Parabrachial and hypothalamic interaction in sodium appetite
| Autor: | Stacey Ruch, Ralph Norgren, Samantha Dayawansa, Steven Peckins |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2011 |
| Předmět: |
Male
medicine.medical_specialty Time Factors Lateral hypothalamus Physiology Sodium media_common.quotation_subject Drinking Hypothalamus chemistry.chemical_element Appetite Lesion Rats Sprague-Dawley chemistry.chemical_compound Eating Physiology (medical) Internal medicine Pons Neural Pathways Weight Loss medicine Animals media_common Parabrachial Nucleus Sodium Dietary Articles Feeding Behavior Rats Neuroanatomical Tract-Tracing Techniques Endocrinology chemistry medicine.symptom Luteinizing hormone Ibotenic acid |
| Popis: | Rats with bilateral lesions of the lateral hypothalamus (LH) fail to exhibit sodium appetite. Lesions of the parabrachial nuclei (PBN) also block salt appetite. The PBN projection to the LH is largely ipsilateral. If these deficits are functionally dependent, damaging the PBN on one side and the LH on the other should also block Na appetite. First, bilateral ibotenic acid lesions of the LH were needed because the electrolytic damage used previously destroyed both cells and axons. The ibotenic LH lesions produced substantial weight loss and eliminated Na appetite. Controls with ipsilateral PBN and LH lesions gained weight and displayed robust sodium appetite. The rats with asymmetric PBN-LH lesions also gained weight, but after sodium depletion consistently failed to increase intake of 0.5 M NaCl. These results dissociate loss of sodium appetite from the classic weight loss after LH damage and prove that Na appetite requires communication between neurons in the LH and the PBN. |
| Databáze: | OpenAIRE |
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