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Mitochondrial oxidant stress in locus coeruleus is regulated by activity and nitric oxide synthase.

Abstract：

:Loss of noradrenergic locus coeruleus (LC) neurons is a prominent feature of aging-related neurodegenerative diseases, such as Parkinson's disease (PD). The basis of this vulnerability is not understood. To explore possible physiological determinants, we studied LC neurons using electrophysiological and optical approaches in ex vivo mouse brain slices. We found that autonomous activity in LC neurons was accompanied by oscillations in dendritic Ca(2+) concentration that were attributable to the opening of L-type Ca(2+) channels. This oscillation elevated mitochondrial oxidant stress and was attenuated by inhibition of nitric oxide synthase. The relationship between activity and stress was malleable, as arousal and carbon dioxide increased the spike rate but differentially affected mitochondrial oxidant stress. Oxidant stress was also increased in an animal model of PD. Thus, our results point to activity-dependent Ca(2+) entry and a resulting mitochondrial oxidant stress as factors contributing to the vulnerability of LC neurons.

journal_name

Nat Neurosci

journal_title

Nature neuroscience

authors

Sanchez-Padilla J,Guzman JN,Ilijic E,Kondapalli J,Galtieri DJ,Yang B,Schieber S,Oertel W,Wokosin D,Schumacker PT,Surmeier DJ

doi

10.1038/nn.3717

subject

Has Abstract

pub_date

2014-06-01 00:00:00

pages

832-40

issue

6

eissn

1097-6256

issn

1546-1726

pii

nn.3717

journal_volume

17

pub_type

杂志文章

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