Josselyn S A, Frankland P W, Petrisano S, Bush D E, Yeomans J S, Vaccarino F J
Department of Psychology, University of Toronto, Ontario, Canada.
Peptides. 1995;16(7):1313-5. doi: 10.1016/0196-9781(95)02013-m.
The neuropeptide cholecystokinin (CCK), via the CCKB receptor, increases behaviors associated with anxiety in laboratory animals and humans. The present experiment assessed the role of endogenous CCKB function in fear-potentiated startle, a test of "anxiety" in rats. The amplitude of the acoustic startle response is potentiated if preceded by a stimulus that has been previously paired with shock. Pretreatment with the CCKB antagonist L-365,260 (0, 0.1, 1.0, and 10.0 mg/kg, IP) did not affect baseline acoustic startle amplitudes, but dose-dependently decreased fear-potentiated startle. These results indicate that the specific attenuation of fear-potentiated startle induced by L-365,260 was not due to a general decrease in motor responsivity. The present findings are consistent with the effects of CCKB antagonists in other tests measuring anxiety in animals.
神经肽胆囊收缩素(CCK)通过CCKB受体,增加实验动物和人类中与焦虑相关的行为。本实验评估了内源性CCKB功能在恐惧增强惊吓反应中的作用,恐惧增强惊吓反应是大鼠“焦虑”的一种测试。如果在声惊吓反应之前出现过与电击配对的刺激,那么声惊吓反应的幅度会增强。用CCKB拮抗剂L-365,260(0、0.1、1.0和10.0mg/kg,腹腔注射)预处理不影响基线声惊吓幅度,但剂量依赖性地降低了恐惧增强惊吓反应。这些结果表明,L-365,260诱导的恐惧增强惊吓反应的特异性减弱并非由于运动反应性的普遍降低。本研究结果与CCKB拮抗剂在其他测量动物焦虑的测试中的作用一致。