Calcium channel, voltage-dependent, T type, alpha 1G subunit, also known as CACNA1G or Cav3.1 is a protein which in humans is encoded by the CACNA1Ggene.[5][6][7] It is one of the primary targets in the pharmacology of absence seizure.
Function
Cav3.1 is a type of low-voltage-activated calcium channel, also known as "T-type" for its transient on and off.[5] It is expressed in thalamocortical relay nucleus, and is responsible for the slow-wave sleep and absence seizure.[8] During a slow-wave sleep, Cav3.1 is put into burst mode, and a self-sustaining synchronous cycle between cortex and thalamus is formed, sensory inputs are isolated from cortex; while awake the thalamus should instead relay sensory inputs from outside the central nervous system. The mechanism of absence seizure has a lot in common with slow-wave sleep. Therefore, a blocker that inhibits the burst mode activation of Cav3.1 is effective in treating absence seizures. Common drugs including ethosuximide, as well as trimethadione.[8]
Interactive pathway map
Click on genes, proteins and metabolites below to link to respective Wikipedia articles.[§ 1]
^Perez-Reyes E, Cribbs LL, Daud A, Lacerda AE, Barclay J, Williamson MP, Fox M, Rees M, Lee JH (February 1998). "Molecular characterization of a neuronal low-voltage-activated T-type calcium channel". Nature. 391 (6670): 896–900. Bibcode:1998Natur.391..896P. doi:10.1038/36110. PMID9495342. S2CID4373283.
^Catterall WA, Perez-Reyes E, Snutch TP, Striessnig J (December 2005). "International Union of Pharmacology. XLVIII. Nomenclature and structure-function relationships of voltage-gated calcium channels". Pharmacol. Rev. 57 (4): 411–25. doi:10.1124/pr.57.4.5. PMID16382099. S2CID10386627.
