The Cacna1e (calcium channel, voltage-dependent, R type, alpha 1E subunit) gene encodes a subunit of the non-L-type high-voltage activated Cav2 channel subfamily. Cav2.3 Ca2+ channels are involved in Ca2+-induced insulin secretion. Cav2.3 knock-out (KO) mice have exon 2 deleted in the Cacna1e gene. Homozygous null mice are viable. Although homozygous females are fertile, homozygous males exhibit reduced fertility. Glucose tolerance is significantly reduced following intraperitoneal injection of D-glucose and insulin release into plasma is impaired in 10 week old mice. In aged mice (42 weeks), insulin release and glucose tolerance are slightly improved. In addition to insulin, secretion of the peptide hormones glucagon and somatostatin is disturbed. Induction of stress in Cav2.3 KO mice results in glucose release rate that is 29% of the release rate in wild-type mice. Cav2.3 KO mice are less susceptible to convulsive drugs, exhibit increased anxiety and aggression, and develop cardiac arrhythmia. These mice may be useful for studying hormone secretion, glucose homeostasis, cardiac arrhythmias, and seizure susceptibility.

Cacna1e (calcium channel, voltage-dependent, R type, alpha 1E subunit) knock-out mice exhibit impaired insulin secretion, reduced glucose tolerance, cardiac arrhythmia, and seizure resistance. These mice may be useful for studying hormone secretion, glucose homeostasis, cardiac arrhythmias, and seizure susceptibility.

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