Corticotropin-releasing hormone in the lateral parabrachial nucleus inhibits sodium appetite in rats
| Autor: | Alan Kim Johnson, Emilio de Castro e Silva, Josmara Bartolomei Fregoneze |
|---|---|
| Rok vydání: | 2006 |
| Předmět: |
Male
endocrine system medicine.medical_specialty Corticotropin-Releasing Hormone Physiology media_common.quotation_subject Sodium Drinking Appetite chemistry.chemical_element Receptors Corticotropin-Releasing Hormone Rats Sprague-Dawley Corticotropin-releasing hormone Furosemide Pons Physiology (medical) Internal medicine medicine Animals Lateral parabrachial nucleus Sodium Chloride Dietary Receptor media_common Body fluid Chemistry Peptide Fragments Rats Endocrinology hormones hormone substitutes and hormone antagonists Homeostasis Hormone |
| Zdroj: | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. 290:R1136-R1141 |
| ISSN: | 1522-1490 0363-6119 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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