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Autism spectrum disorders (ASD) are a group of neurodevelopmental disorders characterized by social and communication deficits, and repetitive and restricted interests and behaviours. A loss of GABAergic inhibition has been described in the autism mouse model, the Rag1 knockout (KO). To investigate mechanisms underlying the loss of GABAergic inhibition in this model, we studied intracellular Ca2+ dynamics in cerebellar granule neurons (CGNs) isolated from Rag1 KO and wild-type (WT) mice. We show that CGNs isolated from Rag1 KO mice showed altered Ca2+ dynamics in the form of increased cytoplasmic Ca2+ activity, resulting in an enhanced Ca2+ efflux through ryanodine receptors. The Ca2+ efflux also appeared to be accelerated by increased levels of the RyR-associated proteins, Ca2+/calmodulin-dependent kinase II (CaMKII) and calbindin-D9k (CABD), and decreased by phosphorylation of RyRs. We further show that CGNs isolated from WT mice showed increased Ca2+ influx and activation of RyRs which was likely due to a reduced ryanodine receptor phosphorylation and an increased association of CaMKII and CABD with the RyR. The altered Ca2+ dynamics observed in Rag1 KO CGNs were not only associated with an overactivation of Ca2+ efflux pathways but also with an overactivation of the Na+/Ca2+ exchanger. Our data show that altered intracellular Ca2+ dynamics in the form of increased Ca2+ efflux and activation of Ca2+ influx mechanisms could
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