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icv四肽Asn-Ala-Gly-Ala(NAGA)能引起大鼠痛阈持续升高,并呈剂量依赖关系(0.03—0.24μmol/rat)。这一作用可被纳洛酮(icv.0.26mg·kg~(-1))翻转。icv甲硫氨酸脑啡肽抗血清或亮氨酸脑啡肽抗血清,能抑制NAGA引起的镇痛作用;icv强啡肽A_(1-13)抗血清或β-内啡肽抗血清不影响NAGA引起的镇痛作用。结果提示NAGA的镇痛作用可能与大鼠脑内甲硫氨酸脑啡肽和亮氨酸脑啡肽的释放有关。
The icv tetrapeptide Asn-Ala-Gly-Ala (NAGA) caused a sustained increase of pain threshold in a dose-dependent manner (0.03-0.24μmol / rat). This effect can be reversed by naloxone (icv 0.26 mg · kg -1). icv methionine enkephalin antiserum or leucine enkephalin antiserum can inhibit the analgesic effect caused by NAGA; icv dynorphin A 1-13 antiserum or β-endorphin antiserum is not Affect the analgesic effect caused by NAGA. The results suggest that the analgesic effect of NAGA may be related to the release of enkephalin and leucine enkephalin in rat brain.