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帕金森病中的纹状体可塑性:中等棘状神经元的营养不良性变化与帕金森病的进展

Striatal plasticity in parkinsonism: dystrophic changes in medium spiny neurons and progression in Parkinson's disease.

作者信息

Deutch A Y

机构信息

Department of Psychiatry, Vanderbilt University Medical Center, Psychiatric Hospital at Vanderbilt, Nashville, TN 37212, USA.

出版信息

J Neural Transm Suppl. 2006(70):67-70. doi: 10.1007/978-3-211-45295-0_12.

Abstract

Striatal dopamine loss in Parkinson's Disease (PD) sets into play a variety of compensatory responses to help counter dopamine depletion. Most of these changes involve surviving dopamine neurons, but there are also changes in striatal medium spiny neurons (MSNs), which are the major target of dopamine axons. Among these changes are decreases in MSN dendritic length and spine density, which may dampen excessive corticostriatal glutamatergic drive onto MSNs that occurs secondary to dopamine loss. An increasing knowledge of dendritic changes in PD suggests strategies for tracking progressive worsening of symptoms and is opening new ideas on novel therapeutic strategies for PD.

摘要

帕金森病(PD)中纹状体多巴胺的丧失引发了多种代偿反应,以帮助对抗多巴胺耗竭。这些变化大多涉及存活的多巴胺能神经元,但纹状体中等棘状神经元(MSNs)也有变化,而MSNs是多巴胺轴突的主要靶点。这些变化包括MSN树突长度和棘密度的降低,这可能会抑制多巴胺丧失继发的皮质纹状体谷氨酸能对MSNs的过度驱动。对PD中树突变化的了解日益增加,这为追踪症状的进行性恶化提供了策略,并为PD的新型治疗策略开启了新思路。

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