Cav3.3
Description: calcium channel, voltage-dependent, T type, alpha 1I subunit Gene: Cacna1i Synonyms: cacna1i, cav3.3, ca3.3, Ca(v)3.3
CACNA1I (also known as Cav3.3; KIAA1120) encodes Cav3.3, a T type LVA calcium channel found in neurons which is also know as a1I. Voltage-dependent calcium channels control the rapid entry of Ca(2+) into a variety of cell types and are therefore involved in both electrical and cellular signaling. T-type channels, such as CACNA1I, are activated by small membrane depolarizations and can generate burst firing and pacemaker activity
http://www.ncbi.nlm.nih.gov/gene/8911
Gene
Transcript
Acc No | Sequence | Length | Source | |
---|---|---|---|---|
NM_020084 | n/A | n/A | NCBI | |
NM_001044308 | n/A | n/A | NCBI | |
NM_021096 | n/A | n/A | NCBI | |
NM_001003406 | n/A | n/A | NCBI |
Ontology
Accession | Name | Definition | Evidence | |||||||
---|---|---|---|---|---|---|---|---|---|---|
GO:0000786 | nucleosome | A complex comprised of DNA wound around a multisubunit core and associated proteins, which forms the primary packing unit of DNA into higher order structures. | IEA | |||||||
GO:0005634 | nucleus | A membrane-bounded organelle of eukaryotic cells in which chromosomes are housed and replicated. In most cells, the nucleus contains all of the cell's chromosomes except the organellar chromosomes, and is the site of RNA synthesis and processing. In some species, or in specialized cell types, RNA metabolism or DNA replication may be absent. | IEA | |||||||
GO:0016020 | membrane | Double layer of lipid molecules that encloses all cells, and, in eukaryotes, many organelles; may be a single or double lipid bilayer; also includes associated proteins. | IEA |
Zinc
CaV 3.2 current (IC50 , 0.8 μM) is significantly more sensitive to Zn2 + than are CaV 3.1 and CaV 3.3 currents (IC50 , 80 μM and ∼160 μM, respectively). This inhibition of CaV 3 currents is associated with a shift to more negative membrane potentials of both steady-state inactivation for CaV 3.1, CaV 3.2 and CaV 3.3 and steady-state activation for CaV 3.1 and CaV 3.3 currents. We also document changes in kinetics, especially a significant slowing of the inactivation kinetics for CaV 3.1 and CaV 3.3, but not for CaV 3.2 currents. (Traboulsie [103])
Phorbol-12-myristate-13-acetate (PMA)
PMA augmented the current amplitudes of the three T-type channel isoforms (Cav3.1, Cav3.2, Cav3.3), but the fold stimulations and time courses differed. (Park [112])
Protein
Structure
Distribution
T-type Ca2+ currents are central determinants of neuronal excitability that are present in the somatodendritic compartment of many types of neurones (Carbone & Lux, 1984 [1238]; Talley et al. 1999 [1242]).
Expression
Functional
Genetic and pharmacological inhibition of T-type Ca2+ currents has demonstrated the importance of these currents in various sensory systems, ranging from pain perception and hyperalgesia (Kim et al. 2003 [1243]; Ikeda et al. 2003 [1244]), mechanoreceptor function (Shin et al. 2003 [1245]) and to olfaction (Kawai & Miyachi, 2001 [1246]).
T-type channels are distinguished from high voltage-activated (HVA)1 Ca2+ channels by their unique biophysical properties, including low voltage activation, fast activation and inactivation kinetics that produce a criss-crossing pattern between successive traces of a current-voltage (IV) protocol, slow deactivation kinetics, and tiny single channel conductance (Perez-Reyes [528], Armstrong [1237], Carbone [1238], Randall [340]).
Expression studies found that Cav3.3 channels generate currents with much slower activation and inactivation kinetics than Cav3.1 and Cav3.2 channels, which show the more typical transient kinetics described for native T-type channels (Perez-Reyes [528], Perez-Reyes [1239], Cribbs [1240], Lee [1241]).
Cav3.1 and Cav3.2 channels are activating and inactivating much faster than Cav3.3 channels. (Park [113])
The kinetics of T-type channels resemble those of Na+ channels, albeit on a slower time scale, suggesting that they may also inactivate by a ball-and-chain mechanism. However, preliminary evidence indicates that T-type channels inactivate by similar processes as HVA Ca2+ channels.Multiple structural elements contribute to the slow kinetics of Cav3.3 channels. (Park [113])
Model
Model Cav3.3 (ID=42) Edit
Animal | CH | |
CellType | CHO | |
Age | 0 Days | |
Temperature | 0.0°C | |
Reversal | 30.0 mV | |
Ion | Ca + | |
Ligand ion | ||
Reference | [103] Achraf Traboulsie et. al; J. Physiol. (Lond.) 2007 Jan 1 | |
mpower | 1.0 | |
m Inf | 1/(1+exp((v- -45.454426)/-5.073015)) | |
m Tau | 3.394938 +( 54.187616 / (1 + exp((v - -40.040397)/4.110392))) | |
hpower | 1.0 | |
h Inf | 1 /(1+exp((v-(-74.031965))/8.416382)) | |
h Tau | 109.701136 + (0.003816 * exp(-v/4.781719)) |
References
Traboulsie A
et al.
Subunit-specific modulation of T-type calcium channels by zinc.
J. Physiol. (Lond.),
2007
Jan
1
, 578 (159-71).
Park JY
et al.
Activation of protein kinase C augments T-type Ca2+ channel activity without changing channel surface density.
J. Physiol. (Lond.),
2006
Dec
1
, 577 (513-23).
Park JY
et al.
Multiple structural elements contribute to the slow kinetics of the Cav3.3 T-type channel.
J. Biol. Chem.,
2004
May
21
, 279 (21707-13).
T-type Ca2+ channels encode prior neuronal activity as modulated recovery rates.
J. Physiol. (Lond.), 2006 Mar 15 , 571 (519-36).
Cataldi M
et al.
Zn(2+) slows down Ca(V)3.3 gating kinetics: implications for thalamocortical activity.
J. Neurophysiol.,
2007
Oct
, 98 (2274-84).
Kovacs K
et al.
Subcellular distribution of low-voltage activated T-type Ca2+ channel subunits (Ca(v)3.1 and Ca(v)3.3) in reticular thalamic neurons of the cat.
J. Neurosci. Res.,
2010
Feb
1
, 88 (448-60).
Perez-Reyes E
Molecular physiology of low-voltage-activated t-type calcium channels.
Physiol. Rev.,
2003
Jan
, 83 (117-61).
Armstrong CM
et al.
Two distinct populations of calcium channels in a clonal line of pituitary cells.
Science,
1985
Jan
4
, 227 (65-7).
Carbone E
et al.
A low voltage-activated, fully inactivating Ca channel in vertebrate sensory neurones.
Nature,
1984 Aug 9-15
, 310 (501-2).
Randall AD
et al.
Contrasting biophysical and pharmacological properties of T-type and R-type calcium channels.
Neuropharmacology,
1997
Jul
, 36 (879-93).
Perez-Reyes E
et al.
Molecular characterization of a neuronal low-voltage-activated T-type calcium channel.
Nature,
1998
Feb
26
, 391 (896-900).
Cribbs LL
et al.
Cloning and characterization of alpha1H from human heart, a member of the T-type Ca2+ channel gene family.
Circ. Res.,
1998
Jul
13
, 83 (103-9).
Lee JH
et al.
Cloning and expression of a novel member of the low voltage-activated T-type calcium channel family.
J. Neurosci.,
1999
Mar
15
, 19 (1912-21).
Talley EM
et al.
Differential distribution of three members of a gene family encoding low voltage-activated (T-type) calcium channels.
J. Neurosci.,
1999
Mar
15
, 19 (1895-911).
Kim D
et al.
Thalamic control of visceral nociception mediated by T-type Ca2+ channels.
Science,
2003
Oct
3
, 302 (117-9).
Ikeda H
et al.
Synaptic plasticity in spinal lamina I projection neurons that mediate hyperalgesia.
Science,
2003
Feb
21
, 299 (1237-40).
Shin JB
et al.
A T-type calcium channel required for normal function of a mammalian mechanoreceptor.
Nat. Neurosci.,
2003
Jul
, 6 (724-30).
Kawai F
et al.
Enhancement by T-type Ca2+ currents of odor sensitivity in olfactory receptor cells.
J. Neurosci.,
2001
May
15
, 21 (RC144).
Credits
Contributors: Rajnish Ranjan, Michael Schartner
To cite this page: [Contributors] Channelpedia https://channelpedia.epfl.ch/ionchannels/87/ , accessed on [date]