Inositol (1,4,5)-trisphosphate receptors (IP3Rs) are intracellular Ca2+ release channels that play a key role in controlling neuronal excitability and plasticity. Production of IP3 is caused by synaptic inputs activating metabotropic neurotransmitter receptors, such as metabotropic glutamate or acetylcholine receptors. The resulting increase in intracellular Ca2+ levels influences a plethora of neuronal processes by activating Ca2+-sensitive enzymes and ion channels. Previous studies have shown that Ca2+-sensitive SK and BK K+ channels are activated by spike-evoked Ca2+ influx in medium spiny neurons (MSNs), the sole output neurons of the striatum, thereby shaping their firing pattern. However, it is not clear how SK and BK channels are coupled to IP3-induced Ca2+ release in these neurons. I use in vitro brain slice electrophysiology recordings in combination with flash photolysis of caged IP3 to address how intracellular Ca2+ release could modulate MSN firing.
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