Osaka T, Kawano S, Ueta Y, Inenaga K, Kannan H, Yamashita H
Department of Physiology, University of Occupational and Environmental Health, Kitakyushu, Japan.
Brain Res Bull. 1993;31(1-2):135-44. doi: 10.1016/0361-9230(93)90020-c.
Kainic acid (KA) and muscimol were injected into the lateral preoptic area (LPO) of the rat to study their effects on drinking behavior. A low dose (5 ng) of KA, which stimulates neurons, decreased the amount of water intake induced by hypertonic saline (IP) and angiotensin II (SC). Injection of 2 ng muscimol, a potent GABAA receptor agonist that suppresses neurons, facilitated drinking responses induced by hypertonic saline, but did not affect angiotensin II-induced drinking. Rats injected with a high dose (150 ng) of KA, which destroys neurons, showed marked polydipsia accompanied by increased urination. One week after the KA lesion, drinking and urine output recovered to normal. During the polydipsia, a small volume of concentrated urine could be excreted if water intake was restricted. After recovery, excessive drinking responses followed water deprivation and hypertonic saline load. The rats normally drank water in response to angiotensin II and to polyethylene glycol solution. The results show that activation of LPO neurons inhibits water intake, and that suppression of LPO neurons facilitates osmotically induced water intake. Therefore, LPO neurons are probably involved in the inhibition of thirst.
将海藻酸（KA）和蝇蕈醇注射到大鼠的外侧视前区（LPO），以研究它们对饮水行为的影响。低剂量（5纳克）的KA可刺激神经元，减少高渗盐水（腹腔注射）和血管紧张素II（皮下注射）诱导的饮水量。注射2纳克蝇蕈醇，一种强效的γ-氨基丁酸A型（GABAA）受体激动剂，可抑制神经元，促进高渗盐水诱导的饮水反应，但不影响血管紧张素II诱导的饮水。注射高剂量（150纳克）的KA可破坏神经元，大鼠出现明显的多饮并伴有尿量增加。KA损伤一周后，饮水和尿量恢复正常。在多饮期间，如果限制水摄入，可排出少量浓缩尿液。恢复后，禁水和高渗盐水负荷后会出现过度饮水反应。大鼠通常会对血管紧张素II和聚乙二醇溶液做出饮水反应。结果表明，LPO神经元的激活会抑制水摄入，而LPO神经元的抑制会促进渗透压诱导的水摄入。因此，LPO神经元可能参与口渴的抑制。
