Abstract：
:Nitric oxide (NO) has a number of physiological and pathophysiological effects in the nervous system. One target of NO is the mitochondrion, where it inhibits respiration and ATP synthesis, which may contribute to NO-mediated neuronal injury. Our recent studies suggested that impaired mitochondrial function impairs mitochondrial trafficking, which could also contribute to neuronal injury. Here, we studied the effects of NO on mitochondrial movement and morphology in primary cultures of forebrain neurons using a mitochondrially targeted enhanced yellow fluorescent protein. NO produced by two NO donors, papa non-oate and diethylamine/NO complex, caused a rapid cessation of mitochondrial movement but did not alter morphology. Movement recovered after removal of NO. The effects of NO on movement were associated with dissipation of the mitochondrial membrane potential. Increasing cGMP levels using 8-bromoguanosine 3',5'-cyclic monophosphate, did not mimic the effects on mitochondrial movement. Furthermore, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), an inhibitor of NO-induced activation of soluble guanylate cyclase, did not block the effects of NO. Thus, neither increasing nor decreasing cGMP levels had an effect on mitochondrial movement. Based on these data, we conclude that NO is a novel modulator of mitochondrial trafficking in neurons, which may act through the inhibition of mitochondrial function.
journal_name
J Neurochemjournal_title
Journal of neurochemistryauthors
Rintoul GL,Bennett VJ,Papaconstandinou NA,Reynolds IJdoi
10.1111/j.1471-4159.2006.03788.xkeywords:
subject
Has Abstractpub_date
2006-05-01 00:00:00pages
800-6issue
3eissn
0022-3042issn
1471-4159pii
JNC3788journal_volume
97pub_type
杂志文章abstract：:The motor signs of Parkinson's disease have been partly attributed to an overinhibition of the external globus pallidus (GP) that results from hyperactivity of striatopallidal GABA/enkephalinergic neurons. The goals of this study were to measure basal levels of extracellular fluid GABA in the GP of normal cats, 1-meth...
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doi：10.1111/j.1471-4159.1985.tb07240.x
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pub_type： 杂志文章
doi：10.1111/j.1471-4159.1981.tb01640.x
更新日期：1981-02-01 00:00:00
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pub_type： 杂志文章
doi：10.1111/j.1471-4159.1986.tb01746.x
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pub_type： 杂志文章
doi：10.1046/j.1471-4159.1995.65030998.x
更新日期：1995-09-01 00:00:00
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journal_title：Journal of neurochemistry
pub_type： 杂志文章
doi：10.1111/j.1471-4159.1989.tb09217.x
更新日期：1989-05-01 00:00:00
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journal_title：Journal of neurochemistry
pub_type： 杂志文章,评审
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更新日期：2007-06-01 00:00:00
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journal_title：Journal of neurochemistry
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更新日期：2006-03-01 00:00:00
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journal_title：Journal of neurochemistry
pub_type： 杂志文章
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更新日期：1998-10-01 00:00:00
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journal_title：Journal of neurochemistry
pub_type： 杂志文章
doi：10.1111/j.1471-4159.1983.tb08041.x
更新日期：1983-03-01 00:00:00
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journal_title：Journal of neurochemistry
pub_type： 杂志文章,评审
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更新日期：2010-08-01 00:00:00
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journal_title：Journal of neurochemistry
pub_type： 杂志文章
doi：10.1111/j.1471-4159.1987.tb05606.x
更新日期：1987-03-01 00:00:00
