Dipsogenic stimulation in ibotenic DRN-lesioned rats induces concomitant sodium appetite

Cavalcante-Lima, H.R.; Lima, H.R.C.; Costa-e-Sousa, Ricardo H.; Olivares, Emerson Lopes; Cedraz-Mercez, P.L.; Reis, Rafael; Badauê‐Passos, Daniel; de-Lucca, W.; Medeiros, Magda Alves de; Cortês, Wellington da Silva; Reis, L. C.

doi:10.1016/j.neulet.2004.10.017

Cited by 20 publications

(15 citation statements)

References 27 publications

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“…Although we did not investigate the forebrain angiotensinergic sensitivity, we recently demonstrated that experiments involving an increase in plasma ANG II levels exarcebate the sodium appetite of iboteniclesioned rats (31). Hence, the view that suppression of neural pathways originating in the DRN reduces the threshold of the sodium appetite response through an increase in angiotensinergic sensitivity of SFO neurons should be considered.…”

Section: Discussionmentioning

confidence: 98%

Chronic excitotoxic lesion of the dorsal raphe nucleus induces sodium appetite

Cavalcante-Lima

Badauê‐Passos

de-Lucca

et al. 2005

Braz J Med Biol Res

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We determined if the dorsal raphe nucleus (DRN) exerts tonic control of basal and stimulated sodium and water intake. Male Wistar rats weighing 300-350 g were microinjected with phosphate buffer (PB-DRN, N = 11) or 1 µg/0.2 µl, in a single dose, ibotenic acid (IBO-DRN, N = 9 to 10) through a guide cannula into the DRN and were observed for 21 days in order to measure basal sodium appetite and water intake and in the following situations: furosemide-induced sodium depletion (20 mg/kg, sc, 24 h before the experiment) and a low dose of dietary captopril (1 mg/g chow). From the 6th day after ibotenic acid injection IBO-DRN rats showed an increase in sodium appetite (12.0 ± 2.3 to 22.3 ± 4.6 ml 0.3 M NaCl intake) whereas PB-DRN did not exceed 2 ml (P < 0.001). Water intake was comparable in both groups. In addition to a higher dipsogenic response, sodium-depleted IBO-DRN animals displayed an increase of 0.3 M NaCl intake compared to PB-DRN (37.4 ± 3.8 vs 21.6 ± 3.9 ml 300 min after fluid offer, P < 0.001). Captopril added to chow caused an increase of 0.3 M NaCl intake during the first 2 days (IBO-DRN, 33.8 ± 4.3 and 32.5 ± 3.4 ml on day 1 and day 2, respectively, vs 20.2 ± 2.8 ml on day 0, P < 0.001). These data support the view that DRN, probably via ascending serotonergic system, tonically modulates sodium appetite under basal and sodium depletion conditions and/or after an increase in peripheral or brain angiotensin II.

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Section: Discussionmentioning

confidence: 98%

Chronic excitotoxic lesion of the dorsal raphe nucleus induces sodium appetite

Cavalcante-Lima

Badauê‐Passos

de-Lucca

et al. 2005

Braz J Med Biol Res

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“…Studies showing enhanced sodium intake in rats with electrolytic or ibotenic acid lesions in the dorsal raphe nucleus (DRN) suggest that the DRN is a source of endogenous serotonin that inhibits salt appetite (20,21). Such inhibition is possibly linked to reduced ANP release and modulation of forebrain activity in circumventricular organs (9,87,109,110).…”

Section: Major Neurohumoral Factors Inhibiting Water And/or Sodium Inmentioning

confidence: 99%

“…Drinking studies in the pigeon suggest that an homologous serotonergic system inhibits fluid intake in both birds and mammals (18). Consistent with the inhibitory effect that serotonin receptor activation has on sodium appetite, early studies also showed that when given systemically, agonists that reduce serotonin release or antagonists that act on 5HT 2 receptors increase sodium intake (29,114).Studies showing enhanced sodium intake in rats with electrolytic or ibotenic acid lesions in the dorsal raphe nucleus (DRN) suggest that the DRN is a source of endogenous serotonin that inhibits salt appetite (20,21). Such inhibition is possibly linked to reduced ANP release and modulation of forebrain activity in circumventricular organs (9,87,109,110).…”

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confidence: 95%

Role of the lateral parabrachial nucleus in the control of sodium appetite

Menani

Luca

Johnson

2014

American Journal of Physiology-Regulatory, Integrative and Comp

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.-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. sodium intake; angiotensin; electrolyte balance; thirst ANIMALS CONSTANTLY LOSE WATER and electrolytes to the external environment, but specific autonomic, hormonal, and behavioral mechanisms operate continuously to adjust and restore body fluid-electrolyte balance. The rate of loss from the kidneys is primarily controlled by neural and hormonal actions, but loss may also occur passively through the largely uncontrolled processes of respiration (evaporation), perspiration, transpiration, and salivation. These later modes of loss are referred to as insensible loss because they cannot be easily measured. Severe loss of both sodium and water may also occur in disorders associated with emesis and diarrhea. However, despite such ongoing challenges, the osmolarity and volume of body fluids are maintained within reasonably narrow limits, thus allowing normal metabolic and cardiovascular functions. Although renal mechanisms can slow water and sodium loss, the restoration of fluid homeostasis is only made possible by the mobilization of behaviors that result in the ingestion of water and sodium (usually NaCl). The behavioral responses of seeking out and consuming water and salty substances involve the motivational states of thirst and salt appetite. Salt appetite is also frequently referred to as sodium appetit...

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“…To inhibit sodium intake, DRN could act on forebrain structures that facilitate sodium intake, such as the nuclei from the lamina terminalis including SFO and OVLT. DRN could also influence another key inhibitor of sodium intake, the lateral parabrachial nucleus (LPBN) [1][2][7][8][9]31,33,40,45,56].…”

Section: Introductionmentioning

confidence: 99%

Role of cerebrospinal fluid-contacting nucleus in sodium sensing and sodium appetite

Xing

et al. 2015

Physiology & Behavior

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Dipsogenic stimulation in ibotenic DRN-lesioned rats induces concomitant sodium appetite

Cited by 20 publications

References 27 publications

Chronic excitotoxic lesion of the dorsal raphe nucleus induces sodium appetite

Chronic excitotoxic lesion of the dorsal raphe nucleus induces sodium appetite

Role of the lateral parabrachial nucleus in the control of sodium appetite

Role of cerebrospinal fluid-contacting nucleus in sodium sensing and sodium appetite

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