ArticlePflugers Archiv : European journal of physiology2005
Influence of Ca2+-binding proteins and the cytoskeleton on Ca2+-dependent inactivation of high-voltage activated Ca2+ currents in thalamocortical relay neurons.
Article in Pflugers Archiv : European journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 26 citations in OpenAlex.
- Decalmodulation of Cav1 channels by CaBPs.Channels (Austin, Tex.) · 2016Review
- CD8(+) T Cell-Mediated Neuronal Dysfunction and Degeneration in Limbic Encephalitis.Frontiers in neurology · 2015Review
- Ca2+-dependent modulation of voltage-gated Ca2+ channels.Biochimica et biophysica acta · 2012Review
- Modulation of calcium-dependent inactivation of L-type Ca2+ channels via β-adrenergic signaling in thalamocortical relay neurons.PloS one · 2011Article
- Two pore domain potassium channels in cerebral ischemia: a focus on K2P9.1 (TASK3, KCNK9).Experimental & translational stroke medicine · 2010Article
- Different distributions of calbindin and calretinin immunostaining across the medial and dorsal divisions of the mouse medial geniculate body.Hearing research · 2009Article
- Differential regulation of endogenous N- and P/Q-type Ca2+ channel inactivation by Ca2+/calmodulin impacts on their ability to support exocytosis in chromaffin cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- Functional stabilization of weakened thalamic pacemaker channel regulation in rat absence epilepsy.The Journal of physiology · 2006Article
- Impaired regulation of thalamic pacemaker channels through an imbalance of subunit expression in absence epilepsy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
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5 authors at 1 institution in 1 country.
Funding
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Abstract
Ca2+-dependent inactivation (CDI) of high-voltage activated (HVA) Ca2+ channels was investigated in acutely isolated and identified thalamocortical relay neurons of the dorsal lateral geniculate nucleus (dLGN) by combining electrophysiological and immunological techniques. The influence of Ca2+-binding proteins, calmodulin and the cytoskeleton on CDI was monitored using double-pulse protocols (a constant post-pulse applied shortly after the end of conditioning pre-pulses of increasing magnitude). Under control conditions the degree of inactivation (34+/-9%) revealed a U-shaped and a sigmoid dependency of the post-pulse current amplitude on pre-pulse voltage and charge influx, respectively. In contrast to a high concentration (5.5 mM) of EGTA (31+/-3%), a low concentration (3 microM) of parvalbumin (20+/-2%) and calbindin(D28K) (24+/-4%) significantly reduced CDI. Subtype-specific Ca2+ channel blockers indicated that L-type, but not N-type Ca2+ channels are governed by CDI and modulated by Ca2+-binding proteins. These results point to the possibility that activity-dependent changes in the intracellular Ca2+-binding capacity can influence CDI substantially. Furthermore, calmodulin antagonists (phenoxybenzamine, 22+/-2%; calmodulin binding domain, 17+/-1%) and cytoskeleton stabilizers (taxol, 23+/-5%; phalloidin, 15+/-3%) reduced CDI. Taken together, these findings indicate the concurrent occurrence of different CDI mechanisms in a specific neuronal cell type, thereby supporting an integrated model of this feedback mechanism and adding further to the elucidation of the role of HVA Ca2+ channels in thalamic physiology.
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