De Castro E Silva E, Ferreira H, Cunha M, Bulcão C, Sarmento C, De Oliveira I, Fregoneze J B
Department of Physiology, Federal University of Bahia, Brazil.
Pharmacol Biochem Behav. 1996 Mar;53(3):687-93. doi: 10.1016/0091-3057(95)02070-5.
The effect of acute third ventricle cadmium administration on the drinking behavior of adult male rats under different situations was studied. Injections of cadmium chloride (0.07, 0.7,and 7.0 ng/rat) significantly attenuated water intake in dehydrated rats. Drinking behavior induced by acute intracerebroventricular injections of carbachol (2 micrograms/rat) or angiotensin II (5 ng/rat) was also inhibited by central cadmium injections. Cadmium-induced blockade in water intake in dehydrated animals was reverted by the previous administration of a 5-HT2 antagonist (RP62203) in different doses (5 and 10 micrograms/rat). The data clearly reveal that cadmium elicits very fast actions on the central nervous system. It is suggested that cadmium-induced attenuation of water intake may rely on at least three different mechanisms: impairment of cholinergic and angiotensinergic systems in the brain and stimulation of a central serotonergic drive acting on 5-HT2 receptors. The study of cadmium neurotoxicity by observation of drinking behavior, a behavioral parameter easy to be recorded and measured, is proposed.
研究了成年雄性大鼠急性经第三脑室给予镉在不同情况下对其饮水行为的影响。注射氯化镉（0.07、0.7和7.0纳克/只大鼠）显著减少了脱水大鼠的饮水量。中枢注射镉也抑制了急性脑室内注射卡巴胆碱（2微克/只大鼠）或血管紧张素II（5纳克/只大鼠）所诱导的饮水行为。预先给予不同剂量（5和10微克/只大鼠）的5-HT2拮抗剂（RP62203）可逆转镉诱导的脱水动物饮水减少。数据清楚地表明，镉对中枢神经系统产生非常快速的作用。提示镉诱导的饮水量减少可能至少依赖三种不同机制：脑内胆碱能和血管紧张素能系统受损以及作用于5-HT2受体的中枢5-羟色胺能驱动的刺激。提出通过观察饮水行为这一易于记录和测量的行为参数来研究镉的神经毒性。
