Increased neuronal cell survival after L‐deprenyl treatment in experimental thiamine deficiency
Identifieur interne : 003973 ( Main/Exploration ); précédent : 003972; suivant : 003974Increased neuronal cell survival after L‐deprenyl treatment in experimental thiamine deficiency
Auteurs : Kathryn G. Todd [Canada] ; Roger F. Butterworth [Canada]Source :
- Journal of Neuroscience Research [ 0360-4012 ] ; 1998-04-15.
English descriptors
Abstract
Experimental thiamine deficiency results in a reproducible pattern of selective neuronal cell death. Events such as blood‐brain barrier breakdown, N‐methyl‐D‐aspartic acid (NMDA) receptor‐mediated excitotoxicity, and increased reactive oxygen species have been implicated in thiamine deficiency‐induced neural loss. L‐deprenyl protects dopaminergic, noradrenergic, and acetylcholinergic neurons from neurotoxic, mechanical, and excitotoxic damage. In the present study, the effects of l‐deprenyl on neuronal cell survival were examined in rats made thiamine deficient by daily administration of the central thiamine antagonist pyrithiamine (0.5 mg/kg s.c.). Rats assigned to thiamine deficient or control groups received daily injections of l‐deprenyl (0.25, 0.5, or 1.0 mg/kg/day i.p.) or vehicle until they reached a state of severe thiamine deficiency (loss of righting reflex). At this stage, thiamine status was restored by daily injections of thiamine (10 mg/kg s.c.) for 3 days, after which the animals were killed, and their brains were processed for neuronal cell counts (cresyl violet staining), astrocytic proliferation [glial fibrillary acidic protein (GFAP) immunohistochemistry], and monoamine oxidase B (MAO‐B) activity. All rats receiving l‐deprenyl (all doses) had significantly decreased neuronal cell loss in thalamic nuclei, in the inferior colliculus, and in the inferior olive and had a concomitant decrease in reactive astrocytic proliferation compared with the thiamine‐deficient, vehicle‐treated rats. The neuroprotective effects of l‐deprenyl in thiamine deficiency induced brain damage most likely result from its properties other than its effects as an MAO‐B inhibitor. J. Neurosci. Res. 52:240–246, 1998. © 1998 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/(SICI)1097-4547(19980415)52:2<240::AID-JNR12>3.0.CO;2-B
Affiliations:
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Events such as blood‐brain barrier breakdown, N‐methyl‐D‐aspartic acid (NMDA) receptor‐mediated excitotoxicity, and increased reactive oxygen species have been implicated in thiamine deficiency‐induced neural loss. L‐deprenyl protects dopaminergic, noradrenergic, and acetylcholinergic neurons from neurotoxic, mechanical, and excitotoxic damage. In the present study, the effects of l‐deprenyl on neuronal cell survival were examined in rats made thiamine deficient by daily administration of the central thiamine antagonist pyrithiamine (0.5 mg/kg s.c.). Rats assigned to thiamine deficient or control groups received daily injections of l‐deprenyl (0.25, 0.5, or 1.0 mg/kg/day i.p.) or vehicle until they reached a state of severe thiamine deficiency (loss of righting reflex). At this stage, thiamine status was restored by daily injections of thiamine (10 mg/kg s.c.) for 3 days, after which the animals were killed, and their brains were processed for neuronal cell counts (cresyl violet staining), astrocytic proliferation [glial fibrillary acidic protein (GFAP) immunohistochemistry], and monoamine oxidase B (MAO‐B) activity. All rats receiving l‐deprenyl (all doses) had significantly decreased neuronal cell loss in thalamic nuclei, in the inferior colliculus, and in the inferior olive and had a concomitant decrease in reactive astrocytic proliferation compared with the thiamine‐deficient, vehicle‐treated rats. The neuroprotective effects of l‐deprenyl in thiamine deficiency induced brain damage most likely result from its properties other than its effects as an MAO‐B inhibitor. J. Neurosci. 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