Ca²⁺ influx through presynaptic voltage-gated Ca²⁺ channels (Caᵥ) is required for neurotransmitter release. Volatile anesthetic effects on synaptic transmission and neurotransmitter release are mediated by inhibition of presynaptic Ca²⁺ influx, but the detailed mechanisms by which anesthetics reduce presynaptic Ca²⁺ are not fully understood. Ligand-gated ion channels, including Naᵥ and Caᵥ, as well as targets regulating intracellular Ca²⁺ stores, are leading candidates for anesthetic effects on intracellular Ca²⁺.
![Rat hippocampal neurons (14 DIV) transfected with vGlut-pHluorin during electrical stimulation [50 action potentials at 50 Hz (open circle)].](https://hemmingsandplatholi-labs.weill.cornell.edu/sites/default/files/styles/panopoly_image_original/public/hhmovie1_stim_1.gif?itok=rEDbR4k1 "Rat hippocampal neurons (14 DIV) transfected with vGlut-pHluorin during electrical stimulation [50 action potentials at 50 Hz (open circle)].")
Rat hippocampal neurons (14 DIV) transfected with ER-GCaMP during electrical stimulation [20 action potentials at 20 Hz (open circle)].
Fluorescence traces of a single bouton from a neuron transfected with vGlut-pHluorin. 𝜔-Aga blocked P/Q-type mediated exocytosis; isoflurane inhibited residual N-type Ca²⁺ channel- mediated exocytosis.
