Abstract
The somatic membrane of guinea-pig olfactory cortex neurons in vitro (23.degree. C) was voltage clamped by means of a single-micro-electrode sample-and-hold technique. In most cells the current-voltage (I-V) relationship showed inward (anomalous) rectification with increasing hyperpolarization beyond the resting potential (.apprx. -80 mV). Under current-clamp conditions a time-dependent sag of the hyperpolarizing electrotonic potentials was observed following an initial overshoot. No depolarizing after-potential was seen on return to the resting potential. Inward rectification was activated 100-110 mV (irrespective of pre-set resting potential) and increased the membrane input conductance by up to 3-fold. The rectification was unaffected by tetrodotoxin or Cd2+. Under somatic voltage clamp, hyperpolarization beyond -110 mV activated a rapid inward relaxation fitted by a single exponential. The relaxation time constant (.tau.on) decreased e-fold for a 40 mV hyperpolarization. (Typical values: 28 ms at -110 mV declining to 13 ms at -140 mV: external K+ concentration 3 mM, 23.degree. C). More extreme hyperpolarizations evoked a slower inactivation phase (.tau. = 40-60 ms). A transient outward-decaying tail current reflecting deactivation of inward rectification was seen on stepping from -140 mV to more positive potentials .tau.off became slower with hyperpolarization. The tail current disappeared at a potential close to the expected VK but was rarely inverted to an inward-decaying tail. The fast inward-rectifying current of olfactory neurons (If.i.r.) is a K+ current analogous to the anomalous K+ rectifier of marine egg and frog muscle membranes. The behavior of the inward rectifier was dependent on external K+ concentration in accordance with the unique V-VK dependence of classical anomalous rectification. Of several agents tested (external Cs+, Ba2+, Rb+, Tl+ or tetraethylammonium), only Cs+ and Ba2+ blocked Ifir in a time- and voltage-dependent manner. The effect of tetraethylammonium resembled that of an increase in external K+. The possible contribution of the inward rectifier to the passive cell membrane properties is discussed.