Sarnyai Z, Höhn J, Szabó G, Penke B
Institute of Pathophysiology, Albert Szent-Györgyi Medical University, Szeged, Hungary.
Life Sci. 1992;51(26):2019-24. doi: 10.1016/0024-3205(92)90151-e.
The role of endogenous CRF in the locomotor hyperactivity induced by cocaine was investigated by using the immunoneutralization of endogenous CRF and an antagonist of CRF-receptors (alpha-helical CRF9-41: alpha h-CRF) in rats. Different dilutions of anti-CRF antibody (1:5, 1:20, but not 1:100) injected intracerebroventricularly (i.c.v.) 24 hours before the cocaine treatment blocked the expression of locomotor hyperactivity. Pretreatment with different doses (0.001, 0.01, 0.1, 1.0 micrograms i.c.v.) of alpha h-CRF inhibited the locomotor hyperactivity induced by cocaine dose-dependently. Neither the immunoneutralization nor the receptor blockade for CRF changed the hyperactivity induced by another locomotor stimulant caffeine. These results serve as indirect in vivo evidence of the selective role of endogenous CRF in the cocaine-induced behavioral alterations. The findings have implications as concerns the possible role of CRF in human psychopathological changes induced by cocaine.
通过在大鼠体内对内源性促肾上腺皮质激素释放因子（CRF）进行免疫中和以及使用CRF受体拮抗剂（α-螺旋CRF9-41：αh-CRF），研究了内源性CRF在可卡因诱导的运动性多动中的作用。在给予可卡因治疗前24小时，脑室内（i.c.v.）注射不同稀释度的抗CRF抗体（1:5、1:20，但不是1:100）可阻断运动性多动的表达。用不同剂量（0.001、0.01、0.1、1.0微克i.c.v.）的αh-CRF进行预处理可剂量依赖性地抑制可卡因诱导的运动性多动。对CRF进行免疫中和或受体阻断均未改变另一种运动兴奋剂咖啡因诱导的多动。这些结果作为内源性CRF在可卡因诱导的行为改变中选择性作用的间接体内证据。这些发现对于CRF在可卡因诱导的人类心理病理变化中可能发挥的作用具有启示意义。
