Probabilistic secretion of quanta from nerve terminals in avian ciliary ganglia modulated by adenosine.

Kerr

Khurana

1992

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) 4 The transient current inactivated slowly (t <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 JM) but reduced on average by 8% with nifedipine (1 JM). 5 The sustained and transient currents were decreased more than 70% by 5 JAM of o-conotoxin and decreased more than 50% by 250 JM verapamil. 6 2-Chloroadenosine (1 JAM) decreased the transient current by over 50% and the sustained current by less than 10%. In the presence of nifedipine (1 JM), 2-chloroadenosine decreased the transient current by over 30% and the remaining sustained current by 35%. In the presence of 8-phenyltheophylline (10 JM), 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.

Section: Introductionmentioning

confidence: 99%

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

Kerr

Khurana

1992

“…The avian ciliary ganglion provides an opportunity to elucidate the mechanism of action of adenosine as transmission is modulated by endogenous purine nucleotides at this synapse (Bennett & Ho, 1991). Furthermore the synapse possesses giant calyciform nerve terminals that are accessible to single electrode voltage clamp (Martin & Pilar, 1963).…”

Section: Introduction Methodsmentioning

confidence: 99%

“…Furthermore the synapse possesses giant calyciform nerve terminals that are accessible to single electrode voltage clamp (Martin & Pilar, 1963). Such studies have shown that adenosine hyperpolarizes nerve terminals, suggesting that its action increases the outward potassium currents (Bennett & Ho, 1991). Adenosine hyperpolarizes atrial cells by activating IM potassium channels via GTP-binding proteins (Kurachi et al, 1986).…”

Section: Introduction Methodsmentioning

confidence: 99%

“…Endogenous adenosine modulates secretion at synapses (Phillis & Wu, 1981), by acting as an autoinhibitory agent which reduces both the mean quantal content of the synaptic potential and its variance (Ribeiro & Sebastiao, 1987;. The avian ciliary ganglion provides an opportunity to elucidate the mechanism of action of adenosine as transmission is modulated by endogenous purine nucleotides at this synapse (Bennett & Ho, 1991). Furthermore the synapse possesses giant calyciform nerve terminals that are accessible to single electrode voltage clamp (Martin & Pilar, 1963).…”

Section: Introduction Methodsmentioning

confidence: 99%

See 1 more Smart Citation

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

Kerr

Nichol

1991

(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 (10pJM).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 (1OpM). 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.

“…In the neurone soma there are delayed rectifier channels, calcium-activated potassium channels, inward rectifier potassium channels, cholinoceptor agonist activated channels, fast-transient potassium channels, and sodium-activated potassium channels . A number of different potassium channels have also been identified in the calyciform nerve terminal: these include delayed rectifier channels, inward rectifier channels and calcium-activated potassium channels (Bennett & Ho, 1991;Fletcher & Chiappinelli, 1992). The identity of the type of Ik(ca) is not clear, although an Ik(Ca) is blocked by tetraethylammonium ions (TEA; Bennett & Ho, 1992), and it is known that the fast Ik(ca), Ic, which contributes to the repolarization of the action potential is very sensitive to TEA in autonomic ganglia (Lancaster & Pennefather, 1987;Marsh & Brown, 1991).…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide modulation of calcium‐activated potassium channels in postganglionic neurones of avian cultured ciliary ganglia

Çetiner

1993

1 A study has been made of the modulation of calcium-activated potassium channels in cultured neurones of avian ciliary ganglia by sodium nitroprusside and L-arginine.2 Sodium nitroprusside (100 gM) reduced the net outward current by 22± 1% at 4.8 ms (mean ± s.e.mean) and 25 ± 1% at 350 ms during a test depolarization to + 40 mV from a holding potential of -40 mV. The outward current remained reduced for the duration of the recording following a single application of sodium nitroprusside. These effects did not occur if the influx of calcium ions was first blocked with Cd2+ (500 ytM). Application of ferrocyanide (100 j.M) reduced the net outward current by only 6 ± 3% at 350 ms during a test depolarization to + 40 mV.3 L-Arginine (270 IM) reduced the net outward current on average by 19 ± 2% at 4.8 ms and 22 ± 2% at 350 ms during a test depolarization to + 40 mV. The current remained in this reduced state for the duration of the recording following a single application of L-arginine. These effects were reduced to 11 ± 1% at 4.8 ms and 11 ± 2% at 350 ms in the presence of Nw-nitro-L-arginine methyl ester (L-NAME, 100 gM). 4 In order to alleviate the dependence of calcium-activated potassium channels (Ik(Ca)) on the inward flux of calcium ions, the patch-clamp pipettes were filled with a solution containing 100 gM CaC12, and the Ca2+ in the bathing solution was replaced with EGTA. Under these conditions sodium nitroprusside reduced the total outward current during a depolarizing pulse of + 40 mV by 9 ± 1% at 4.8 ms and by 36 ± 3% at 350 ms. L-Arginine (270 gM) reduced this current under the same conditions by 9 ± 1% at 4.8ms and by 35 ± 2% at 350ms. 5 Calcium-activated potassium currents were sensitive to apamin (50 nM), as this reduced the outward current by 23 ± 3% at 350 ms when a high calcium-containing pipette was used during a depolarizing command to +40 mV. L-Arginine still decreased the outward current in the presence of apamin (50 nM), by 5 ± 1% at 4.8 ms and by 19 ± 2% at 350 ms, indicating that L-arginine could reduce an apamin-insensitive Ik(Ca) 6 Calcium-activated potassium currents were also sensitive to charybdotoxin (10 nM), as this reduced the outward current by 34 ± 4% at 350 ms when a high calcium-containing pipette was used during a depolarizing command to + 40 mV. L-Arginine still decreased the outward current in the presence of charybdotoxin, by 6 ± 1% at 4.8 ms and 12 ± 4% at 350 ms, showing that L-arginine could reduce a charybdotoxin-insensitive Ik(Ca). 7 The present results indicate that NO-synthase in ciliary ganglia can modulate Ik(Ca) by a method which is independent of the action of NO on the calcium channels. The Ik(ca) is decreased significantly at 4.8 ms into a depolarizing pulse, at a time that would decrease the rate of repolarization of the action potential. Ik(Ca) is also reduced at longer times (350 ms), indicating an affect on the inactivating process.