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

L-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 Ca(V)1.3. Mice lacking Ca(V)1.3 are reported to have impairments in fear conditioning and depressive-like behaviors, which have been linked to Ca(V)1.3 function in the hippocampus and amygdala. Genetic variation in Ca(V)1.3 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 Ca(V)1.3 plays a role in these behaviors. We found that Ca(V)1.3 knockout mice have deficits in rotarod learning despite normal locomotor function. Deletion of Ca(V)1.3 is also associated with impaired gait adaptation and associative learning on the Erasmus Ladder. We did not observe any impairments in Ca(V)1.3 knockout mice on assays of anxiety-like, depression-like or social preference behaviors. Our results suggest an important role for Ca(V)1.3 in neural circuits involved in motor learning and concur with previous data showing its involvement in associative learning.

Automated summary

L-type voltage-gated calcium channel Ca(V)1.3 plays an important role in regulating neuronal activity in the brain. It has been linked to impairments in fear conditioning and depressive-like behaviors, as well as genetic variations associated with psychiatric disorders. Knockout of Ca(V)1.3 in mice led to deficits in motor learning and impaired associative learning.