Fig. 1.

σ-1R enhancement of NMDAR function. σ-1Rs adapt a multi-component approach to promote NMDAR function, including the inhibition of SK channels (a), G proteins (identity is unclear; b), and intracellular kinases (c) alongside with an increase in the expression, trafficking, and surface levels (d) of NMDARs. In addition, σ-1R-mediated Ca²⁺ mobilization from ER via IP3 receptors may contribute to functional enhancement of NMDARs (e). The resultant increase in the influx of Ca²⁺ (blue arrow) further promotes synaptic plasticity [9,11,18,19,20,21,22].