Fregoneze J B, Ferreira H, Soares T, Luz C P, Bulcão C, Nascimento T, Marinho C A, Sarmento C, De-Oliveira I R, Cunha M
Departamento de Fisiologia, Universidade Federal da Bahia, Salvador, Brasil.
Braz J Med Biol Res. 1995 Jun;28(6):711-4.
Zinc is found in many brain regions where it participates in important processes such as neurotransmission and neuromodulation. We previously demonstrated that acute third ventricle injection of zinc inhibits water intake in dehydrated rats. The present study was undertaken to explore a possible link between zinc-induced inhibition of water intake in dehydrated rats and serotonergic systems in the brain. Adult, male Wistar rats had the third ventricle cannulated a week before the experiments. After an overnight period of water deprivation, the animals (N = 12 per group) received acute intracerebroventricular injections (2 microliters) of Zn(Ac)2 (6.7, 67.1 and 671.6 ng/rat). Control animals (N = 12) received NaAc (671.6 ng/rat). Zinc-treated animals displayed a significant, dose-dependent reduction in water intake. Water intake after 120 min was 7.70 +/- 0.50 ml in control (NaAc-treated) dehydrated rats while animals treated with the highest dose of Zn(Ac)2 drank 2.63 +/- 0.73 ml. Third ventricle injections of SDZ 216-525, a selective 5-HT1A receptor antagonist, 45 min before zinc administration, generated a dose-dependent reversal of zinc-induced thirst blockade in water-deprived rats. At the highest dose used (10 micrograms/rat), the water intake of the animals after 120 min was 7.30 +/- 0.23 ml, a value equal to that of control animals. These data suggest that zinc may decrease water intake in dehydrated rats by activation of a 5-HT1A receptor-related mechanism.
锌存在于许多脑区，参与神经传递和神经调节等重要过程。我们之前证明，向第三脑室急性注射锌可抑制脱水大鼠的饮水。本研究旨在探讨脱水大鼠中锌诱导的饮水抑制与大脑中血清素能系统之间的可能联系。成年雄性Wistar大鼠在实验前一周进行第三脑室插管。经过一夜的禁水后，动物（每组N = 12）接受急性脑室内注射（2微升）Zn(Ac)2（6.7、67.1和671.6纳克/大鼠）。对照动物（N = 12）接受NaAc（671.6纳克/大鼠）。锌处理的动物饮水量显著降低，且呈剂量依赖性。对照（NaAc处理）脱水大鼠120分钟后的饮水量为7.70±0.50毫升，而用最高剂量Zn(Ac)2处理的动物饮水量为2.63±0.73毫升。在给予锌前45分钟，向第三脑室注射选择性5-HT1A受体拮抗剂SDZ 216-525，可使缺水大鼠中锌诱导的口渴阻断产生剂量依赖性逆转。在使用的最高剂量（10微克/大鼠）下，动物120分钟后的饮水量为7.30±0.23毫升，与对照动物的值相等。这些数据表明，锌可能通过激活5-HT1A受体相关机制来减少脱水大鼠的饮水量。
