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Regional activation of L-type voltage-sensitive calcium channels in experimental thiamine deficiency

✍ Scribed by Alan S. Hazell; Antoine M. Hakim; Mary K. Senterman; Matthew J. Hogan

Publisher: John Wiley and Sons
Year: 1998
Tongue: English
Weight: 378 KB
Volume: 52
Category: Article
ISSN: 0360-4012
DOI: 10.1002/(sici)1097-4547(19980615)52:6<742::aid-jnr13>3.0.co;2-0

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✦ Synopsis

During pyrithiamine-induced thiamine deficiency (PTD), specific regions of the brain develop histological damage. The basis of this selective vulnerability is unknown but the mechanism may involve a glutamatemediated excitotoxic process in affected structures, leading to alterations in membrane potential and disturbances in calcium homeostasis. In this study, we have examined the volume of distribution of [ 3 H]nimodipine, an L-type voltage-sensitive calcium channel (VSCC) antagonist, in the brain of the PTD rat. An increase in specific binding of [ 3 H]nimodipine was detected only in the posterior thalamus at the symptomatic stage, immediately following the loss of righting reflexes (P F 0.0001). There was also an increase in nonspecific binding in the medial geniculate and inferior colliculi. Replenishment with thiamine at the symptomatic stage returned [ 3 H]nimodipine binding to normal levels. These findings provide evidence that depolarization and activation of L-type VSCCs occur in the posterior thalamus and may contribute to the appearance of histological lesions in this structure during experimental thiamine deficiency.

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