De Castro-e-Silva E, Sarmento C, Nascimento T A, Luz C P, Soares T, Marinho A, Cunha M, Bulcäo C, De Oliveira I R, Fregoneze J B
Department of Physiology, Federal University of Bahia, Salvador, Brazil.
Pharmacol Biochem Behav. 1997 Aug;57(4):749-54. doi: 10.1016/s0091-3057(96)00457-1.
L-694,247, a selective 5-HT1D receptor agonist, injected directly into the third ventricle (2.5, 5.0, and 10.0 micrograms/rat) of dehydrated rats induced a dose-dependent partial blockade of water intake. Injected in this way, the compound abolishes drinking behavior induced by third ventricle administration of carbachol (2 micrograms/rat), angiotensin II (5 ng/rat), and isoproterenol (40 micrograms/rat). In addition, intraventricular injections of L-694,247 did not modify water intake in normohydrated rats. The effects of L-694,247 are due to a specific interaction with 5-HT1D receptors, because its inhibitory effect on water intake in dehydrated rats is blocked by the previous administration of a 5-HT1D antagonist, GR 127935 (5 micrograms/rat), directly into the third ventricle. It is concluded that central 5-HT1D receptor activation disrupts the functional integrity of central pathways related to drinking behavior.
L-694,247是一种选择性5-羟色胺1D（5-HT1D）受体激动剂，直接注射到脱水大鼠的第三脑室（2.5、5.0和10.0微克/大鼠）会引起饮水的剂量依赖性部分阻断。以这种方式注射时，该化合物可消除由第三脑室注射卡巴胆碱（2微克/大鼠）、血管紧张素II（5纳克/大鼠）和异丙肾上腺素（40微克/大鼠）诱导的饮水行为。此外，脑室内注射L-694,247不会改变正常水合大鼠的饮水量。L-694,247的作用是由于与5-HT1D受体的特异性相互作用，因为其对脱水大鼠饮水的抑制作用可被预先直接注射到第三脑室的5-HT1D拮抗剂GR 127935（5微克/大鼠）所阻断。得出的结论是，中枢5-HT1D受体激活会破坏与饮水行为相关的中枢通路的功能完整性。
