Corticotropin-releasing hormone in the lateral parabrachial nucleus inhibits sodium appetite in rats

2006 ◽  
Vol 290 (4) ◽  
pp. R1136-R1141 ◽  
Author(s):  
Emilio De Castro e Silva ◽  
Josmara B. Fregoneze ◽  
Alan Kim Johnson

The present study investigated the role of corticotropin-releasing hormone (CRH) in the lateral parabrachial nucleus (LPBN) in the behavioral control of body fluid homeostasis by determining the effect of bilateral injections of the CRH receptor antagonist, α-helical corticotropin-releasing factor (CRF)9–41, and the CRH receptor agonist, CRH, on sodium chloride (salt appetite) and water (thirst) intake. Groups of adult, male Sprague-Dawley rats had stainless-steel cannulas implanted bilaterally into the LPBN and were sodium depleted or water deprived. Bilateral injections of α-helical CRF9–41 into the LPBN significantly potentiated water and salt intake in the sodium-depleted rats when access to fluids was restored. Bilateral injections of α-helical CRF9–41 into the LPBN (1.0 μg) also increased sodium appetite in water-deprived rats. Conversely, in sodium-depleted animals, bilateral injections of CRH inhibited sodium chloride intake. These results suggest that there is an endogenous CRH inhibitory mechanism operating in the LPBN to modulate the intake of sodium (salt appetite). This mechanism may contribute to the behavioral control of restoration of body fluid homeostasis in sodium-deficient states.

1986 ◽  
Vol 251 (3) ◽  
pp. R504-R509 ◽  
Author(s):  
L. E. Ohman ◽  
A. K. Johnson

The lateral parabrachial nucleus (LPBN) has been shown to be anatomically linked to a number of forebrain nuclei and medullary structures implicated in the control of body fluid balance and cardiovascular regulation. Although these connections suggest a role for the LPBN in body fluid homeostasis, there is currently little or no physiological or behavioral data to support this notion. The purpose of the present series of experiments was to determine the importance of the ventrolateral region of the LPBN (VLLPBN) in the behavioral response to various thirst challenges. Rats with electrolytic lesions of the VLLPBN and control rats were studied after administration of angiotensin II (ANG II) (1.5 and 3.0 mg/kg), isoproterenol (30 and 100 micrograms/kg), polyethylene glycol (20%) and hypertonic saline (4 and 12%). It was found that rats with lesions drank more in response to ANG II and isoproterenol administration than did control animals.


1994 ◽  
Vol 267 (1) ◽  
pp. R337-R348 ◽  
Author(s):  
D. E. Carlson ◽  
A. M. Nabavian ◽  
D. S. Gann

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.


2014 ◽  
Vol 306 (4) ◽  
pp. R201-R210 ◽  
Author(s):  
Jose V. Menani ◽  
Laurival A. De Luca ◽  
Alan Kim Johnson

In states of sodium deficiency many animals seek and consume salty solutions to restore body fluid homeostasis. These behaviors reflect the presence of sodium appetite that is a manifestation of a pattern of central nervous system (CNS) activity with facilitatory and inhibitory components that are affected by several neurohumoral factors. The primary focus of this review is on one structure in this central system, the lateral parabrachial nucleus (LPBN). However, before turning to a more detailed discussion of the LPBN, a brief overview of body fluid balance-related body-to-brain signaling and the identification of the primary CNS structures and humoral factors involved in the control of sodium appetite is necessary. Angiotensin II, mineralocorticoids, and extracellular osmotic changes act on forebrain areas to facilitate sodium appetite and thirst. In the hindbrain, the LPBN functions as a key integrative node with an ascending output that exerts inhibitory influences on forebrain regions. A nonspecific or general deactivation of LPBN-associated inhibition by GABA or opioid agonists produces NaCl intake in euhydrated rats without any other treatment. Selective LPBN manipulation of other neurotransmitter systems [e.g., serotonin, cholecystokinin (CCK), corticotrophin-releasing factor (CRF), glutamate, ATP, or norepinephrine] greatly enhances NaCl intake when accompanied by additional treatments that induce either thirst or sodium appetite. The LPBN interacts with key forebrain areas that include the subfornical organ and central amygdala to determine sodium intake. To summarize, a model of LPBN inhibitory actions on forebrain facilitatory components for the control of sodium appetite is presented in this review.


2014 ◽  
Vol 47 (1) ◽  
pp. 11-18 ◽  
Author(s):  
C.A.F. Andrade ◽  
G.M.F. Andrade-Franzé ◽  
P.M. De Paula ◽  
L.A. De Luca Jr. ◽  
J.V. Menani

1996 ◽  
Vol 270 (1) ◽  
pp. R162-R168 ◽  
Author(s):  
J. V. Menani ◽  
R. L. Thunhorst ◽  
A. K. Johnson

This study investigated the effects of bilateral injections of serotonergic receptor agonist and antagonist into the lateral parabrachial nucleus (LPBN) on the ingestion of water and 0.3 M NaCl induced by intracerebroventricular angiotensin II (ANG II) or by combined subcutaneous injections of the diuretic furosemide (Furo) and the angiotensin-converting enzyme inhibitor captopril (Cap). Rats had stainless steel cannulas implanted bilaterally into the LPBN and into the left lateral ventricle. Bilateral LPBN pretreatment with the serotonergic 5-HT1/5-HT2 receptor antagonist methysergide (4 micrograms/200 nl each site) increased 0.3 M NaCl and water intakes induced by intracerebroventricular ANG II (50 ng/microliter) and 0.3 M NaCl intake induced by subcutaneous Furo + Cap. Pretreatment with bilateral LPBN injections of a serotonergic 5-HT2A/2C receptor agonist DOI (5 micrograms/200 nl) significantly reduced 0.3 M NaCl intake induced by subcutaneous Furo + Cap. Pretreatment with methysergide or DOI into the LPBN produced no significant changes in the water intake induced by subcutaneous Furo + Cap. These results suggest that serotonergic mechanisms associated with the LPBN may have inhibitory roles in water and sodium ingestion in rats.


2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Silvia Gasparini ◽  
Joelma Maria Cardoso Gomide ◽  
Glaucia Maria Fabricio Andrade-Franzé ◽  
Carina Aparecida Fabricio Andrade ◽  
Débora Simões Almeida Colombari ◽  
...  

Neuroscience ◽  
2011 ◽  
Vol 183 ◽  
pp. 160-170 ◽  
Author(s):  
L.B. De Oliveira ◽  
E.H. Kimura ◽  
J.C. Callera ◽  
L.A. De Luca ◽  
D.S.A. Colombari ◽  
...  

1996 ◽  
Vol 271 (6) ◽  
pp. R1470-R1476 ◽  
Author(s):  
D. S. Colombari ◽  
J. V. Menani ◽  
A. K. Johnson

This study investigated the roles of serotonin (5-HT) receptors in the lateral parabrachial nucleus (LPBN) and brain angiotensin type 1 (AT1) receptors in the intake of 0.3 M NaCl and water induced by angiotensin II (ANG II). Rats were implanted with stainless steel cannulas for injections into the subfornical organ (SFO) and into the LPBN. Bilateral LPBN pretreatment with the nonselective serotonergic 5-HT1/5-HT2 receptor antagonist methysergide (4 micrograms/200 nl) markedly enhanced 0.3 M NaCl intake induced by injections of ANG II (20 ng/200 nl) into the SFO. Pretreatment of the SFO with the AT1 receptor antagonist losartan (1 microgram/200 nl) blocked the intake of 0.3 M NaCl induced by ANG II in combination with LPBN methysergide injections. These results suggest that serotonergic mechanisms associated with the LPBN inhibit the expression of salt appetite induced by ANG II injections into the SFO. In addition, the results indicate that the enhanced NaCl intake generated by central administration of ANG II in the presence of LPBN 5-HT blockade is mediated by brain AT1 receptors.


Sign in / Sign up

Export Citation Format

Share Document