ADENOSINE MODULATION OF POTASSIUM CURRENTS IN POSTGANGLIONIC NEURONS OF CULTURED AVIAN CILIARY GANGLIA

1 Potassium currents in cultured postganglionic neurones of avian ciliary ganglia were analysed under whole-cell voltage clamp and their modulation by adenosine determined. 2 In the presence of tetrodotoxin (200 nM), and with moderate holding potentials (Vh = -40 mV), the steady-state current-voltage (I/V) curve was N-shaped over the range from -70 mV to +155 mV. CsCl (1 M) blocked the current, indicating that it was carried by K+. If Ca2+ influx was blocked by CdCl2 (500-mu-M) then the outward current was reduced and the N-shaped I-V curve lost, indicating the presence of a calcium-activated potassium current (I(K(Ca)); the remaining current, due to the delayed rectifier (I(K)), increased with depolarization up to about a conductance of 10 nS near +50 mV. This I(K) was 50% activated at about +20 mV and 50% inactivated at about -50 mV. Adenosine (10-mu-M) had similar affects on the N-shaped I/V curve as did CdCl2, indicating that it blocked I(K(Ca)). However, adenosine had little affect on the steady-state current in the presence of CdCl2, indicating that it did not much affect I(K). 3 In the presence of tetrodotoxin (200 nM), a large inward current occurred for large hyperpolarizations from a Vh = -50 mV. This inward rectifying current (I(IR)) had a reversal potential near E(K) and showed 50% activation at about -130 mV. Adenosine (10-mu-M) reduced I(IR), by as much as 50% at large hyperpolarizations beyond -80 mV. 4 Relaxations of the outward current on hyperpolarization from Vh = -30 mV were blocked by carbachol (10-mu-M), had a reversal potential near E(K), and an I/V curve typical of I(M) currents. These currents were little affected by adenosine (10-mu-M). 5 A fast transient outward current, due to depolarizing pulses from a large Vh = -110 mV was observed in the presence of tetrodotoxin (200 nM). This had the characteristics of an I(A) current as it could be blocked with 4-aminopyridine (5 mM) and was 50% activated at about -20 mV and 50% inactivated at about -94 mV. The I(A) current was reduced by 42% at a depolarization of -20 mV by adenosine (10-mu-M). 6 Many neurones possessed a fast transient outward current that was blocked by tetrodotoxin (200 nM). This current could be blocked with 4-aminopyridine (5 mM); it therefore has the characteristics of a sodium-activated potassium current (I(K(Na)). This I(K(Na)) was unaffected by adenosine (10-mu-M). 7 These results are discussed in relation to the role of adenosine in blocking Ca2+ channels and thereby modifying calcium-dependent components of K+ currents.