Thornberg S A, Saklad S R
Department of Pharmacy Practice and Administration, College of Pharmacy at Rutgers, State University of New Jersey, New Brunswick, USA.
Pharmacotherapy. 1996 Jan-Feb;16(1):82-93.
Current models of drug-induced psychosis insufficiently describe the symptoms of schizophrenia. Phencyclidine-induced psychosis is a model that more completely reflects the pathophysiology of the disease. By decreasing glutamatergic neurotransmission, phencyclidine decreases gamma-aminobutyric acid release from the nucleus accumbens, striatum, and hippocampus (manifested by MK-801); may inhibit tonic release of dopamine from the nucleus accumbens and striatum, resulting in increased dopamine phasic reactivity; and decreases long-term potentiation. Glutamatergic system dysfunction may be involved, but pharmacologic manipulation has not revealed a clear mechanism of this dysfunction.
当前药物性精神病模型对精神分裂症症状的描述不够充分。苯环己哌啶所致精神病是一种能更全面反映该疾病病理生理学的模型。通过降低谷氨酸能神经传递，苯环己哌啶减少伏隔核、纹状体和海马体中γ-氨基丁酸的释放（以MK-801为表现）；可能抑制伏隔核和纹状体中多巴胺的紧张性释放，导致多巴胺相位反应性增加；并降低长时程增强。谷氨酸能系统功能障碍可能与之有关，但药物操作尚未揭示这种功能障碍的明确机制。
