2+ stores abolished the increase in [Ca2+]i and reduced responders. Blockade of voltage‐dependent Ca2+ channels abolished the α1‐AR induced increase in [Ca2+]i and number of responders, as did inhibition of phospholipase C inhibitor, protein kinase C and inositol triphosphate receptors. Spontaneous phasic Ca2+ events, however, were not altered by NE, PE or CLON. Repeated K+‐induced membrane depolarisation produced repetitive [Ca2+]i elevations. NE and PE increased baseline Ca2+, whereas NE decreased the peak amplitude. CLON also decreased peak amplitude but did not affect baseline [Ca2+]i. Taken together, these data suggest receptor‐specific influence of α1 and α2 receptors on the various modes of calcium entry in PVN neurones. They further suggest Ca2+ increase via α1‐ARs is co‐dependent on extracellular Ca2+ influx and intracellular Ca2+ release, possibly via a phospholipase C inhibitor‐mediated signalling cascade.

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Mapping study of noradrenergic stimulation of vasopressin release

Cited by 46 publications

References 49 publications

Neuronal activity and axonal sprouting differentially regulate CNTF and CNTF receptor complex in the rat supraoptic nucleus

Neuronal activity and axonal sprouting differentially regulate CNTF and CNTF receptor complex in the rat supraoptic nucleus

Stress activation of IL-6 neurons in the hypothalamus

Activation of alpha‐1 adrenergic receptors increases cytosolic calcium in neurones of the paraventricular nucleus of the hypothalamus

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