Involvement of serotonergic systems in the lateral parabrachial nucleus in sodium and water intake: a microdialysis study in the rat

Tanaka, Junichi; Hayashi, Yasushi; Yamato, Koichi; Miyakubo, Hiroko; Nomura, Masahiko

doi:10.1016/j.neulet.2003.12.040

Cited by 34 publications

(25 citation statements)

References 10 publications

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“…However, in hypovolemia, similarly to what happened in the present work, increased Fos-ir in the AP, mNTS and PVNparvo preceded the ingestion of 0.3 M NaCl intake [46][47][48]. Such increase in Fos-ir coincides with the time of reduced serotonergic activation in the LPBN, before hypovolemic rats start to ingest hypertonic NaCl [49]. Taken together, the results indicate that increased cell activity in those areas anticipates the time when sodium intake occurs.…”

Section: Discussionsupporting

confidence: 87%

Sodium intake, brain c-Fos protein and gastric emptying in cell-dehydrated rats treated with methysergide into the lateral parabrachial nucleus

David

Roncari

Lauar

et al. 2015

Physiology & Behavior

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Section: Discussionsupporting

confidence: 87%

Sodium intake, brain c-Fos protein and gastric emptying in cell-dehydrated rats treated with methysergide into the lateral parabrachial nucleus

David

Roncari

Lauar

et al. 2015

Physiology & Behavior

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“…In contrast to the effects of methysergide, LPBN injections of the 5HT 2 receptor agonist 2,5-dimethoxy-4-iodoamphetamine hydrochloride (DOI) reduces Furo ϩ CAP-induced 0.3 M NaCl intake (96). Consistent with these functional results, the release of serotonin and its metabolite 5-hydroxyindoleacetic acid is reduced in the PBN after Furo ϩ CAP treatment and enhanced by 0.3 M NaCl intake (126).…”

Section: Neurotransmitter and Receptor Distribution In The Lpbn: Basimentioning

confidence: 85%

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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“…In integrative means, LPBN interacts reciprocally with DRN and receives afferents of NTS transmitters of visceral sensory information concerning alterations in the volume and ECF electrolyte composition (Petrov et al 1992a, b). This postulation was recently reassessed in an article, in which it was demonstrated that hypertonic saline and water ingestion increase signifi cantly 5-HT and 5-HIAA levels in LPBN (Tanaka et al 2004). On the other hand, the combined treatment of furosemide + low dose of captopril evoked a reduction in the 5-HT and 5-HIAA concentration in LPBN.…”

Section: Salt Intake Increases the Fos Protein Expression 5-htergic Nmentioning

confidence: 96%

“…However, considering the role of SFO in the sodium appetite expression and AT1 receptors identifi cation over there, the hypothesis of 5-HTergic transmission in this structure to influence the angiotensinergic activity must not be excluded. Tanaka's group has evidenced through the microdialysis that microinjection of ANG II into SFO reduces the extracellular 5-HT and its metabolites levels (Tanaka et al 2004).…”

Section: Regulationmentioning

confidence: 99%

Role of the serotoninergic system in the sodium appetite control

Reis

2007

An. Acad. Bras. Ciênc.

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The present article reviews the role of the serotoninergic system in the regulation of the sodium appetite. Data from the peripheral and icv administration of serotoninergic (5-HTergic) agents showed the participation of 5-HT2/3 receptors in the modulation of sodium appetite. These observations were extended with the studies carried out after brain serotonin depletion, lesions of DRN and during blockade of 5-HT2A/2C receptors in lateral parabrachial nucleus (LPBN). Brain serotonin depletion and lesions of DRN increased the sodium appetite response, in basal conditions, after sodium depletion and hypovolemia or after beta-adrenergic stimulation as well. These observations raised the hypothesis that the suppression of ascending pathways from the DRN, possibly, 5-HTergic fi bers, modifi es the angiotensinergic or sodium sensing mechanisms of the subfornical organ involved in the control of the sodium appetite. 5-HTergic blockade in LPBN induced to similar results, particularly those regarded to the natriorexigenic response evoked by volume depletion or increase of the hypertonic saline ingestion induced by brain angiotensinergic stimulation. In conclusion, many evidences lead to acceptation of an integrated participation resulting of an interaction, between DRN and LPBN, for the sodium appetite control.

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Involvement of serotonergic systems in the lateral parabrachial nucleus in sodium and water intake: a microdialysis study in the rat

Cited by 34 publications

References 10 publications

Sodium intake, brain c-Fos protein and gastric emptying in cell-dehydrated rats treated with methysergide into the lateral parabrachial nucleus

Sodium intake, brain c-Fos protein and gastric emptying in cell-dehydrated rats treated with methysergide into the lateral parabrachial nucleus

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

Role of the serotoninergic system in the sodium appetite control

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