CACNA1C and Anxiety: Cav1.2-associated alterations in HPA originate developmentally, with evidence from neuron-specific Cacna1c−/− mice that spontaneous calcium activity is perturbed from early embryogenesis, which is associated with altered brain structure (including the hippocampus) and anxiety in adulthood [71], and that embryonic, but not adult-induced, Cacna1c depletion results in impaired hippocampal function, synaptic plasticity and anxiety coupled with an increased vulnerability to the effects of stress [19].