Presynaptic calcium channels mediating synaptic transmission in submucosal neurones of the guinea‐pig caecum

Cunningham, Shauna M. C.; Mihara, S.; Higashi, Hideho

doi:10.1111/j.1469-7793.1998.425bn.x

Cited by 16 publications

(18 citation statements)

References 38 publications

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“…Acetylcholine, substance P and 5‐HT are mediators of sEPSPs in myenteric AH neurons 2,32,33 . Previous work has shown that N‐type Ca 2+ channels contribute to Ca 2+ entry required for acetylcholine release from myenteric neurons, 18 while N‐ and P/Q‐type channels contribute to cholinergic fast synaptic excitation in the guinea pig submucosal plexus 24 17,18 .…”

Section: Discussionmentioning

confidence: 98%

“…N‐type Ca 2+ channels contribute to the Ca 2+ component of the action potential in AH neurons 9,21 . N‐type Ca 2+ channels also contribute to neurotransmitter release from enteric neurons 17,18,22–24 . P/Q channels are blocked by ω‐agatoxin GIVA and are composed of Ca V 2.1 subunits 13,14 .…”

Section: Introductionmentioning

confidence: 99%

“…P/Q channels are blocked by ω‐agatoxin GIVA and are composed of Ca V 2.1 subunits 13,14 . P/Q type Ca 2+ channels also contribute neurotransmitter release from enteric neurons 17,18,24 . R‐type Ca 2+ channels are blocked by SNX‐482 and low concentrations (≤50 μmol L −1 ) of NiCl 2 11,25,26 and are composed of Ca V 2.3 subunits 11,27 .…”

Section: Introductionmentioning

confidence: 99%

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R-type Ca2+ channels contribute to fast synaptic excitation and action potentials in subsets of myenteric neurons in the guinea pig intestine

Naidoo

Dai

Galligan

2010

Neurogastroenterology &Amp; Motility

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These data show that R-type Ca(2+) channels contribute to action potentials, but not slow synaptic transmission, in AH neurons. R-type Ca(2+) channels contribute to release of acetylcholine as the mediator of fEPSPs in some S neurons. These data indicate that R-type Ca(2+) channels may be a target for drugs that selectively modulate activity of AH neurons or could alter fast synaptic excitation in specific pathways in the myenteric plexus.

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Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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R-type Ca2+ channels contribute to fast synaptic excitation and action potentials in subsets of myenteric neurons in the guinea pig intestine

Naidoo

Dai

Galligan

2010

Neurogastroenterology &Amp; Motility

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“…This observation might suggest that there is ‘residual release’ in the cat bronchiole. In the submucosal plexus of the guinea‐pig caecum, furthermore, release of noradrenaline from extrinsic nerve terminals (sympathetic origin) is regulatd by N‐type calcium channels, whereas release of ACh from intrinsic nerve terminals (enteric origin) involves several types of calcium channels (Cunningham et al ., 1998). Therefore, it seems that N‐type calcium channels are the dominant channel controlling transmitter release in peripheral nervous system, but additional calcium channels are recruited especially when the stimulation frequency is increased.…”

Section: Discussionmentioning

confidence: 99%

Multiple calcium channels regulate neurotransmitter release from vagus nerve terminals in the cat bronchiole

Fujisawa

Onoue

Abe³

et al. 1999

British J Pharmacology

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1 Twitch-like contractions and non-adrenergic non-cholinergic (NANC) relaxations evoked by electrical ®eld stimulation (EFS) of the cat bronchiole were used to examine the voltage-activated calcium channels involved in excitatory and inhibitory neurotransmission in the cat bronchiole. 2 Nifedipine (50 mM), the L-type calcium channel antagonist, did not aect the twitch-like contraction and NANC relaxations. However, low concentrations of the N-type calcium channel blocker o-conotoxin GVIA (o-CgTX GVIA) (0.1 mM) irreversibly abolished twitch-like contractions evoked by trains of EFS 410 stimuli at 20 Hz. 3 After the prolonged treatment with 0.1 mM o-CgTX GVIA, EFS evoked initial fast and later slow NANC relaxations in the presence of 5-HT (10 mM), atropine and guanethidine (1 mM each). However increased concentration of o-CgTX GVIA (1 mM) completely suppressed the slow NANC relaxation without aecting the initial fast component. 4 o-agatoxin IVA (100 nM), the P-and Q-type calcium channel inhibitor, and nimodipine (10 mM), the L-and T-type calcium channel blocker, did not aect the amplitude of the initial fast NANC relaxation in the absence or presence of o-CgTX GVIA (1 mM). 5 The contraction or relaxation induced by exogenous acetylcholine (ACh) (0.5 mM) or the nitric oxide donor, s-nitroso-N-acetyl penicillamine (SNAP) (1 mM) were not aected by o-CgTX GVIA (1 mM). 6 Taken together, these results suggest that generation of twitch-like contraction and later slow NANC relaxation are regulated by N-type calcium channels, whereas generation of the initial fast NANC relaxation possibly involves R-type calcium channel.

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“…(1993) concluded that the P‐channels alone are responsible for the release of glutamate from striatal synaptosomes, whereas both the P‐ and the N‐channels play a role in the release of dopamine. On a similar vein, Cunningham et al . (1998) found that, in the ileum, the release of noradrenaline is mediated by the N‐type channels, whereas that of acetylcholine depends on both the N‐ and the P‐channel types.…”

Section: Introductionmentioning

confidence: 99%

Calcium channels involved in the inhibition of acetylcholine release by presynaptic muscarinic receptors in rat striatum

Doležal

Tuček

1999

British J Pharmacology

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1 The mechanism of the inhibitory action of presynaptic muscarinic receptors on the release of acetylcholine from striatal cholinergic neurons is not known. We investigated how the electrically stimulated release of [ 3 H]-acetylcholine from superfused rat striatal slices and its inhibition by carbachol are aected by speci®c inhibitors of voltage-operated calcium channels of the L-type (nifedipine), N-type (o-conotoxin GVIA) and P/Q-type (o-agatoxin IVA). 2 The evoked release of [ 3 H]-acetylcholine was not diminished by nifedipine but was lowered by oconotoxin GVIA and by o-agatoxin IVA, indicating that both the N-and the P/Q-type (but not the L-type) channels are involved in the release. The N-type channels were responsible for approximately two thirds of the release. The release was 497% blocked when both o-toxins acted together.3 The inhibition of [ 3 H]-acetylcholine release by carbachol was not substantially aected by the blockade of the L-or P/Q-type channels. It was diminished but not eliminated by the blockade of the N-type channels. 4 In experiments on slices in which cholinesterases had been inhibited by paraoxon, inhibition of [ 3 H]-acetylcholine release by endogenous acetylcholine accumulating in the tissue could be demonstrated by the enhancement of the release after the addition of atropine. The inhibition was higher in slices with functional N-type than with functional P/Q-type channels. 5 We conclude that both the N-and the P/Q-type calcium channels contribute to the stimulationevoked release of acetylcholine in rat striatum, that the quantitative contribution of the N-type channels is higher, and that the inhibitory muscarinic receptors are more closely coupled with the Ntype than with the P/Q-type calcium channels.

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Presynaptic calcium channels mediating synaptic transmission in submucosal neurones of the guinea‐pig caecum

Cited by 16 publications

References 38 publications

R-type Ca2+ channels contribute to fast synaptic excitation and action potentials in subsets of myenteric neurons in the guinea pig intestine

R-type Ca2+ channels contribute to fast synaptic excitation and action potentials in subsets of myenteric neurons in the guinea pig intestine

Multiple calcium channels regulate neurotransmitter release from vagus nerve terminals in the cat bronchiole

Calcium channels involved in the inhibition of acetylcholine release by presynaptic muscarinic receptors in rat striatum

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