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Intracellular Ca2+ release-dependent inactivation of Ca2+ currents in thalamocortical relay neurons.

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Title: Intracellular Ca2+ release-dependent inactivation of Ca2+ currents in thalamocortical relay neurons.
Authors: Rankovic, Vladan (AUTHOR), Ehling, Petra (AUTHOR), Coulon, Philippe (AUTHOR), Landgraf, Peter (AUTHOR), Kreutz, Michael R. (AUTHOR), Munsch, Thomas (AUTHOR), Budde, Thomas (AUTHOR)
Source: European Journal of Neuroscience. Feb2010, Vol. 31 Issue 3, p439-449. 11p. 7 Graphs.
Subjects: Thalamus, Cerebral cortex, Laboratory rats, Pulse (Heart beat), Caffeine, Ryanodine receptors
Abstract: Neuronal Ca2+ channels are rapidly inactivated by a mechanism that is termed Ca2+-dependent inactivation (CDI). In this study we investigated the influence of intracellular Ca2+ release on CDI of high-voltage-activated Ca2+ channels in rat thalamocortical relay neurons by combining voltage-clamp, Ca2+ imaging and immunological techniques. Double-pulse protocols revealed CDI, which depended on the length of the conditioning pulses. Caffeine caused a concentration-dependent increase in CDI that was accompanied by an increase in the duration of Ca2+ transients. Inhibition of ryanodine receptors and endoplasmic Ca2+ pumps (by thapsigargin or cyclopiazonic acid) resulted in a reduction of CDI. In contrast, inhibition of inositol 1,4,5-tris-phosphate receptors by intracellular application of 2-aminoethoxy diphenyl borate or heparin did not influence CDI. The block of transient receptor potential channels by extracellular application of 2-aminoethoxy diphenyl borate, however, resulted in a significant reduction of CDI. The central role of L-type Ca2+ channels was emphasized by the near-complete block of CDI by nifedipine, an effect only surpassed when Ca2+ was replaced by Ba2+ and chelated by 1,2-bis(o-aminophenoxy)ethane-N,N,N′,N′,-tetraacetic acid (BAPTA). Trains of action potential-like stimuli induced a strong reduction in high-voltage-activated Ca2+ current amplitude, which was significantly reduced when intracellular Ca2+ stores were made inoperative by thapsigargin or Ba2+/BAPTA. Western blotting revealed expression of L-type Ca2+ channels in thalamic and hippocampal tissue but not liver tissue. In summary, these results suggest a cross-signalling between L-type Ca2+ channels and ryanodine receptors that controls the amount of Ca2+ influx during neuronal activity. [ABSTRACT FROM AUTHOR]
Copyright of European Journal of Neuroscience is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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PubType: Academic Journal
PubTypeId: academicJournal
PreciseRelevancyScore: 0
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Items – Name: Title
  Label: Title
  Group: Ti
  Data: Intracellular Ca<superscript>2+</superscript> release-dependent inactivation of Ca<superscript>2+</superscript> currents in thalamocortical relay neurons.
– Name: Author
  Label: Authors
  Group: Au
  Data: <searchLink fieldCode="AR" term="%22Rankovic%2C+Vladan%22">Rankovic, Vladan</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Ehling%2C+Petra%22">Ehling, Petra</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Coulon%2C+Philippe%22">Coulon, Philippe</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Landgraf%2C+Peter%22">Landgraf, Peter</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Kreutz%2C+Michael+R%2E%22">Kreutz, Michael R.</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Munsch%2C+Thomas%22">Munsch, Thomas</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Budde%2C+Thomas%22">Budde, Thomas</searchLink> (AUTHOR)
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  Data: <searchLink fieldCode="JN" term="%22European+Journal+of+Neuroscience%22">European Journal of Neuroscience</searchLink>. Feb2010, Vol. 31 Issue 3, p439-449. 11p. 7 Graphs.
– Name: Subject
  Label: Subjects
  Group: Su
  Data: <searchLink fieldCode="DE" term="%22Thalamus%22">Thalamus</searchLink><br /><searchLink fieldCode="DE" term="%22Cerebral+cortex%22">Cerebral cortex</searchLink><br /><searchLink fieldCode="DE" term="%22Laboratory+rats%22">Laboratory rats</searchLink><br /><searchLink fieldCode="DE" term="%22Pulse+%28Heart+beat%29%22">Pulse (Heart beat)</searchLink><br /><searchLink fieldCode="DE" term="%22Caffeine%22">Caffeine</searchLink><br /><searchLink fieldCode="DE" term="%22Ryanodine+receptors%22">Ryanodine receptors</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Neuronal Ca2+ channels are rapidly inactivated by a mechanism that is termed Ca2+-dependent inactivation (CDI). In this study we investigated the influence of intracellular Ca2+ release on CDI of high-voltage-activated Ca2+ channels in rat thalamocortical relay neurons by combining voltage-clamp, Ca2+ imaging and immunological techniques. Double-pulse protocols revealed CDI, which depended on the length of the conditioning pulses. Caffeine caused a concentration-dependent increase in CDI that was accompanied by an increase in the duration of Ca2+ transients. Inhibition of ryanodine receptors and endoplasmic Ca2+ pumps (by thapsigargin or cyclopiazonic acid) resulted in a reduction of CDI. In contrast, inhibition of inositol 1,4,5-tris-phosphate receptors by intracellular application of 2-aminoethoxy diphenyl borate or heparin did not influence CDI. The block of transient receptor potential channels by extracellular application of 2-aminoethoxy diphenyl borate, however, resulted in a significant reduction of CDI. The central role of L-type Ca2+ channels was emphasized by the near-complete block of CDI by nifedipine, an effect only surpassed when Ca2+ was replaced by Ba2+ and chelated by 1,2-bis(o-aminophenoxy)ethane-N,N,N′,N′,-tetraacetic acid (BAPTA). Trains of action potential-like stimuli induced a strong reduction in high-voltage-activated Ca2+ current amplitude, which was significantly reduced when intracellular Ca2+ stores were made inoperative by thapsigargin or Ba2+/BAPTA. Western blotting revealed expression of L-type Ca2+ channels in thalamic and hippocampal tissue but not liver tissue. In summary, these results suggest a cross-signalling between L-type Ca2+ channels and ryanodine receptors that controls the amount of Ca2+ influx during neuronal activity. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
  Group: Ab
  Data: <i>Copyright of European Journal of Neuroscience is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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RecordInfo BibRecord:
  BibEntity:
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      – Type: doi
        Value: 10.1111/j.1460-9568.2010.07081.x
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      – Code: eng
        Text: English
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      Pagination:
        PageCount: 11
        StartPage: 439
    Subjects:
      – SubjectFull: Thalamus
        Type: general
      – SubjectFull: Cerebral cortex
        Type: general
      – SubjectFull: Laboratory rats
        Type: general
      – SubjectFull: Pulse (Heart beat)
        Type: general
      – SubjectFull: Caffeine
        Type: general
      – SubjectFull: Ryanodine receptors
        Type: general
    Titles:
      – TitleFull: Intracellular Ca2+ release-dependent inactivation of Ca2+ currents in thalamocortical relay neurons.
        Type: main
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            NameFull: Rankovic, Vladan
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            NameFull: Ehling, Petra
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            NameFull: Coulon, Philippe
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            NameFull: Landgraf, Peter
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            NameFull: Kreutz, Michael R.
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              M: 02
              Text: Feb2010
              Type: published
              Y: 2010
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              Value: 31
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            – TitleFull: European Journal of Neuroscience
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