Impaired drinking responses of rats with lesions on the subfornical organ
| Autor: | Edward M. Stricker, Jean A. Hosutt, Neil Rowland |
|---|---|
| Rok vydání: | 1981 |
| Předmět: |
Male
medicine.medical_specialty Drinking Stimulation Thirst Polyethylene Glycols chemistry.chemical_compound Internal medicine Hypovolemia medicine Animals Receptors Angiotensin Dose-Response Relationship Drug business.industry Angiotensin II General Medicine Water-Electrolyte Balance Neurosecretory Systems Subfornical organ Hypertonic saline Rats medicine.anatomical_structure Endocrinology chemistry Tonicity medicine.symptom business Caffeine Subfornical Organ |
| Zdroj: | Journal of comparative and physiological psychology. 95(1) |
| ISSN: | 0021-9940 |
| Popis: | electrolytic lesions of the subfornical organ (SFO) in rats are known to abolish their drinking response to intravenous infusion of angiotensin II (AII). Such lesions also attenuate drinking after 20% polyethylene glycol solution (PEG) is given subcutaneously, which suggests that AII may play an important role in mediating thirst during hypovolemia. However, the present studies show that such rats with SFO lesions may drink normal amounts when larger plasma volume deficits are caused by 30% PEG treatment. They also may drink normal amounts in response to 20% PEG when pretreated either with caffeine or hypertonic NaCl solution. Furthermore, they may not drink in response to relatively low doses of hypertonic saline but drink normal amounts when given larger doses. These and other results suggest that the SFO is involved in a control system for thirst and that after damage to it, greater stimulation than usual may be required for drinking to be initiated. From this perspective, drinking would be expected following either suprathreshold stimulation or drug-induced lowering of the activation threshold in these animals, as was observed, with the loss of putative AII receptors in the SFO also contributing to their particularly severe deficits in thirst induced by AII. |
| Databáze: | OpenAIRE |
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