Alterations in neurotransmitter co-release in Parkinson's disease

被引：15

作者：

Barcomb, Kelsey ^{[1
]}

Ford, Christopher P. ^{[1
,2
]}

机构：

[1] Univ Colorado, Sch Med, Dept Pharmacol, Anschutz Med Campus, Aurora, CO 80045 USA

[2] Univ Colorado, Dept Pharmacol, Sch Med, 12800 19 th Ave, Aurora, CO 80045 USA

来源：

EXPERIMENTAL NEUROLOGY | 2023年 / 370卷

关键词：

Parkinson 's; Dopamine; GABA; Glutamate; Co-release; Striatum; Basal ganglia; STRIATAL SYNAPTIC PLASTICITY; MIDBRAIN DOPAMINE NEURONS; ALPHA-SYNUCLEIN; CHOLINERGIC INTERNEURONS; GLUTAMATE CORELEASE; RELEASE; VGLUT2; SYNAPSES; TRANSMISSION; MODULATION;

D O I：

10.1016/j.expneurol.2023.114562

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Parkinson's disease is a neurological disorder characterized by degeneration of midbrain dopamine neurons, which results in numerous adaptations in basal ganglia circuits. Research over the past twenty-five years has identified that midbrain dopamine neurons of the substantia nigra pars compacta (SNc) and ventral tegmental area (VTA) co-release multiple other transmitters including glutamate and GABA, in addition to their canonical transmitter, dopamine. This review summarizes previous work characterizing neurotransmitter co-release from dopamine neurons, work examining potential changes in co-release dynamics that result in animal models of Parkinson's disease, and future opportunities for determining how dysfunction in co-release may contribute to circuit dysfunction in Parkinson's disease.

引用

页数：9

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