Conceivably, deficits in TBS-induced LTP may represent a commonality across neuropsychiatric disorders with dysregulated local protein synthesis and cognitive deficits [55,56].In conclusion, this previously unknown role of Cav1.2 in TBS-induced LTPprovidesnew direction for studying Cav1.2 channel mechanisms in this form of LTP and developing potential therapeutics in neuropsychiatric and neurodegenerative disease. The gene discussed is CACNA1C; the disease is Cognitive impairment.