Heal D J, Akagi H, Bowdler J M, Green A R
Eur J Pharmacol. 1981 Nov 5;75(4):231-7. doi: 10.1016/0014-2999(81)90549-5.
Clonidine administration at low dose produces hypoactivity in both rats and mice, probably by stimulation of presynaptic alpha 2-adrenoceptors in the brain. This behaviour is antagonised by yohimbine pretreatment but is unaffected by pretreatment with prazosin. An electroconvulsive shock (ECS) given once daily for 10 days markedly attenuated the hypoactivity in both species when tested 24 h after the final shock. The attenuation in mice was not found after either a single ECS or 10 subconvulsive shocks. Ten ECS did not alter the hypoactivity response produced by (+/-)-propranolol in mice. Clonidine administration decreased rat brain MOPEG-SO4 concentrations. A single ECS given daily for 10 days abolished this decrease. These results suggest that repeated ECS causes a subsensitivity of alpha 2-adrenoceptors in the brain and that these receptors may be located presynaptically.
低剂量可乐定给药会使大鼠和小鼠活动减少，这可能是通过刺激大脑中的突触前α2-肾上腺素能受体实现的。这种行为可被育亨宾预处理拮抗，但不受哌唑嗪预处理的影响。每天给予一次电惊厥休克（ECS），持续10天，在最后一次休克后24小时进行测试时，两种动物的活动减少均明显减弱。单次ECS或10次亚惊厥性休克后，小鼠未出现活动减少减弱的情况。10次ECS并未改变（±）-普萘洛尔在小鼠中产生的活动减少反应。可乐定给药会降低大鼠脑内MOPEG-SO4浓度。每天给予一次ECS，持续10天可消除这种降低。这些结果表明，重复给予ECS会导致大脑中α2-肾上腺素能受体的敏感性降低，且这些受体可能位于突触前。
