Adenosine modulation of calcium currents in postganglionic neurones of avian cultured ciliary ganglia.
1. Calcium currents in postganglionic neurones of cultured 7- to 10-day embryonic avian ciliary ganglia were analyzed under whole-cell voltage-clamp and their modulation by 2-chloroadenosine determined. 2. In the presence of tetrodotoxin (200 nM) in the medium to block the Na+ current and CsCl (105 mM) in the patch-clamp electrode to block the K+ current, two different components of the calcium currents (transient and sustained) were identified on the basis of their voltage-dependent kinetics as well as their sensitivity to the dihydropyridine agonist Bay K 8644 and antagonist nifedipine. 3. The sustained current inactivated very slowly (tau greater than 1000 ms; for test potentials from -20 mV to +40 mV) but was reactivated at a holding potential (Vh) of -40 mV. The current was increased on average over 50% by 1 microM of Bay K 8644 at a test potential of 0 mV and decreased over 35% by 1 microM of nifedipine. 4. The transient current inactivated slowly (tau less than 200 ms; for test potentials from -20 mV to +40 mV), and could be completely reactivated at a Vh of -80 mV. This current was unaffected by Bay K 8644 (1 microM) but reduced on average by 8% with nifedipine (1 microM). 5. The sustained and transient currents were decreased more than 70% by 5 microM of omega-conotoxin and decreased more than 50% by 250 microM verapamil. 6. 2-Chloroadenosine (1 microM) decreased the transient current by over 50% and the sustained current by less than 10%. In the presence of nifedipine (1 microM), 2-chloroadenosine decreased the transient current by over 30% and the remaining sustained current by 35%.In the presence of 8-phenyltheophylline (10 microM), 2-chloroadenosine no longer decreased either the transient or sustained currents but did have a slight potentiating effect on both the transient and sustained currents.7. These observations of the effects of 2-chloroadenosine on the transient and sustained currents are discussed in relation to the different calcium channel types at preganglionic nerve terminals.
Bennett
M R
MR
Neurobiology Research Centre, University of Sydney, N.S.W., Australia.
Kerr
R
R
Khurana
G
G
D015762:2-Chloroadenosine / Q000494:pharmacology*; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000187:drug effects* / Q000378:metabolism; D002478:Cells, Cultured; D002642:Chick Embryo; D004553:Electric Conductivity; D005726:Ganglia, Parasympathetic / Q000187:drug effects* / Q000378:metabolism; D008564:Membrane Potentials / Q000187:drug effects; D009474:Neurons / Q000187:drug effects* / Q000378:metabolism; D009543:Nifedipine / Q000494:pharmacology; D010456:Peptides, Cyclic / Q000494:pharmacology; D013806:Theophylline / Q000031:analogs & derivatives / Q000494:pharmacology; D014700:Verapamil / Q000494:pharmacology; D020960:omega-Conotoxins
D015220:Calcium Channels; D010456:Peptides, Cyclic; D020960:omega-Conotoxins; C053423:Conus magus toxin; D015762:2-Chloroadenosine; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D013806:Theophylline; D014700:Verapamil; C028322:8-phenyltheophylline; D009543:Nifedipine; D002118:Calcium