Moxonidine into the lateral parabrachial nucleus reduces renal and hormonal responses to cell dehydration

Corticotropin-releasing hormone (CRH)-containing processes were found by immunohistochemistry in the dorsal and lateral parabrachial nucleus extending medially over the dorsal aspect of the brachium and then along the lateral and medial aspects of the mesencephalic trigeminal tract. Reactivity of lesser density extended ventrally from the medial parabrachial nucleus into the locus ceruleus and subceruleus. To determine if CRH acts in these areas to modulate plasma adrenocorticotropic hormone (ACTH) and arginine vasopressin (AVP), acutely prepared, chloralose-anesthetized cats were tested with microinjections (100 nl/min, 2 min). Plasma ACTH increased significantly after injections of CRH (2 pmol) along the dorsal aspect of the brachium and in the locus subceruleus (P < 0.05 and P < 0.01, respectively). Plasma AVP increased significantly after injections of CRH into the medial parabrachial nucleus (P < 0.01). These responses of ACTH and AVP differed significantly from those to injections of either vehicle or glutamate at identical sites and from those to CRH injected in other areas. None of these latter responses was significant. CRH was without effect on arterial pressure even though glutamate (30 nmol) injected into the area ventral and medial to the brachium elicited a significant pressor response. We suggest that excitatory amino acids such as glutamate act in this area to activate neurons with descending projections that influence autonomic function. In contrast, CRH appears to activate other neurons with ascending projections that drive neuroendocrine release.

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Serotonergic mechanisms of the lateral parabrachial nucleus in renal and hormonal responses to isotonic blood volume expansion

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00351.2006 ◽

2007 ◽

Vol 292 (3) ◽

pp. R1190-R1197 ◽

Cited By ~ 14

Author(s):

Lisandra Oliveira Margatho ◽

Alexandre Giusti-Paiva ◽

Jose Vanderlei Menani ◽

Lucila Leico Kagohara Elias ◽

Laura M. Vivas ◽

...

Keyword(s):

Blood Volume ◽

Volume Expansion ◽

Parabrachial Nucleus ◽

Urinary Volume ◽

Hormonal Responses ◽

Water Excretion ◽

Lateral Parabrachial Nucleus ◽

Blood Volume Expansion ◽

Male Wistar Rats ◽

Serotonergic Receptor

This study investigated the involvement of serotonergic mechanisms of the lateral parabrachial nucleus (LPBN) in the control of sodium (Na+) excretion, potassium (K+) excretion, and urinary volume in unanesthetized rats subjected to acute isotonic blood volume expansion (0.15 M NaCl, 2 ml/100 g of body wt over 1 min) or control rats. Plasma oxytocin (OT), vasopressin (VP), and atrial natriuretic peptide (ANP) levels were also determined in the same protocol. Male Wistar rats with stainless steel cannulas implanted bilaterally into the LPBN were used. In rats treated with vehicle in the LPBN, blood volume expansion increased urinary volume, Na+ and K+ excretion, and also plasma ANP and OT. Bilateral injections of serotonergic receptor antagonist methysergide (1 or 4 μg/200 ηl) into the LPBN reduced the effects of blood volume expansion on increased Na+ and K+ excretion and urinary volume, while LPBN injections of serotonergic 5-HT2a/HT2c receptor agonist, 2.5-dimetoxi-4-iodoamphetamine hydrobromide (DOI; 1 or 5 μg/200 ηl) enhanced the effects of blood volume expansion on Na+ and K+ excretion and urinary volume. Methysergide (4 μg) into the LPBN decreased the effects of blood volume expansion on plasma ANP and OT, while DOI (5 μg) increased them. The present results suggest the involvement of LPBN serotonergic mechanisms in the regulation of urinary sodium, potassium and water excretion, and hormonal responses to acute isotonic blood volume expansion.

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GLP-1 Receptor Stimulation of the Lateral Parabrachial Nucleus Reduces Food Intake: Neuroanatomical, Electrophysiological, and Behavioral Evidence

Endocrinology ◽

10.1210/en.2014-1248 ◽

2014 ◽

Vol 155 (11) ◽

pp. 4356-4367 ◽

Cited By ~ 46

Author(s):

Jennifer E. Richard ◽

Imre Farkas ◽

Fredrik Anesten ◽

Rozita H. Anderberg ◽

Suzanne L. Dickson ◽

...

Keyword(s):

Feeding Behavior ◽

Fluorescent Protein ◽

Yellow Fluorescent Protein ◽

Parabrachial Nucleus ◽

Lateral Parabrachial Nucleus ◽

Electrophysiological Studies ◽

Glucagon Like Peptide 1 ◽

Behavioral Evidence ◽

Stimulation Of

Abstract The parabrachial nucleus (PBN) is a key nucleus for the regulation of feeding behavior. Inhibitory inputs from the hypothalamus to the PBN play a crucial role in the normal maintenance of feeding behavior, because their loss leads to starvation. Viscerosensory stimuli result in neuronal activation of the PBN. However, the origin and neurochemical identity of the excitatory neuronal input to the PBN remain largely unexplored. Here, we hypothesize that hindbrain glucagon-like peptide 1 (GLP-1) neurons provide excitatory inputs to the PBN, activation of which may lead to a reduction in feeding behavior. Our data, obtained from mice expressing the yellow fluorescent protein in GLP-1-producing neurons, revealed that hindbrain GLP-1-producing neurons project to the lateral PBN (lPBN). Stimulation of lPBN GLP-1 receptors (GLP-1Rs) reduced the intake of chow and palatable food and decreased body weight in rats. It also activated lPBN neurons, reflected by an increase in the number of c-Fos-positive cells in this region. Further support for an excitatory role of GLP-1 in the PBN is provided by electrophysiological studies showing a remarkable increase in firing of lPBN neurons after Exendin-4 application. We show that within the PBN, GLP-1R activation increased gene expression of 2 energy balance regulating peptides, calcitonin gene-related peptide (CGRP) and IL-6. Moreover, nearly 70% of the lPBN GLP-1 fibers innervated lPBN CGRP neurons. Direct intra-lPBN CGRP application resulted in anorexia. Collectively, our molecular, anatomical, electrophysiological, pharmacological, and behavioral data provide evidence for a functional role of the GLP-1R for feeding control in the PBN.

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Rapid stimulation of sodium intake combining aldosterone into the 4th ventricle and the blockade of the lateral parabrachial nucleus

Neuroscience ◽

10.1016/j.neuroscience.2017.01.005 ◽

2017 ◽

Vol 346 ◽

pp. 94-101 ◽

Cited By ~ 1

Author(s):

S. Gasparini ◽

M.R. Melo ◽

G.F. Leite ◽

P.A. Nascimento ◽

G.M.F. Andrade-Franzé ◽

...

Keyword(s):

Sodium Intake ◽

Parabrachial Nucleus ◽

Lateral Parabrachial Nucleus ◽

Rapid Stimulation ◽

4Th Ventricle ◽

Stimulation Of

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Activation of P2X‐purinergic receptors in the lateral parabrachial nucleus increases renal sympathetic nerve discharge and mean arterial pressure in anesthetized rats (686.13)

The FASEB Journal ◽

10.1096/fasebj.28.1_supplement.686.13 ◽

2014 ◽

Vol 28 (S1) ◽

Author(s):

Miguel Menezes ◽

Michele Favero ◽

Kenta Yamamoto ◽

Jose Menani ◽

Patricia Paula ◽

...

Keyword(s):

Mean Arterial Pressure ◽

Arterial Pressure ◽

Sympathetic Nerve ◽

Purinergic Receptors ◽

Parabrachial Nucleus ◽

Renal Sympathetic Nerve ◽

Anesthetized Rats ◽

Lateral Parabrachial Nucleus ◽

Renal Sympathetic ◽

Nerve Discharge

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Divergent neural pathways emanating from the lateral parabrachial nucleus mediate distinct components of the pain response

10.1101/602466 ◽

2019 ◽

Cited By ~ 1

Author(s):

Michael C. Chiang ◽

Eileen K. Nguyen ◽

Andrew E. Papale ◽

Sarah E. Ross

Keyword(s):

Ventromedial Hypothalamus ◽

Parabrachial Nucleus ◽

Projection Neurons ◽

Pain Response ◽

Neural Pathways ◽

Bed Nucleus ◽

Lateral Parabrachial Nucleus ◽

Efferent Projections ◽

Efferent Neurons ◽

Nociceptive Input

ABSTRACTThe lateral parabrachial nucleus (lPBN) is a major target of spinal projection neurons conveying nociceptive input into supraspinal structures. However, the functional role of distinct lPBN efferents for diverse nocifensive responses have remained largely uncharacterized. Here, we show that two populations of efferent neurons from different regions of the lPBN collateralize to distinct targets. Activation of efferent projections to the ventromedial hypothalamus (VMH) or lateral periaqueductal gray (lPAG) drive escape behaviors, whereas the activation of lPBN efferents to the bed nucleus stria terminalis (BNST) or central amygdala (CEA) generates an aversive memory. Finally, we provide evidence that dynorphin expressing neurons span cytoarchitecturally distinct domains of the lPBN to coordinate these distinct aspects of the nocifensive response.HIGHLIGHTSSpatially segregated neurons in the lPBN collateralize to distinct targets.Distinct output pathways give rise to separate aspects of the pain response.Dynorphin neurons within the lPBN convey noxious information across subdivisions.eTOC BLURBChiang et al. reveal that neurons in spatially segregated regions of the lateral parabrachial nucleus collateralize to distinct targets, and that activation of distinct efferents gives rise to separate components of the nocifensive response.

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