Central effects of various ligands on drinking behavior in eels acclimated to seawater
Central effects of various ligands on drinking behavior in eels acclimated to seawater
复制标题
DOI：
10.1242/jeb.00146
复制
发表时间：
2003-02-01
影响因子：
2.8
通讯作者：
Ando, M
中科院分区：
文献类型：
--
作者：
Kozaka, T;Fujii, Y;Ando, M
脑内注射血管紧张素II(Eang II，5×10(-13)-5×10(-8))、乙酰胆碱(ACh，5×10(-12)-5×10(-9)摩尔)、P物质(5×10(-10)摩尔)和异丙肾上腺素(一种β-肾上腺素能受体激动剂，5×10(-11)-5×10(-9)摩尔)可增加海水鳗鱼的摄水量。Eang II、ACh和异丙肾上腺素的作用呈剂量依赖性。脑室注射鳗鱼心钠素(eANP，5x10(-13)-5x10(-10)mol)、5-羟色胺(5-羟色胺，5x10(-12)-5x10(-8)mol)、生长激素(ghrelin，5x10(-12)-5x10(-10)摩尔)、γ-氨基丁酸(GABA，5x10(-11)-5x10(-8)摩尔)、催乳素(PRL，5x10(-10)-5x10(-9)摩尔)、精氨酸血管妥英素(AVT，5x10(-12)摩尔)、血管活性肠肽(VIP，5x10(-11)-5x10(-8)摩尔)可抑制大鼠的饮水摄取。5×10(-11)摩尔)、去甲肾上腺素(5×10(-9)摩尔L(-1))和苯肾上腺素(α-肾上腺素受体激动剂，5×10(-11)-5x10(-9)摩尔)。EANP、5-羟色胺、Ghrelin、GABA、PRL和苯肾上腺素的抑制作用呈剂量依赖性。与静脉给药相比，Eang II对颅内的刺激作用相对持久。静脉注射eang II的刺激作用立即消失，随后被抑制，这可以很好地解释为心房分泌eANP的增加。
Intracranial injection of eel angiotensin II (eANG II, 5x10(-13)-5x10(-8) mol), acetylcholine (ACh, 5x10(-12)-5x10(-9) mol), substance P (5x10(-10) mol) and isoproterenol (a beta-adrenoceptor agonist, 5x10(-11)-5x10(-9) mol) enhanced water intake in the seawater eel. The effects of eANG II, ACh and isoproterenol were dose-dependent. By contrast, water intake was inhibited by intracranial injection of eel atrial natriuretic peptide (eANP, 5x10(-13)-5x10(-10) mol), serotonin (5-HT, 5x10(-12)-5x10(-8) mol), ghrelin (5x10(-12)-5x10(-10) mol), gamma-amino butyric acid (GABA, 5x10(-11)-5x10(-8) mol), prolactin (PRL, 5x10(-10)-5x10(-9) mol), arginine vasotocin (AVT, 5x10(-12) mol), vasoactive intestinal peptide (VIP, 5x10(-11) mol), noradrenaline (5x10(-9) mol l(-1)) and phenylephrine (alpha-adrenoceptor agonist, 5x10(-11)-5x10(-9) mol). The inhibitory effects of eANP, 5-HT, ghrelin, GABA, PRL and phenylephrine were dose-dependent. The intracranial stimulatory effect of eANG II was relatively long-lasting compared with the intravenous effect. The stimulatory effect of intravenous eANG II disappeared immediately, and was followed by an inhibition, which could be well explained by an increase in eANP secretion from the atrium.