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Proteins that control calcium influx and efflux. Numbers in red circles reflect the number of C. elegans genes in each category, although some of the homologs may not be expressed in the nervous system. Sources of calcium influx are nicotinic acetylcholine receptors (nAChR; 61 C. elegans genes; Table 9), AMPA and NMDA-type glutamate receptors (at least 10 C. elegans genes; Table 11), transient receptor potential type C channels (TRPC; 3 C. elegans genes; Table 7) and voltage-gated calcium channels (VGCC; 9 C. elegans genes; Table 4). Calcium release from internal stores is mediated by inositol trisphosphate receptors (IP3R; 1 C. elegans gene) and ryanodine receptors (RyR; 1 C. elegans gene). Inositol trisphosphate can be generated by metabotropic glutamate receptors (mGluR; 5 C. elegans genes; Table 19) as well as by other Gq coupled GPCRs. Calcium efflux is mediated by the plasma membrane calcium ATPase (PMCA; 3 C. elegans genes), the sodium-calcium exchanger (NCX; 10 C. elegans genes; Table 5), and the sarco-endoplasmic reticulum calcium ATPase (SERCA; 1 C. elegans genes). Intracellular calcium is sensed and buffered by calcium binding proteins, of which there are many dozens in the worm genome (Table 6). Mitochondria also play important roles in neuronal calcium homeostasis; the C. elegans calcium uniporter is encoded by mcu-1. This figure is a modified version of a figure taken from (Grienberger and Konnerth, 2012).