Specific expression of low-voltage-activated calcium channel isoforms and splice variants in thalamic local circuit interneurons

被引:35
作者
Broicher, Tilman
Kanyshkova, Tatyana
Landgraf, Peter
Rankovic, Vladan
Meuth, Patrick
Meuth, Sven G.
Pape, Hans-Chiristian
Budde, Thomas
机构
[1] Univ Munster, Inst Physiol, D-48149 Munster, Germany
[2] Leibniz Inst Neurobiol, D-39118 Magdeburg, Germany
[3] Otto Von Guericke Univ, Inst Physiol, D-39120 Magdeburg, Germany
[4] Univ Wurzburg, Neurol Klin, D-97080 Wurzburg, Germany
[5] Inst Expt Epilepsieforsch, D-48149 Munster, Germany
关键词
patch clamp; T-type Ca2+ channel; absence epilepsy; thalamus; real time PCR;
D O I
10.1016/j.mcn.2007.05.013
中图分类号
Q189 [神经科学];
学科分类号
071006 [神经生物学];
摘要
It has been suggested that the specific burst firing patterns of thalamic neurons reflect differential expression of low-voltage-activated (LVA) Ca2+ channel subtypes and their splice variants. By combining electrophysiological, molecular biological, immunological, and computational modeling techniques we here show that diverging LVA Ca2+ currents of thalamocortical relay (TC) and GABAergic interneurons of the dLGN correlate with a differential expression of LVA Ca2+ channel splice variations and isoforms (alpha 1G-a in TC; alpha 1G-bc and alpha 1I in interneurons). Implementation of the observed LVA Ca2+ current differences into a TC neuron model changed the burst firing from TC-like to interneuron-like. We conclude that alternative splicing of the alpha 1G isoform in dLGN TC and interneurons, and the exclusive expression of the alpha 1I isoform in interneurons play a prominent role in setting the different LVA Ca2+ current properties of TC and interneurons, which critically contribute to the diverging burst firing behavior of these neurons. (c) 2007 Elsevier Inc. All rights reserved.
引用
收藏
页码:132 / 145
页数:14
相关论文
共 68 条
[1]
INHIBITION FROM THE BRAIN-STEM OF INHIBITORY INTERNEURONES OF THE CATS DORSAL LATERAL GENICULATE-NUCLEUS [J].
AHLSEN, G ;
LINDSTROM, S ;
LO, FS .
JOURNAL OF PHYSIOLOGY-LONDON, 1984, 347 (FEB) :593-609
[2]
Thalamic Cav3.1 T-type Ca2+ channel plays a crucial role in stabilizing sleep [J].
Anderson, MP ;
Mochizuki, T ;
Xie, J ;
Fischler, W ;
Manger, JP ;
Talley, EM ;
Scammell, TE ;
Tonegawa, S .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2005, 102 (05) :1743-1748
[3]
Impaired regulation of thalamic pacemaker channels through an imbalance of subunit expression in absence epilepsy [J].
Budde, T ;
Caputi, L ;
Kanyshkova, T ;
Staak, R ;
Abrahamczik, C ;
Munsch, T ;
Pape, HC .
JOURNAL OF NEUROSCIENCE, 2005, 25 (43) :9871-9882
[4]
Budde T, 2006, MODELS OF SEIZURES AND EPILEPSY, P73, DOI 10.1016/B978-012088554-1/50009-8
[5]
DISCHARGE PATTERNS OF PRINCIPAL CELLS AND INTERNEURONES IN LATERAL GENICULATE NUCLEUS OF RAT [J].
BURKE, W ;
SEFTON, AJ .
JOURNAL OF PHYSIOLOGY-LONDON, 1966, 187 (01) :201-&
[6]
Presence of mRNA for glutamic acid decarboxylase in both excitatory and inhibitory neurons [J].
Cao, YX ;
Wilcox, KS ;
Martin, CE ;
Rachinsky, TL ;
Eberwine, J ;
Dichter, MA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (18) :9844-9849
[7]
Specific contribution of human T-type calcium channel isotypes (α1G, α1H and α1I) to neuronal excitability [J].
Chemin, J ;
Monteil, A ;
Perez-Reyes, E ;
Bourinet, E ;
Nargeot, J ;
Lory, P .
JOURNAL OF PHYSIOLOGY-LONDON, 2002, 540 (01) :3-14
[8]
Alternatively spliced α1G (Cav3.1) intracellular loops promote specific T-type Ca2+ channel gating properties [J].
Chemin, J ;
Monteil, A ;
Bourinet, E ;
Nargeot, J ;
Lory, P .
BIOPHYSICAL JOURNAL, 2001, 80 (03) :1238-1250
[9]
T-type Cav3.3 calcium channels produce spontaneous low-threshold action potentials and intracellular calcium oscillations [J].
Chevalier, Marc ;
Lory, Philippe ;
Mironneau, Chantal ;
Macrez, Nathalie ;
Quignard, Jean-Francois .
EUROPEAN JOURNAL OF NEUROSCIENCE, 2006, 23 (09) :2321-2329
[10]
Genetic animal models for absence epilepsy: A review of the WAG/Rij strain of rats [J].
Coenen, AML ;
van Luijtelaar, ELJM .
BEHAVIOR GENETICS, 2003, 33 (06) :635-655