Characterization of voltage-activated currents in Hermissenda type B-photoreceptors.
Two distinct voltage-dependent K+ currents have been previously identified in the type B-photoreceptors of Hermissenda: an early, rapidly inactivating K+ current (IA), and a late, 4-AP- and TEA-resistant voltage and Ca(2+)-dependent current (IK(Ca)). Using conventional two-electrode voltage-clamp techniques, we have characterized two additional currents, a late voltage-dependent outward K+ current (IK(v)) and a voltage-dependent inward current identified as an inward rectifier (Iir). In addition, we have further studied the activation-inactivation kinetics of IA. In 0-Na+ ASW, Iir activates at a potential of > -50 mV, is steeply voltage-dependent and noninactivating, and reaches steady-state within 800 msec to 3 sec at -100 mV. In addition to the variability in activation kinetics, there was also considerable variability in Iir magnitude (-5 to -80 nA, at -100 mV). Iir was blocked by external 4-AP (5 mM), external and internal TEA, internal Cs+, but not external Ba2+. The major component of outward K+ current in type B-photoreceptors is IK(v), the delayed rectifier. IK(v) was isolated after removal of IA and IK(Ca). IK(v) activates at around -25 mV or more positive membrane potentials and its activation and inactivation are strongly voltage dependent. IK(v) inactivation to steady state is reached within 1.5-2.5 sec. The wide range of activation-inactivation rates suggests that there may be kinetic subtypes of IK(v). The proposed "slow" IK(v) peaked in 50-90 msec at +30 mV, and decayed with a single exponential component with an average tau off of 279 msec. Proposed "intermediate" and "fast" IK(v) subtypes peaked within 12-50 msec at +30 mV, and had a decay fitted by two exponentials, with an average tau 1 of 147 msec and tau 2 of 275 msec, respectively. IK(v) exhibited marked twin-pulse inactivation with a recovery time of 30-40 sec, and also exhibited time- and voltage-dependent cumulative inactivation to repeated depolarizing pulses. Both types of inactivation were quickly removed by a prepulse hyperpolarization. 4-AP (5 mM) produced partial to complete block of the inactivating component of IK(v), leaving only a residual sustained component. Complete block of the transient and sustained components of IK(v) was obtained by 100 mM TEA. Reliable voltage separation of IA from IK(v) was achieved by activating IA in the range of -50 to -20 mV, from a Vh of -80 mV. Voltage-dependent steady-state inactivation curves for IA were determined, yielding an average h0.5 value of -56 mV.(ABSTRACT TRUNCATED AT 250 WORDS)
Acosta-Urquidi
J
J
Department of Neurobiology and Anatomy, University of Texas Medical School, Houston 77225.
Crow
T
T
D015761:4-Aminopyridine / Q000494:pharmacology; D000818:Animals; D001464:Barium / Q000494:pharmacology; D002586:Cesium / Q000494:pharmacology; D004594:Electrophysiology; D007700:Kinetics; D008974:Mollusca / Q000502:physiology*; D017956:Photoreceptor Cells, Invertebrate / Q000502:physiology*; D026902:Potassium Channel Blockers; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology
D026902:Potassium Channel Blockers; D013757:Tetraethylammonium Compounds; D002586:Cesium; D001464:Barium; D019789:Tetraethylammonium; D015761:4-Aminopyridine