Deletion of the voltage-gated calcium channel, CaV1.3, causes deficits in motor performance and associative learning

Abstract

AbstractL-type voltage-gated calcium channels are important regulators of neuronal activity and are widely expressed throughout the brain. One of the major L-type voltage-gated calcium channel isoforms in the brain is CaV1.3. Mice lacking CaV1.3 are reported to have impairments in fear conditioning and depressive-like behaviors, which have been linked to CaV1.3 function in the hippocampus and amygdala. Genetic variation in CaV1.3 has been linked to a variety of psychiatric disorders, including autism and schizophrenia, which are associated with altered motor learning, associative learning, and social function. Here, we explored whether CaV1.3 plays a role in these behaviors. We found that CaV1.3 knockout mice have deficits in rotarod learning despite normal locomotor function. Deletion of CaV1.3 is also associated with impaired gait adaptation and associative learning on the Erasmus Ladder. We did not observe any impairments in CaV1.3 knockout mice on assays of anxiety-like, depression-like, or social preference behaviors. Our results suggest an important role for CaV1.3 in neural circuits involved in motor learning and concur with previous data showing its involvement in associative learning.