Abstract：
:The decrease of pyruvate and ketoglutarate dehydrogenase complex activities is the main cause of energy and acetyl-CoA deficits in thiamine deficiency-evoked cholinergic encephalopathies. However, disturbances in pathways of acetyl-CoA metabolism leading to appearance of cholinergic deficits remain unknown. Therefore, the aim of this work was to investigate alterations in concentration and distribution of acetyl-CoA and in acetylcholine metabolism in brain nerve terminals, caused by thiamine deficits. They were induced by the pyrithiamine, a potent inhibitor of thiamine pyrophosphokinase. The thiamine deficit reduced metabolic fluxes through pyruvate and ketoglutarate dehydrogenase steps, yielding deficits of acetyl-CoA in mitochondrial and cytoplasmic compartments of K-depolarized nerve terminals. It also inhibited indirect transport of acetyl-CoA though ATP-citrate lyase pathway being without effect on its direct Ca-dependent transport to synaptoplasm. Resulting suppression of synaptoplasmic acetyl-CoA correlated with inhibition of quantal acetylcholine release (r = 0.91, p = 0.012). On the other hand, thiamine deficiency activated non-quantal acetylcholine release that was independent of shifts in intraterminal distribution of acetyl-CoA. Choline acetyltransferase activity was not changed by these conditions. These data indicate that divergent alterations in the release of non-quantal and quantal acetylcholine pools from thiamine deficient nerve terminals could be caused by the inhibition of acetyl-CoA and citrate synthesis in their mitochondria. They in turn, caused inhibition of acetyl-CoA transport to the synaptoplasmic compartment through ATP-citrate lyase pathway yielding deficits of cholinergic functions.
journal_name
J Neurochemjournal_title
Journal of neurochemistryauthors
Jankowska-Kulawy A,Bielarczyk H,Pawełczyk T,Wróblewska M,Szutowicz Adoi
10.1111/j.1471-4159.2010.06919.xsubject
Has Abstractpub_date
2010-10-01 00:00:00pages
333-42issue
2eissn
0022-3042issn
1471-4159pii
JNC6919journal_volume
115pub_type
杂志文章abstract：:Neuronal nicotinic acetylcholine receptors labelled with tritiated agonists are reduced in the cerebral cortex in Alzheimer's disease (AD), but to date it has not been demonstrated which nicotinic receptor subunits contribute to this deficit. In the present study, autopsy tissue from the temporal cortex of 14 AD cases...
journal_title：Journal of neurochemistry
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journal_title：Journal of neurochemistry
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journal_title：Journal of neurochemistry
pub_type： 杂志文章
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pub_type： 杂志文章
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pub_type： 杂志文章
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更新日期：1991-03-01 00:00:00
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pub_type： 杂志文章
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更新日期：1992-07-01 00:00:00
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pub_type： 杂志文章
doi：10.1111/j.1471-4159.1980.tb06298.x
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journal_title：Journal of neurochemistry
pub_type： 杂志文章
doi：10.1111/j.1471-4159.2004.02706.x
更新日期：2004-10-01 00:00:00
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pub_type： 临床试验,杂志文章
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更新日期：2009-01-01 00:00:00
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journal_title：Journal of neurochemistry
pub_type： 杂志文章
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journal_title：Journal of neurochemistry
pub_type： 杂志文章
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更新日期：2010-01-01 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：2006-11-01 00:00:00
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更新日期：1986-05-01 00:00:00
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pub_type： 杂志文章
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journal_title：Journal of neurochemistry
pub_type： 杂志文章
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更新日期：1989-11-01 00:00:00
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pub_type： 杂志文章
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更新日期：1999-10-01 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：1989-05-01 00:00:00
abstract：:Using nuclear reaction 6Li(n, alpha)3H and dielectric detectors, we have studied the distribution of Li in the brain of adult mice, following Li treatment of the animals. Two strains of animals were used in parallel: "quaking" dysmyelinating mutants and normally myelinated controls. The distribution appeared to be sha...
journal_title：Journal of neurochemistry
pub_type： 杂志文章
doi：10.1111/j.1471-4159.1986.tb00657.x
更新日期：1986-04-01 00:00:00
