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Motor Nerve Endings (motor + nerve_ending)
Selected AbstractsMechanisms of ATP action on motor nerve terminals at the frog neuromuscular junctionEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 5 2005S. Grishin Abstract We have shown previously that ATP inhibits transmitter release at the neuromuscular junction through the action on metabotropic P2Y receptors coupled to specific second messenger cascades. In the present study we recorded K+ or Ca2+ currents in motor nerve endings or blocked K+ or Ca2+ channels in order to explore the nature of downstream presynaptic effectors. Endplate currents were presynaptically depressed by ATP. Blockers of Ca2+ -activated K+ -channels, such as iberiotoxin, apamin or tetraethylammonium, did not change the depressant action of ATP. By contrast, K+ channel blocker 4-aminopyridine (4-AP) and raised extracellular Ca2+ attenuated the effect of ATP. However, these effects of 4-AP and high Ca2+ were reversed by Mg2+, suggesting Ca2+ -dependence of the ATP action. Ba2+ promoted the depressant action of ATP as did glibenclamide, a blocker of ATP-sensitive K+ channels, or mild depolarization produced by 7.5 mm K+. None of the K+ channel blockers affected the depressant action of adenosine. Focal recording revealed that neither ATP nor adenosine affected the fast K+ currents of the motor nerve endings. However, unlike adenosine, ATP or UTP, an agonist of P2Y receptors, reversibly reduced the presynaptic Ca2+ -current. This effect was abolished by suramin, an antagonist of P2 receptors. Depressant effect of ATP on the endplate and Ca2+ -currents was mimicked by arachidonate, which precluded the action of ATP. ATP reduced acetylcholine release triggered by ionomycin or sucrose, suggesting inhibition of release machinery. Thus, the presynaptic depressant action of ATP is mediated by inhibition of Ca2+ channels and by mechanism acting downstream of Ca2+ entry. [source] A2A Adenosine Receptor Facilitation of Neuromuscular TransmissionJOURNAL OF NEUROCHEMISTRY, Issue 6 2000Influence of Stimulus Paradigm on Calcium Mobilization Abstract: The influence of stimulus pulse duration on calcium mobilization triggering facilitation of evoked [3H]acetylcholine ([3H]ACh) release by the A2A adenosine receptor agonist CGS 21680C was studied in the rat phrenic nerve-hemidiaphragm. The P-type calcium channel blocker ,-agatoxin IVA (100 nM) decreased [3H]ACh release evoked with pulses of 0.04-ms duration, whereas nifedipine (1 ,M) inhibited transmitter release with pulses of 1-ms duration. Depletion of intracellular calcium stores by thapsigargin (2 ,M) decreased [3H]ACh release evoked by pulses of 1 ms, an effect observed even in the absence of extracellular calcium. With short (0.04-ms) stimulation pulses, when P-type calcium influx triggered transmitter release, facilitation of [3H]ACh release by CGS 21680C (3 nM) was attenuated by both thapsigargin (2 ,M) and nifedipine (1 ,M). With longer stimuli (1 ms), a situation in which both thapsigargin-sensitive internal stores and L-type channels are involved in ACh release, pretreatment with either ,-agatoxin IVA (100 nM) or nifedipine (1 ,M) reduced the facilitatory effect of CGS 21680C (3 nM). The results suggest that A2A receptor activation facilitates ACh release from motor nerve endings through alternatively mobilizing the available calcium pools (thapsigargin-sensitive internal stores and/or P- or L-type channels) that are not committed to the release process in each stimulation condition. [source] Phorbol esters and adenosine affect the readily releasable neurotransmitter pool by different mechanisms at amphibian motor nerve endingsTHE JOURNAL OF PHYSIOLOGY, Issue 2 2003T. J. Searl Phorbol esters and adenosine have been proposed to interact at common sites downstream of calcium entry at amphibian motor nerve endings. We thus studied the actions and interactions of phorbol esters and adenosine using electrophysiological recording techniques in conjunction with both binomial statistical analysis and high-frequency stimulation at the amphibian neuromuscular junction. To begin this study, we confirmed previous observations that synchronous evoked acetylcholine (ACh) release (reflected as endplate potentials, EPPs) is well described by a simple binomial distribution. We then used binomial analysis to study the effects of the phorbol ester phorbol dibutyrate (PDBu, 100 nm) and adenosine (50 µm) on the binomial parameters n (the number of calcium charged ACh quanta available for release) and p (the average probability of release), where the mean level of evoked ACh release (m) =np. We found that PDBu increased m by increasing the parameter n whilst adenosine reduced m by reducing n; neither agent affected the parameter p. PDBu had no effect on either the potency or efficacy of the inhibition produced by adenosine. Subtle differences between these two agents were revealed by the patterns of EPPs evoked by high-frequency trains of stimuli. Phorbol esters increased ACh release during the early phase of stimulation but not during the subsequent plateau phase. The inhibitory effect of adenosine was maximal at the beginning of the train and was still present with reduced efficacy during the plateau phase. When taken together with previous findings, these present results suggest that phorbol esters increase the immediately available store of synaptic vesicles by increasing the number of primed vesicles whilst adenosine acts at a later stage of the secretory process to decrease the number of calcium-charged primed vesicles. [source] Antagonism of calcium currents and neurotransmitter release by barium ions at frog motor nerve endingsBRITISH JOURNAL OF PHARMACOLOGY, Issue 2 2000Eugene M Silinsky The effects of Ba2+ (0.1,2 mM) on the component of the perineural voltage change associated with nerve terminal calcium currents (prejunctional Ca2+ currents) were compared with the effects of this ion to antagonize calcium-dependent acetylcholine (ACh) release. These experiments were made on isolated neuromuscular junctions of the frog. In the presence of sufficient concentrations of K+ channel blockers to eliminate measurable prejunctional K+ currents, low concentrations of Ba2+ selectively antagonized prejunctional Ca2+ currents in normal Ca2+ solutions. Higher concentrations of Ba2+ also substantially reduced the Na+ component of the perineural waveform. Ba2+ inhibited the prolonged prejunctional Ca2+ currents that developed in the presence of higher concentrations of K+ channel blockers. Simultaneous measurements of the prejunctional Ca2+ currents and the electrophysiological correlates of ACh release (i.e. end-plate potentials, EPPs) were made under conditions of modest K+ channel blockade. Under these conditions, Ba2+ generally produced simultaneous decreases in both Ca2+ currents and EPP amplitudes. In some instances, a prolongation of prejunctional Ca2+ currents and a transient increase in EPP amplitudes preceded the decreases in both electrophysiological events. These results suggest that Ba2+ ions can antagonize the entry of calcium into motor nerve endings and this effect is likely to be responsible for the inhibitory effects of Ba2+ on evoked ACh release. British Journal of Pharmacology (2000) 129, 360,366; doi:10.1038/sj.bjp.0703036 [source] | ||||||||||