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慢性电惊厥后局部脑葡萄糖利用率:对电惊厥治疗作用模式的启示。

Local cerebral glucose utilization after chronic electroconvulsive shock: implications for the mode of action of electroconvulsive therapy.

机构信息

University of Liverpool, Liverpool L69 3BX.

出版信息

J Psychopharmacol. 1991 Jan;5(2):111-9. doi: 10.1177/026988119100500204.

Abstract

The [(14)C]2-deoxyglucose autoradiographic technique measures local rates of glucose utilization simul taneously in all functional and anatomical subunits of the CNS and provides a measure of the functional consequences in the CNS of any manipulation. Glucose utilization was measured in 24 regions of the CNS in conscious rats one day after the end of a 7-day course of electroconvulsive shock (chronic ECS). Chronic ECS had minimal effects on local glucose utilization in most brain areas (including extrapyramidal, cortical, hippocampal and other limbic structures) with only the nucleus accumbens displaying a significant alteration (reduced by 25% from sham-treated animals). These data suggest that functional alterations in the nucleus accumbens may underly a unique therapeutic mechanism of electroconvulsive therapy (ECT), which is known to be effective in a wide variety of psychiatric syndromes characterized by mixed depressive and 'positive' psychotic symptoms. Our findings (supported by preliminary data from a study of sub-convulsive ECS) suggest that the functional sequelae of repeated electroconvulsions in selectively vulnerable limbic and hippocampal structures-more likely to underly ECT's unwanted cognitive side effect than its wanted therapeutic effect-may be attenuated by reducing the power of the stimulus required to induce seizures.

摘要

[(14)C]2-脱氧葡萄糖放射自显影技术可同时测量中枢神经系统所有功能和解剖亚单位的局部葡萄糖利用率,并提供中枢神经系统中任何操作的功能后果的测量。在电惊厥治疗(慢性 ECS)结束后一天,对清醒大鼠的中枢神经系统的 24 个区域进行了葡萄糖利用测量。慢性 ECS 对大多数脑区(包括锥体外系、皮质、海马和其他边缘结构)的局部葡萄糖利用几乎没有影响,只有伏隔核显示出明显的改变(与假处理动物相比减少了 25%)。这些数据表明,伏隔核的功能改变可能是电惊厥治疗(ECT)的一种独特治疗机制的基础,ECT 已知对各种以混合抑郁和“阳性”精神病症状为特征的精神综合征有效。我们的发现(由一项亚惊厥 ECS 研究的初步数据支持)表明,在选择性易受影响的边缘和海马结构中反复电惊厥的功能后果——比其预期的治疗效果更有可能导致 ECT 的认知副作用——可能通过降低诱发癫痫所需的刺激强度来减轻。

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