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Adenosine modulation of potassium currents in postganglionic neurones of cultured avian ciliary ganglia
Author(s) -
Bennett Max R.,
Kerr Rod,
Nichol Kerry
Publication year - 1991
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1991.tb12451.x
Subject(s) - chemistry , adenosine , tetrodotoxin , biophysics , depolarization , 4 aminopyridine , cardiac transient outward potassium current , reversal potential , potassium , membrane potential , voltage clamp , potassium channel , patch clamp , medicine , endocrinology , biochemistry , biology , receptor , organic chemistry
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 n m ), 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 Ca 2+ influx was blocked by CdCl 2 (500 μ 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 μ m ) had similar affects on the N‐shaped I / V curve as did CdCl 2 , indicating that it blocked I K(Ca) . However, adenosine had little affect on the steady‐state current in the presence of CdCl 2 , indicating that it did not much affect I K . 3 In the presence of tetrodotoxin (200 n m ), 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 μ 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 μ 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 μ 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 n m ). This had the characteristics of an I A current as it could be blocked with 4‐aminopyridine (5 m m ) 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 μ m ). 6 Many neurones possessed a fast transient outward current that was blocked by tetrodotoxin (200 n m ). This current could be blocked with 4‐aminopyridine (5 m m ); it therefore has the characteristics of a sodium‐activated potassium current ( I K(Na) ). This I K(Na) was unaffected by adenosine (10 μ m ). 7 These results are discussed in relation to the role of adenosine in blocking Ca 2+ channels and thereby modifying calcium‐dependent components of K + currents.