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Localized IP₃-Evoked Ca²⁺ Release Activates a K⁺ Current in Primary Vagal Sensory Neurons

¹Medical Biotechnology Center, University of Maryland Biotechnology Institute; and Departments of ²Physiology and ³Pharmacology and Experimental Therapeutics, University of Maryland School of Medicine, Baltimore, Maryland 21201

Submitted 20 October 2003; accepted in final form 4 December 2003

Electrophysiological and microfluorimetric techniques were used to determine whether intracellular photorelease of caged IP₃, and the consequent release of Ca²⁺, could trigger a Ca²⁺-activated K⁺ current (I_IP3). Photorelease of caged IP₃ evoked an I_IP3 that averaged 2.36 ± 0.35 (SE) pA/pF in 24 of 28 rabbit primary vagal sensory neurons (nodose ganglion neurons, NGNs) voltage-clamped at –50 mV. I_IP3 was abolished by intracellular BAPTA (2 mM), a Ca²⁺ chelator. Changing the K⁺ equilibrium potential by increasing extracellular K⁺ ion concentration caused a predicted Nernstian shift in the reversal potential of I_IP3. These results indicated that I_IP3 was a Ca²⁺-dependent K⁺ current. I_IP3 was unaffected by three common antagonists of Ca²⁺-activated K⁺ currents: bath-applied iberiotoxin (50 nM) or apamin (100 nM), and intracellular 8-Br-cAMP (100 µM) included in the patch pipette. We have previously demonstrated that both IP₃-evoked Ca²⁺ release and Ca²⁺-induced Ca²⁺ release (CICR) are co-expressed in NGNs and that CICR can trigger a Ca²⁺-activated K⁺ current. In the present study, using caffeine, a CICR agonist, to selectively attenuate intracellular Ca²⁺ stores, we showed that IP₃-evoked Ca²⁺ release occurs independently of CICR, but interestingly, that a component of I_IP3 requires CICR. These data suggest that IP₃-evoked Ca²⁺ release activates a K⁺ current that is pharmacologically distinct from other Ca²⁺-activated K⁺ currents in NGNs. We describe several models that explain our results based on Ca²⁺ signaling microdomains in NGNs.