Gray J A, Joseph M H, Hemsley D R, Young A M, Warburton E C, Boulenguez P, Grigoryan G A, Peters S L, Rawlins J N, Taib C T
Department of Psychology and MRC Behavioural Neurochemistry Group, Institute of Psychiatry, Denmark Hill, London, UK.
Behav Brain Res. 1995 Nov;71(1-2):19-31. doi: 10.1016/0166-4328(95)00154-9.
Latent inhibition (LI) consists in a retardation of conditioning seen when the to-be-conditioned stimulus is first presented a number of times without other consequence. Disruption of LI has been proposed as a possible model of the cognitive abnormality that underlies the positive psychotic symptoms of acute schizophrenia. We review here evidence in support of the model, including experiments tending to show that: (1) disruption of LI is characteristic of acute, positively-symptomatic schizophrenia; (2) LI depends upon dopaminergic activity; (3) LI depends specifically upon dopamine release in n. accumbens; (4) LI depends upon the integrity of the hippocampal formation and the retrohippocampal region reciprocally connected to the hippocampal formation; (5) the roles of n. accumbens and the hippocampal system in LI are interconnected.
潜伏抑制(LI)表现为当待条件刺激首次多次呈现且无其他结果时,条件作用出现延迟。LI的破坏已被提出作为急性精神分裂症阳性精神病性症状背后认知异常的一种可能模型。我们在此回顾支持该模型的证据,包括倾向于表明以下几点的实验:(1)LI的破坏是急性、有阳性症状的精神分裂症的特征;(2)LI依赖于多巴胺能活动;(3)LI特别依赖于伏隔核中的多巴胺释放;(4)LI依赖于海马结构以及与海马结构相互连接的海马后区域的完整性;(5)伏隔核和海马系统在LI中的作用是相互关联的。