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in a first attempt to explain changes in brain structure, previous work in animal models showed that a knockdown of cacna2d2 results in an increase in the length of the regenerating axons in the spinal cord, even in injured adult animals. to test the hypothesis that an increase in the activity of the channel might enhance axonal regrowth, we developed an experimental paradigm that allows the effects of cacna2d2 downregulation to be probed in vivo. we found that the pharmacological inhibition of the alpha2delta2 channel by pregabalin (pgb) increases the growth of injured axons and promotes the recovery of motor function in adult mice after a spinal cord injury (sci).
we hypothesized that neurons that survive after an injury must be able to regenerate their axons to reconstitute their target regions. however, it has been shown that neurons that undergo apoptosis during development are unable to regenerate their axons. to assess the functional consequences of in vivo gene deletion of cacna2d2, we generated a new model of inducible cacna2d2 conditional knockout mice. using this novel model, we found that the functional recovery in adult mice after sci was improved by the deletion of cacna2d2, as assessed by motor and sensory tests. moreover, the number of dopaminergic neurons that survived the injury was increased in conditional knockout mice. these data strongly indicate that the survival of injured neurons is a key determinant in the limited ability of adult cns axons to regenerate and that targeting the alpha2delta2 channel can improve functional recovery after sci.
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