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. |
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| 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] |
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| Database: | Psychology and Behavioral Sciences Collection |
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| 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] |
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| ISSN: | 0953816X |
| DOI: | 10.1111/j.1460-9568.2010.07081.x |
