Literature DB >> 1317497

Calbindin-D28K-containing neurons in animal models of neurodegeneration: possible protection from excitotoxicity.

A Iacopino1, S Christakos, D German, P K Sonsalla, C A Altar.   

Abstract

Brain levels of the calcium binding protein Calbindin-D28K (CaBP28K) and CaBP28K mRNA were measured for various animal models of neurodegenerative diseases (MPTP-treated C57BL/6J mice and Sprague-Dawley rats receiving striatal/intraperitoneal kainic acid or quinolinic acid into the nucleus basalis magnocellularis). Brain areas were tested (radioimmunoassay, Western blot, slot blot, and Northern blot) for levels of CaBP28K and CaBP28K mRNA. The various models did not exhibit any changes in protein or mRNA levels from the controls, suggesting that CaBP28K-containing neurons were not lost after exposure to these neurotoxins. Immunocytochemical characterization of the substantia nigra of the MPTP-treated mice revealed that there was significant dopaminergic cell loss in this brain area after MPTP treatment. The majority of dopaminergic neurons that degenerated did not contain CaBP28K. The small percentage of surviving neurons were CaBP28K-positive. These results suggest that the presence of CaBP28K may protect neurons from calcium-mediated neurotoxicity.

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Year:  1992        PMID: 1317497     DOI: 10.1016/0169-328x(92)90033-8

Source DB:  PubMed          Journal:  Brain Res Mol Brain Res        ISSN: 0169-328X


  23 in total

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7.  Systematic differences in time of dopaminergic neuron origin between normal mice and homozygous weaver mutants.

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8.  Selective vulnerability of late-generated dopaminergic neurons of the substantia nigra in weaver mutant mice.

Authors:  S A Bayer; K V Wills; L C Triarhou; T Verina; J D Thomas; B Ghetti
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Review 9.  Chronic MPTP administration regimen in monkeys: a model of dopaminergic and non-dopaminergic cell loss in Parkinson's disease.

Authors:  Gunasingh J Masilamoni; Yoland Smith
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10.  Effect of serum on intracellular calcium homeostasis and survival of primary cortical and hippocampal CA1 neurons following brief glutamate treatment.

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