Yee B K, Feldon J, Rawlins J N
Department of Experimental Psychology, University of Oxford, England.
Behav Neurosci. 1995 Apr;109(2):227-40. doi: 10.1037//0735-7044.109.2.227.
Latent inhibition (LI) refers to the retardation in learning about the significance of a neutral stimulus that results from its nonreinforced preexposure. There is evidence that electrolytic or aspiration lesions of the hippocampal formation can disrupt LI (see I. Weiner, 1990). It has been suggested that this effect may stem from the interruption of a projection from the retrohippocampal region to the nucleus accumbens (A. J. M. Clark et al., 1992). The present experiment assessed this possibility by comparing LI in rats with retrohippocampal N-methyl-D-aspartate (NMDA) lesions extending from the entorhinal cortex to the ventral subiculum to that seen in vehicle controls and unoperated controls. LI was abolished by the retrohippocampal lesion. The effect of the lesion on LI was prevented by treatment with systemic haloperidol (0.2 mg/kg). The results are discussed with respect to an animal model of schizophrenia.
潜伏抑制(LI)是指由于中性刺激在无强化条件下的预先暴露而导致其在学习该刺激意义时出现的延迟。有证据表明,海马结构的电解或损毁会破坏潜伏抑制(见I. 维纳,1990年)。有人提出,这种效应可能源于海马后区域向伏隔核投射的中断(A. J. M. 克拉克等人,1992年)。本实验通过比较海马后N-甲基-D-天冬氨酸(NMDA)损毁从内嗅皮质延伸至腹侧下托的大鼠与溶剂对照组及未手术对照组大鼠的潜伏抑制情况,对这一可能性进行了评估。海马后损毁消除了潜伏抑制。全身给予氟哌啶醇(0.2毫克/千克)可防止损毁对潜伏抑制的影响。本文结合精神分裂症动物模型对结果进行了讨论。