Atp2a2, also known as SERCA2, encodes a Ca2+ pump on the endoplasmic reticulum (ER) membrane. It is crucial for intracellular Ca2+ signaling, which is involved in multiple biological processes. Mutations in Atp2a2 are associated with various disorders, highlighting its importance in maintaining normal physiological functions. Genetic models, such as knockout (KO) or conditional knockout (CKO) mouse models, are valuable for studying its function [1].

In Atp2a2 heterozygous brain-specific conditional knockout (hetero cKO) mice, the ER membranes from the brain showed decreased Ca2+ uptake activity. In hetero cKO neurons, the decay of cytosolic Ca2+ level was slower after depolarization. These mice exhibited altered behavioral responses and fear memory impairments, along with higher extracellular dopamine levels in the NAc, suggesting that haploinsufficiency of Atp2a2 in the brain leads to prolonged cytosolic Ca2+ transients and enhanced dopamine signaling [1].

In conclusion, Atp2a2 is essential for regulating intracellular Ca2+ levels and signaling. Studies using CKO mouse models have revealed its role in the development of behavioral abnormalities and a hyper-dopaminergic state, indicating its significance in neuropsychiatric disorders. Understanding Atp2a2 function through such models provides insights into the mechanisms underlying these diseases [1].