Hosutt J A, Rowland N, Stricker E M
J Comp Physiol Psychol. 1981 Feb;95(1):104-13. doi: 10.1037/h0077759.
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.
已知大鼠穹窿下器（SFO）的电解损伤会消除其对静脉注射血管紧张素II（AII）的饮水反应。此类损伤还会减弱皮下注射20%聚乙二醇溶液（PEG）后的饮水行为，这表明AII可能在低血容量期间介导口渴方面发挥重要作用。然而，目前的研究表明，当30%PEG处理导致更大的血浆容量不足时，此类有SFO损伤的大鼠可能会正常饮水。当用咖啡因或高渗NaCl溶液预处理时，它们对20%PEG的反应也可能正常饮水。此外，它们对相对低剂量的高渗盐水可能无饮水反应，但给予更大剂量时则会正常饮水。这些以及其他结果表明，SFO参与了口渴控制系统，并且在其受损后，可能需要比平常更大的刺激才能引发饮水行为。从这个角度来看，正如所观察到的，在这些动物中，超阈值刺激或药物诱导的激活阈值降低后会出现饮水行为，SFO中假定的AII受体的丧失也导致了它们对AII诱导的口渴特别严重的缺陷。
