Potentiation of miniature endplate potential frequency by ATP in <i>Xenopus</i> tadpoles

Fu, Wen‐Mei; Yang, Shiau‐Hui; Lin‐Shiau, Shoei‐Yn

doi:10.1111/j.1476-5381.1993.tb13468.x

Cited by 9 publications

(2 citation statements)

References 48 publications

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“…Similar modulatory effects of ACh channels were also observed recently with the calcitonin gene-related peptide (CGRP) through the activation of protein kinase A in embryonic Xenopus cell cultures (Lu, Fu, Greengard & Poo, 1993). Furthermore, ATP (1 mM) had no effect on the amplitude and decay time of miniature endplate potentials in Xenopus tadpoles, which represent the latter stages of embryos (Fu, Yang & Lin-Shiau, 1993).…”

Section: Postsynaptic Potentiation Effect Of Atpsupporting

confidence: 78%

Potentiation by ATP of the postsynaptic acetylcholine response at developing neuromuscular synapses in Xenopus cell cultures.

Fu¹

1994

The Journal of Physiology

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1. Extracellular application of ATP to developing Xenopus neuromuscular synapses in culture resulted in a marked increase in the amplitude and frequency of spontaneous synaptic currents, using whole-cell recording. 2. The postsynaptic action of ATP was examined by studying the response of isolated muscle cells to iontophoretically applied acetylcholine (ACh). ATP enhanced the responses of the muscle membrane to ACh. The order of potency for various nucleotides (ATP = ADP > AMP, adenosine, GTP) suggests that ATP acts through P2-purinoceptors. The effect of ATP on whole-cell currents was also abolished by the protein kinase inhibitor H-7. 3. Single-channel measurements indicate that ATP increased the mean open time of lowconductance ACh channels. No change in the conductance of ACh channels was observed. 4. Local application of ATP to one region of the elongated myocyte surface resulted in potentiated ACh responses only at the ATP-treated region, suggesting that the cytosolic second messengers were effectively confined within the muscle cytoplasm. 5. The results of the present study suggest that ATP released from the nerve terminals may potentiate the ACh response of developing muscle cells during the early phase of synaptogenesis, and that the action of ATP can be restricted to the subsynaptic region exposed to the secreted ATP.

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Section: Postsynaptic Potentiation Effect Of Atpsupporting

confidence: 78%

Potentiation by ATP of the postsynaptic acetylcholine response at developing neuromuscular synapses in Xenopus cell cultures.

Fu¹

1994

The Journal of Physiology

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“…If this were the case, application of 10 mM H-7, a PKC blocker at that concentration (Fu et al, 1993;Plomp & Molenaar, 1996), should reverse the presynaptic inhibition induced by CCPA. Addition of H-7 to the solution containing CCPA did not modify the effect of the A 1 analog on mepp frequency (55.671.9% of control values, n ¼ 4, Figure 4b).…”

Section: Mechanism Of Action Of Ccpa On L-type Vdccsmentioning

confidence: 99%

Presynaptic inhibition of spontaneous acetylcholine release induced by adenosine at the mouse neuromuscular junction

Lorenzo

Veggetti

Muchnik

et al. 2004

British J Pharmacology

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1 At the mouse neuromuscular junction, adenosine (AD) and the A 1 agonist 2-chloro-N 6 -cyclopentyl-adenosine (CCPA) induce presynaptic inhibition of spontaneous acetylcholine (ACh) release by activation of A 1 AD receptors through a mechanism that is still unknown. To evaluate whether the inhibition is mediated by modulation of the voltage-dependent calcium channels (VDCCs) associated with tonic secretion (L-and N-type VDCCs), we measured the miniature endplate potential (mepp) frequency in mouse diaphragm muscles. 2 Blockade of VDCCs by Cd 2 þ prevented the effect of the CCPA. Nitrendipine (an L-type VDCC antagonist) but not o-conotoxin GVIA (an N-type VDCC antagonist) blocked the action of CCPA, suggesting that the decrease in spontaneous mepp frequency by CCPA is associated with an action on L-type VDCCs only. 3 As A 1 receptors are coupled to a G i/o protein, we investigated whether the inhibition of PKA or the activation of PKC is involved in the presynaptic inhibition mechanism. Neither N-(2[p-bromocinnamylamino]-ethyl)-5-isoquinolinesulfonamide (H-89, a PKA inhibitor), nor 1-(5-isoquinolinesulfonyl)-2-methyl-piperazine (H-7, a PKC antagonist), nor phorbol 12-myristate 13-acetate (PHA, a PKC activator) modified CCPA-induced presynaptic inhibition, suggesting that these second messenger pathways are not involved. 4 The effect of CCPA was eliminated by the calmodulin antagonist N-(6-aminohexil)-5-chloro-1-naphthalenesulfonamide hydrochloride (W-7) and by ethylene glycol-bis(b-aminoethyl ether)-N,N,N 0 ,N 0 -tetraacetic acid-acetoxymethyl ester e6TD-BM, which suggests that the action of CCPA to modulate L-type VDCCs may involve Ca 2 þ -calmodulin. 5 To investigate the action of CCPA on diverse degrees of nerve terminal depolarization, we studied its effect at different external K þ concentrations. The effect of CCPA on ACh secretion evoked by 10 mM K þ was prevented by the P/Q-type VDCC antagonist o-agatoxin IVA. 6 CCPA failed to inhibit the increases in mepp frequency evoked by 15 and 20 mM K þ . We demonstrated that, at high K þ concentrations, endogenous AD occupies A1 receptors, impairing the action of CCPA, since incubation with 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, an A 1 receptor antagonist) and adenosine deaminase (ADA), which degrades AD into the inactive metabolite inosine, increased mepp frequency compared with that obtained in 15 and 20 mM K þ in the absence of the drugs. Moreover, CCPA was able to induce presynaptic inhibition in the presence of ADA. It is concluded that, at high K þ concentrations, the activation of A 1 receptors by endogenous AD prevents excessive neurotransmitter release.

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Purinoceptors: Ontogeny and phylogeny

Burnstock

1996

Drug Dev. Res.

108

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Potentiation of miniature endplate potential frequency by ATP in Xenopus tadpoles

Abstract: 1 Extracellular application of ATP (1 mM), a substance co-stored and co-released with acetylcholine in peripheral nervous systems, potentiated the spontaneous secretion of acetylcholine (ACh) but had no effect on

Cited by 9 publications

References 48 publications

Potentiation by ATP of the postsynaptic acetylcholine response at developing neuromuscular synapses in Xenopus cell cultures.

Potentiation by ATP of the postsynaptic acetylcholine response at developing neuromuscular synapses in Xenopus cell cultures.

Presynaptic inhibition of spontaneous acetylcholine release induced by adenosine at the mouse neuromuscular junction

Purinoceptors: Ontogeny and phylogeny

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