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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Bennett, M. R. Kerr, R. Nichol, K. |
| Description | Author Affiliation: Bennett MR ( Neurobiology Research Centre, University of Sydney, N.S.W., Australia.) |
| Abstract | 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. |
| ISSN | 00071188 |
| e-ISSN | 14765381 |
| Journal | British Journal of Pharmacology |
| Issue Number | 2 |
| Volume Number | 104 |
| Language | English |
| Publisher | Wiley Online Library(on behalf of The British Pharmacological Society) |
| Publisher Date | 1991-10-01 |
| Publisher Place | Great Britain (UK) |
| Access Restriction | Open |
| Subject Keyword | Adenosine Physiology Ganglia Neurons Potassium Channels Animals Carbachol Cells, Cultured Cytology Membrane Potentials Sodium Pharmacology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Pharmacology |
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