Javascript must be enabled to continue!
Presynaptic ‘Cav2.3‐containing’ E‐type Ca2+ channels share dual roles during neurotransmitter release
View through CrossRef
AbstractCa2+ influx into excitable cells is a prerequisite for neurotransmitter release and regulated exocytosis. Within the group of ten cloned voltage‐gated Ca2+ channels, the Cav2.3‐containing E‐type Ca2+ channels are involved in various physiological processes, such as neurotransmitter release and exocytosis together with other voltage‐gated Ca2+ channels of the Cav1, Cav2 and Cav3 subfamily. However, E‐type Ca2+ channels also exhibit several subunit‐specific features, most of which still remain poorly understood. Cav2.3‐containing R‐type channels (here called ‘E‐type channels’) are also located in presynaptic terminals and interact with some synaptic vesicle proteins, the so‐called SNARE proteins, although lacking the classical synprint interaction site. E‐type channels trigger exocytosis and are also involved in long‐term potentiation. Recently, it was shown that the interaction of Cav2.3 with the EF‐hand motif containing protein EFHC1 is involved in the aetiology and pathogenesis of juvenile myoclonic epilepsy.
Title: Presynaptic ‘Cav2.3‐containing’ E‐type Ca2+ channels share dual roles during neurotransmitter release
Description:
AbstractCa2+ influx into excitable cells is a prerequisite for neurotransmitter release and regulated exocytosis.
Within the group of ten cloned voltage‐gated Ca2+ channels, the Cav2.
3‐containing E‐type Ca2+ channels are involved in various physiological processes, such as neurotransmitter release and exocytosis together with other voltage‐gated Ca2+ channels of the Cav1, Cav2 and Cav3 subfamily.
However, E‐type Ca2+ channels also exhibit several subunit‐specific features, most of which still remain poorly understood.
Cav2.
3‐containing R‐type channels (here called ‘E‐type channels’) are also located in presynaptic terminals and interact with some synaptic vesicle proteins, the so‐called SNARE proteins, although lacking the classical synprint interaction site.
E‐type channels trigger exocytosis and are also involved in long‐term potentiation.
Recently, it was shown that the interaction of Cav2.
3 with the EF‐hand motif containing protein EFHC1 is involved in the aetiology and pathogenesis of juvenile myoclonic epilepsy.
Related Results
Na+/Ca2+ exchange current in ventricular myocytes of fish heart: contribution to sarcolemmal Ca2+ influx
Na+/Ca2+ exchange current in ventricular myocytes of fish heart: contribution to sarcolemmal Ca2+ influx
ABSTRACT
Influx of extracellular Ca2+ plays a major role in the activation of contraction in fish cardiac cells. The relative contributions of Na+/Ca2+ exchange and ...
Ca2+ entry through Na(+)‐Ca2+ exchange can trigger Ca2+ release from Ca2+ stores in Na(+)‐loaded guinea‐pig coronary myocytes.
Ca2+ entry through Na(+)‐Ca2+ exchange can trigger Ca2+ release from Ca2+ stores in Na(+)‐loaded guinea‐pig coronary myocytes.
1. The ionized cytosolic calcium concentration ([Ca2+]i) was monitored in voltage‐clamped coronary myocytes at 36 degrees C and 2.5 mM [Ca2+]o using the Ca2+ indicator indo‐1. [Ca2...
Brevity of the Ca2+ Microdomain and Active Zone Geometry Prevent Ca2+-Sensor Saturation for Neurotransmitter Release
Brevity of the Ca2+ Microdomain and Active Zone Geometry Prevent Ca2+-Sensor Saturation for Neurotransmitter Release
The brief time course of the calcium (Ca2+) channel opening combined with the molecular-level colocalization of Ca2+ channels and synaptic vesicles in presynaptic terminals predict...
Computational analysis of Ca2+ dynamics in isolated cardiac mitochondria predicts two distinct modes of Ca2+ uptake
Computational analysis of Ca2+ dynamics in isolated cardiac mitochondria predicts two distinct modes of Ca2+ uptake
Key points
Cytosolic, but not matrix, Mg2+ inhibits mitochondrial Ca2+ uptake through the Ca2+ uniporter (CU).
The majority of mitochondrial Ca2+ uptake under physiological levels ...
A rationally designed peptidomimetic modulator of CaV2.2 (N-type) voltage-gated calcium channels for chronic pain
A rationally designed peptidomimetic modulator of CaV2.2 (N-type) voltage-gated calcium channels for chronic pain
Background and Purpose Transmembrane Cav2.2 (N-type) voltage-gated
calcium channels are genetically and pharmacologically validated pain
targets. Clinical block of Cav2.2 (e.g., wi...
Altered Seizure Susceptibility in Mice Lacking the Cav2.3 E‐type Ca2+ Channel
Altered Seizure Susceptibility in Mice Lacking the Cav2.3 E‐type Ca2+ Channel
Summary: Purpose: Recently the Cav2.3 (E/R‐type) voltage‐gated calcium channel (VGCC) has turned out to be not only a potential target for different antiepileptic drugs (e.g., la...
A Mechanism for Both Capacitative Ca2+Entry and Excitation-Contraction Coupled Ca2+Release by the Sarcoplasmic Reticulum of Skeletal Muscle Cells
A Mechanism for Both Capacitative Ca2+Entry and Excitation-Contraction Coupled Ca2+Release by the Sarcoplasmic Reticulum of Skeletal Muscle Cells
We have previously established that L6 skeletal muscle cell cultures display capacitative calcium entry (CCE), a phenomenon established with other cells in which Ca2+uptake from ou...
Regulation of cochlear hair cell function by intracellular calcium stores
Regulation of cochlear hair cell function by intracellular calcium stores
IntroductionMammalian hearing depends on the dual mechanosensory and motor functions of cochlear hair cells. Both these functions may be regulated by Ca2+ release from intracellula...

