Release Activates a K Current in Primary Vagal Sensory Neurons

Hoesch, Robert E., Daniel Weinreich, and Joseph P. Y. Kao. Localized IP3-evoked Ca 2 release activates a K current in primary vagal sensory neurons. J Neurophysiol 91: 2344–2352, 2004. First published December 10, 2003; 10.1152/jn.01008.2003. Electrophysiological and microfluorimetric techniques were used to determine whether intracellular photorelease of caged IP3, and the consequent release of Ca , could trigger a Ca -activated K current (IIP3). Photorelease of caged IP3 evoked an IIP3 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. IIP3 was abolished by intracellular BAPTA (2 mM), a Ca chelator. Changing the K equilibrium potential by increasing extracellular K ion concentration caused a predicted Nernstian shift in the reversal potential of IIP3. These results indicated that IIP3 was a Ca 2 -dependent K current. IIP3 was unaffected by three common antagonists of Ca 2 activated K currents: bath-applied iberiotoxin (50 nM) or apamin (100 nM), and intracellular 8-Br-cAMP (100 M) included in the patch pipette. We have previously demonstrated that both IP3-evoked Ca release and Ca -induced Ca release (CICR) are co-expressed in NGNs and that CICR can trigger a Ca -activated K current. In the present study, using caffeine, a CICR agonist, to selectively attenuate intracellular Ca stores, we showed that IP3evoked Ca release occurs independently of CICR, but interestingly, that a component of IIP3 requires CICR. These data suggest that IP3-evoked Ca 2 release activates a K current that is pharmacologically distinct from other Ca -activated K currents in NGNs. We describe several models that explain our results based on Ca signaling microdomains in NGNs.