Evidence for impaired long-term potentiation in schizophrenia and its relationship to motor skill leaning
Evidence for impaired long-term potentiation in schizophrenia and its relationship to motor skill leaning
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DOI：
10.1093/cercor/bhm151
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发表时间：
2008-05-01
期刊：
影响因子：
3.7
通讯作者：
Daskalakis, Zafiris J.
中科院分区：
文献类型：
--
作者：
Frantseva, Marina V.;Fitzgerald, Paul B.;Daskalakis, Zafiris J.
几条证据表明，精神分裂症（SCZ）与大脑皮层可塑性受损有关。然而，很少有直接的神经生理学证据表明SCZ中异常的长时程增强（LTP）样可塑性，也很少有人类证据表明LTP与学习和记忆之间存在联系。使用称为配对联想刺激（PAS）的神经生理学范式评价LTP。PAS涉及配对正中神经电刺激与经颅磁刺激（TMS）在对侧运动皮层（拇短展肌肌肉激活）在25毫秒的刺激间隔。这种配对被提供在0.1 Hz的频率为30分钟。LTP反映了运动诱发电位（MEP）的变化之前和之后PAS。此外，运动技能学习进行了评估，使用旋转追求任务。与健康受试者相比，SCZ患者表现出明显的MEP易化缺陷后PAS和受损的旋转追踪运动学习。在所有受试者中，LTP和运动技能学习之间存在显着关联。这些数据为SCZ中LTP中断提供了证据，而LTP与运动技能学习之间的关联表明，SCZ中学习和记忆的缺陷可能是通过LTP紊乱介导的。
Several lines of evidence suggest that schizophrenia (SCZ) is associated with disrupted plasticity in the cortex. However, there is little direct neurophysiological evidence of aberrant long-term potentiation (LTP)-like plasticity in SCZ and little human evidence to establish a link between LTP to learning and memory. LTP was evaluated using a neurophysiological paradigm referred to as paired associative stimulation (PAS). PAS involves pairing of median nerve electric stimulation with transcranial magnetic stimulation (TMS) over the contralateral motor cortex (for abductor pollicis brevis muscle activation) delivered at 25-ms interstimulus interval. This pairing was delivered at a frequency of 0.1 Hz for 30 min. LTP was reflected by the change in motor evoked potentials (MEPs) before and after PAS. In addition, motor skill learning was assessed using the rotary pursuit task. Compared with healthy subjects, patients with SCZ demonstrated significant MEP facilitation deficits following PAS and impaired rotary-pursuit motor learning. Across all subjects there was a significant association between LTP and motor skill learning. These data provide evidence for disrupted LTP in SCZ, whereas the association between LTP with motor skill learning suggests that the deficits in learning and memory in SCZ may be mediated through disordered LTP.