Cacna1g encodes the α1G subunit of the thalamus-enriched T-type calcium channel, also known as Ca(V)3.1, a low-threshold voltage-gated T-type calcium channel. This channel is involved in various cellular processes, especially those related to neural activity, and is crucial for normal neurological function [1,2].

In mouse models, reduced Cacna1g expression in Scn1a+/- Dravet syndrome mouse models led to partial amelioration of disease phenotypes, with improved survival and reduced spontaneous seizure frequency, suggesting Cacna1g is a genetic modifier in this syndrome [3]. In Scn2a(Q54) transgenic epilepsy mouse models, increased Cacna1g expression led to an increased spontaneous seizure frequency, while decreased expression led to a decreased seizure frequency, indicating Cacna1g as an epilepsy modifier gene [4].

In conclusion, Cacna1g plays a vital role in neural activity, especially in relation to epilepsy. The study of Cacna1g using gene-knockout (KO) and conditional-knockout (CKO) mouse models has provided valuable insights into its role in Dravet syndrome and other epilepsy-related conditions, highlighting its potential as a therapeutic target for these neurological disorders.