Adenosine modulation of calcium currents in postganglionic neurones of avian cultured ciliary ganglia

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Abstract
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 (τ > 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 μm of Bay K 8644 at a test potential of 0 mV and decreased over 35% by 1 μm of nifedipine. 4 The transient current inactivated slowly (τ < 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 μm) but reduced on average by 8% with nifedipine (1 μm). 5 The sustained and transient currents were decreased more than 70% by 5 μm of ω-conotoxin and decreased more than 50% by 250 μm verapamil. 6 2-Chloroadenosine (1 μm) decreased the transient current by over 50% and the sustained current by less than 10%. In the presence of nifedipine (1 μm), 2-chloroadenosine decreased the transient current by over 30% and the remaining sustained current by 35%. In the presence of 8-phenyltheophylline (10 μm), 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.