Variations in the gene CACNA1C, which encodes the protein Cav1.2, has been identified as a risk factor for a number of neuropsychiatric disorders including major depressive disorder, schizophrenia, bipolar disorder, attention deficit hyperactivity disorder and autism spectrum disorder. Follow up studies revealed that an intronic single nucleotide polymorphism (SNP) rs1006737 of CACNA1C can lead to both higher or lower CACNA1C expression as well as altered Cav1.2 function in neurons. Therefore, in this dissertation, I use cacna1c transgenic mouse models that harbor Cav1.2 knockout in specific brain regions and cell types to study the role of the L-type calcium channel, Cav1.2 in neuropsychiatric disorders. Using a transgenic mouse model, I discovered that Cav1.2 in the glutamatergic neurons of the forebrain regulate anxiety-like behaviors in mice. Using stereotaxic delivery of virus mediated gene transfer, I further showed that Cav1.2 in the glutamatergic neurons of the prefrontal cortex within the forebrain regulates anxiety-like behaviors in mice. I also report a role for Cav1.2 in regulating depressive-like behaviors via Regulated in Development and DNA Damage (Redd1) in the prefrontal cortex. More specifically, Cav1.2 in non-glutamatergic neurons of the prefrontal cortex was found to modulate depressive-like behaviors in mice. Since hippocampal adult neurogenesis is a process that has been associated with anxiety and depression, I studied the role of Cav1.2 in this process. I found that Cav1.2, but not Cav1.3, is necessary for the survival, but not proliferation, of new born neuronal progenitor cells. Since carriers of the SNP rs1006737 have been shown to have deficits in reward response, and drug addiction is so often co-morbid with anxiety and depression, I studied the role of Cav1.2 in cocaine addiction using the cocaine conditioned place preference behavioral paradigm. I found that Cav1.2 in the hippocampus is required for the normal decay of cocaine-context association memories following a long-term withdrawal from cocaine. I discovered that decreased Cav1.2 in the hippocampus leads to the preferential activation of the calcium calmodulin kinase pathway and increased phosphorylation of nuclear factor of activated T-cells (NFATc) in the nucleus accumbens, which underlies the maintenance or decay of cocaine-context association memories by Cav1.2.