As a genetic variation in CACNA1C (the alpha-1 subunit of CaV1.2, L-type voltage-dependent Ca2+ channels) is demonstrated to be a risk factor for both bipolar disorder and schizophrenia, using a Cacna1c+/− rat model [77], Tigaret et al. examined cognitive and synaptic phenotypes of the animal models and found synaptic and cognitive abnormalities in the rats, which were also rescued by LM22B-10, an agonist for the TrkB/TrkC receptor [17]. Here, NTRK2 is linked to schizophrenia.