The effects of TMB-8 on acetylcholine release from frog motor nerve: interactions with adenosine

Hunt, James M.; Silinsky, Eugene M.; Hirsh, Jody K.; Ahn, Dean; Solsona, Carles

doi:10.1016/0014-2999(90)90104-e

Cited by 12 publications

(8 citation statements)

References 29 publications

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“…3 B) ( P Ͼ 0.5, ANOVA). Pretreatment of the cultures with another ryanodine receptor antagonist 8-(dethylamino)octyl 3, 4, 5-trimethoxybenzoate (TMB-8) (30 M) (Hunt et al, 1990) also blocked the NT3 effects ( Fig. 3B).…”

Section: Role Of Intracellular Ca 2 ϩ Storesmentioning

confidence: 83%

Intracellular Ca2+ and Ca2+/Calmodulin-Dependent Kinase II Mediate Acute Potentiation of Neurotransmitter Release by Neurotrophin-3

Yang

Xie

et al. 2000

The Journal of Cell Biology

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Neurotrophins have been shown to acutely modulate synaptic transmission in a variety of systems, but the underlying signaling mechanisms remain unclear. Here we provide evidence for an unusual mechanism that mediates synaptic potentiation at the neuromuscular junction (NMJ) induced by neurotrophin-3 (NT3), using Xenopus nerve–muscle co-culture. Unlike brain-derived neurotrophic factor (BDNF), which requires Ca2+ influx for its acute effect, NT3 rapidly enhances spontaneous transmitter release at the developing NMJ even when Ca2+ influx is completely blocked, suggesting that the NT3 effect is independent of extracellular Ca2+. Depletion of intracellular Ca2+ stores, or blockade of inositol 1, 4, 5-trisphosphate (IP3) or ryanodine receptors, prevents the NT3-induced synaptic potentiation. Blockade of IP3 receptors can not prevent BDNF-induced potentiation, suggesting that BDNF and NT3 use different mechanisms to potentiate transmitter release. Inhibition of Ca2+/calmodulin-dependent kinase II (CaMKII) completely blocks the acute effect of NT3. Furthermore, the NT3-induced potentiation requires a continuous activation of CaMKII, because application of the CaMKII inhibitor KN62 reverses the previously established NT3 effect. Thus, NT3 potentiates neurotransmitter secretion by stimulating Ca2+ release from intracellular stores through IP3 and/or ryanodine receptors, leading to an activation of CaMKII.

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Section: Role Of Intracellular Ca 2 ϩ Storesmentioning

confidence: 83%

Intracellular Ca2+ and Ca2+/Calmodulin-Dependent Kinase II Mediate Acute Potentiation of Neurotransmitter Release by Neurotrophin-3

Yang

Xie

et al. 2000

The Journal of Cell Biology

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“…To identify the source of Ca 2ϩ underlying these stimulusdependent signals, we applied 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate hydrochloride (TMB-8), an inhibitor of Ca 2ϩ -induced Ca 2ϩ release (Hunt et al, 1990;Narita et al, 1998) or -CgTx GVIA, an N-type Ca 2ϩ channel blocker that completely blocks transmitter release from this synapse (Kerr and Yoshikami, 1984). Action potential-evoked Ca 2ϩ signals were unaffected by a 30 min treatment with 10 M TMB-8 (data not shown).…”

Section: Resultsmentioning

confidence: 99%

Spatial Distribution of Calcium Entry Evoked by Single Action Potentials within the Presynaptic Active Zone

Wachman

Poage²,

Stiles³

et al. 2004

J. Neurosci.

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The nature of presynaptic calcium (Ca 2ϩ ) signals that initiate neurotransmitter release makes these signals difficult to study, in part because of the small size of specialized active zones within most nerve terminals. Using the frog motor nerve terminal, which contains especially large active zones, we show that increases in intracellular Ca 2ϩ concentration within 1 msec of action potential invasion are attributable to Ca 2ϩ entry through N-type Ca 2ϩ channels and are not uniformly distributed throughout active zone regions. Furthermore, changes in the location and magnitude of Ca 2ϩ signals recorded before and after experimental manipulations (-conotoxin GVIA, diaminopyridine, and lowered extracellular Ca 2ϩ ) support the hypothesis that there is a remarkably low probability of a single Ca 2ϩ channel opening within an active zone after an action potential. The trial-to-trial variability observed in the spatial distribution of presynaptic Ca 2ϩ entry also supports this conclusion, which differs from the conclusions of previous work in other synapses.

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“…TMB-8 is an inhibitor of calcium mobilization from intracellular calcium stores (Chiou and Malagodi, 1976;Hunt, Silinsky, Hirsh, Ahn, and Solsona, 1990). It has been shown that in vascular smooth muscle with plasma membrane permeabilized with detergent, bath application of TMB-8 exerts its full effect within 1 min (Ishihara and Karaki, 1991).…”

Section: Effect Of Agents Affecting Pathways Other Than That Via Protmentioning

confidence: 99%

The transduction system in the isoproterenol activation of the Ca(2+)-activated K+ channel in guinea pig taenia coli myocytes.

Fan

Wang

Kao

1993

The Journal of General Physiology

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A B S T RAC T In freshly dispersed guinea pig taenia coli myocytes the activity of the large conductance Ca2+-activated K + channel (maxi-K ÷ channel) predominates. The open probability (Po) of this channel is increased by micromolar concentrations of the 13-adrenergic agonist isoproterenol (ISO). Low concentrations of cholera toxin (CTX, 1 pM) and guanosine 5'-O-2-thiodiphosphate (GDPI3S, 0.5 mM) suppress the ISO-induced increase of Po-Higher concentrations of CTX (e.g., 0.5 nM) as well as forskolin and dibutyryl cAMP increase the Po. 1,9-Dideoxyforskolin, the forskolin analogue, which lacks the adenylate cyclase-stimulating effect, does not. A specific protein kinase A inhibitor (Wiptide), applied intracellularly via diffusion from the patch electrode, suppresses the ISO-induced increase of whole-cell outward K + current during step depolarization. In contrast, intracellularly applied protein kinase C (19-36), a specific protein kinase C inhibitor, has no effect on the whole-cell current. TMB-8, an inhibitor of intracellular calcium mobilization, does not affect either the whole-cell outward K + current during step depolarization or the Po. These observations show that ISO increases the Po of the maxi-K + channels in the guinea pig taenia coli myocytes through the G protein-adenylate cyclaseprotein kinase A system. INTRODUCTIONCellular systems for the transduction of extracellular stimuli into intracellular signals may involve the following components: (a) interaction of extracellular-facing receptors with stimuli, e.g., hormones, neurotransmitters, and drugs, etc.; (b) transduction through intermediate coupling proteins between the receptors and the effector molecules, a family of guanine nucleotide binding proteins (G proteins;Gilman, 1984); and (c) actions of effector molecules, which might be the ion channels (Breitwieser and Szabo, 1985; Pfaffinger, Martin, Hunter, Nathanson, and Hille, 1985) 258THE JOURNAL OF GENERAL PHYSIOLOGY • VOLUME 102 • 1993 messenger cyclic 3',5'-adenosine triphosphate (cAMP) (Lefkowitz, Stadel, and Carm, 1983). In the cell membrane there is a group of receptors coupled with the adenylate cyclase-stimulating G protein (G~). Among that group is beta-adrenoceptor, a transmembrane glycoprotein mediating the action of catecholamine.[3-Adrenergic agonists increase the potassium current (IK) of cardiac myocytes (e.g., Brown and Noble, 1974;Umeno, 1984;Bennett and Begenisich, 1987;Walsh and Kass, 1988), possibly through a process involving cAMP-dependent phosphorylation (by protein kinase A) of the relevant protein (Tsien, Giles, and Greengard, 1972; Brum, Flockerzi, Hofmann, Osterrieder, and Trautwein, 1983;Kameyama, Hescheler, Hofmann, and Trautwein, 1986;Walsh and Kass, 1988). However, there are indications that IK may also be regulated by protein kinase C as well as by protein kinase A (Tohse, Kameyama, and Irisawa, 1987;Walsh and Kass, 1988).In mammalian intestinal smooth myocytes, isoproterenol (ISO) causes hyperpolarization (Kao, Inomata, McCullough, and Yuan, 1975; Biilbr...

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The effects of TMB-8 on acetylcholine release from frog motor nerve: interactions with adenosine

Cited by 12 publications

References 29 publications

Intracellular Ca2+ and Ca2+/Calmodulin-Dependent Kinase II Mediate Acute Potentiation of Neurotransmitter Release by Neurotrophin-3

Intracellular Ca2+ and Ca2+/Calmodulin-Dependent Kinase II Mediate Acute Potentiation of Neurotransmitter Release by Neurotrophin-3

Spatial Distribution of Calcium Entry Evoked by Single Action Potentials within the Presynaptic Active Zone

The transduction system in the isoproterenol activation of the Ca(2+)-activated K+ channel in guinea pig taenia coli myocytes.

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