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  Calbindin-D28K (CaBP) levels and calcium currents in acutely dissociated epileptic neurons

Köhr, G., Lambert, C. E., & Mody, I. (1991). Calbindin-D28K (CaBP) levels and calcium currents in acutely dissociated epileptic neurons. Experimental Brain Research, 85(3), 543-551. doi:10.1007/BF00231738.

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 Creators:
Köhr, Georg1, 2, 3, Author              
Lambert, C. E., Author
Mody, Istvan, Author
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1Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society, ou_1497704              
2Directly responsible to the Managing Director, Max Planck Institute for Medical Research, Max Planck Society, ou_persistent22              
3Georg Köhr Group, Max Planck Institute for Medical Research, Max Planck Society, ou_1497714              

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Free keywords: Voltage-dependent Ca2+-currents (HVA or L-type); Inactivation; Intraneuronal Ca2+; Buffering; Dentate gyrus granule cells; Kindling-induced epilepsy; Rat
 Abstract: Nerve cells that lack the cytoplasmic Ca2+ binding protein Calbindin-D28K (CaBP) appear to be selectively vulnerable to Ca(2+)-related injury consistent with a postulated intraneuronal Ca(2+)-buffering role of CaBP. We have confirmed the selective loss of CaBP from the dentate gyrus during kindling-induced epilepsy in acutely dissociated granule cells (GCs) from kindled rats. Immunohistochemically stained kindled neurons showed a significant loss of CaBP when compared to controls (p less than 0.001; ANOVA). The Ca(2+)-buffering role of CaBP was assessed in acutely dissociated control and kindled GCs by examining a physiological process highly sensitive to intracellular Ca(2+)-buffering: the Ca(2+)-dependent inactivation of high-voltage activated (HVA or L-type) Ca2+ currents in the absence (or presence) of exogenous Ca(2+)-chelators. Whole-cell patch clamp recordings in kindled GCs demonstrated a markedly enhanced Ca(2+)-dependent inactivation of Ca(2+)-currents. After brief conditioning Ca2+ currents, in the absence of an exogenous intraneuronal Ca(2+)-chelator, subsequent test Ca2+ currents were inactivated by 58.3% in kindled GCs, a significant increase from the 37.4% inactivation observed in control GCs (p less than 0.005; ANOVA). The differential Ca2+ current decay and Ca(2+)-dependent inactivation were prevented in both control and kindled GCs upon loading the neurons with the exogenous Ca(2+)-chelator BAPTA. These experiments demonstrate a high correlation between the loss of CaBP and changes in Ca2+ current inactivation and are consistent with the hypothesis that CaBP contributes to the physiological Ca(2+)-buffering in mammalian neurons.

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Language(s): eng - English
 Dates: 1990-11-271991-02-061991-07
 Publication Status: Published in print
 Pages: 9
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
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Title: Experimental Brain Research
  Other : Exp. Brain Res.
Source Genre: Journal
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Publ. Info: Heidelberg : Springer-Verlag
Pages: - Volume / Issue: 85 (3) Sequence Number: - Start / End Page: 543 - 551 Identifier: ISSN: 0014-4819
CoNE: https://pure.mpg.de/cone/journals/resource/954925398496