Adenosine modulation of potassium currents in postganglionic neurones 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 microM) then the outward current was reduced and the N-shaped I-V curve lost, indicating the presence of a calcium-activated potassium current (IK(Ca)); the remaining current, due to the delayed rectifier (IK), increased with depolarization up to about a conductance of 10 nS near + 50 mV. This IK was 50% activated at about +20 mV and 50% inactivated at about -50 mV. Adenosine (10 microM) had similar affects on the N-shaped I/V curve as did CdCl2, indicating that it blocked IK(Ca). However, adenosine had little affect on the steady-state current in the presence of CdCl, indicating that it did not much affect IK. 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 (IIR) had a reversal potential near EK and showed 50% activation at about -130 mV. Adenosine (10 microM) reduced IIR, by as much as 50% at large hyperpolarizations beyond -80 mV. 4. Relaxations of the outward current on hyperpolarization from Vh = -30mV were blocked by carbachol (10 microM), had a reversal potential near EK, and an I/V curve typical of 1M currents. These currents were little affected by adenosine (10 microM). 5. A fast transient outward current, due to depolarizing pulses from a large Vh = -110mV was observed in the presence of tetrodotoxin (200 nM). This had the characteristics of an IA 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 IA current was reduced by 42% at a depolarization of -20 mV by adenosine (10 microM). 6. Many neurones possessed a fast transient outward current that was blocked by tetrodotoxin (200nM). This current could be blocked with 4-aminopyridine (5mM); it therefore has the characteristics of a sodium-activated potassium current ('K(Na)). This IK(Na) was unaffected by adenosine (1O microM). 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.
Bennett
M R
MR
Neurobiology Research Centre, University of Sydney, N.S.W., Australia.
Kerr
R
R
Nichol
K
K
D000241:Adenosine / Q000502:physiology*; D000818:Animals; D002217:Carbachol; D002478:Cells, Cultured; D002645:Chickens; D005724:Ganglia / Q000166:cytology / Q000502:physiology*; D008564:Membrane Potentials / Q000502:physiology; D009474:Neurons / Q000502:physiology*; D015221:Potassium Channels / Q000502:physiology*; D012964:Sodium / Q000502:physiology
D015221:Potassium Channels; D002217:Carbachol; D012964:Sodium; D000241:Adenosine