Transduction of the modulatory effect of catecholamines at the mammalian motor neuron terminal

Chen, Hsinyo; Dryden, William F.; Singh, Yadhu N.

doi:10.1002/syn.890070202

Cited by 12 publications

(7 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is known that catecholamines facilitate neuromuscular transmission (Orbeli, 1923; Burn, 1945) by increasing EPC amplitude. This has been attributed to an increase in quantal content (Jenkinson et al 1968; Hidaka & Kuriyama, 1969; Kuba, 1970; Kuba & Tomita, 1971; Wessler & Anschuetz, 1988; Vizi, 1991), an increase in quantum size (Van der Kloot & Van der Kloot, 1986) and a greater sensitivity of the subsynaptic membrane to ACh (Chen et al 1991). For example, when a decrease in quantal content and longer latencies are observed, NA removes activity‐induced fatigue (Ruzzier & Scuka, 1986).…”

mentioning

confidence: 99%

Protein kinase A cascade regulates quantal release dispersion at frog muscle endplate

Bukharaeva

Samigullin

Nikolsky

et al. 2002

The Journal of Physiology

View full text Add to dashboard Cite

Uniquantal endplate currents (EPCs) were recorded simultaneously at the proximal, central and distal parts of the frog neuromuscular synapse, and their minimal synaptic latencies, latency dispersions and sensitivity to noradrenaline, cAMP and protein kinase A inhibition were measured. The latency dispersion was highest in the proximal part (P 90 = 1.25 ms); it decreased to P 90 = 0.95 ms in the central part and to P 90 = 0.75 ms (60 % of the proximal part) in the distal part. In the proximal parts of the long neuromuscular synapse, stimulation-evoked EPCs with long release latencies were eliminated when the intracellular cAMP was increased by b1 activation by noradrenaline, by the permeable analogue db-cAMP, by activation of adenylyl cyclase or by inhibition of cAMP hydrolysis. This makes the evoked release more compact, and the amplitude of the reconstructed multiquantal currents increases. Protein kinase A is a target of this regulation, since a specific inhibitor, Rp-cAMP, prevents the action of cAMP in the proximal parts and increases the occurrence of long-latency events in the distal parts of the synapse. Our results show that protein kinase A is involved in the timing of quantal release and can be regulated by presynaptic adrenergic receptors. Journal of Physiology (2002), 538.3, pp. 837-848 DOI: 10.1013/jphysiol.2001.012752 © The Physiological Society 2002 www.jphysiol.org 1984 Shakiryanova et al. 1994), non-uniform spontaneous and evoked release (Zefirov, 1983; Mallart, 1984; D'Alonzo & Grinnell, 1989) as well as different structural characteristics of the proximal and distal endplate regions (Davey & Bennett, 1982; Robitaille & Tremblay, 1987). We therefore estimated the latencies of EPCs simultaneously at the proximal, central and distal parts of the synapse and found substantial differences between these parts in minimal synaptic latencies, latency dispersions and sensitivity to NA, cAMP manipulations and PKA inhibition. Preliminary results with cAMP in the proximal part of the synapse have already been presented as a short report (Bukharaeva et al. 2000). METHODS Animals and drugsThe experimental preparation, bathing solutions and focal extracellular recording technique have been described in a previous paper (Bukharaeva et al. 1999). Briefly, experiments were carried out on the cutaneous pectoris muscle from the frog Rana ridibunda from November to April. Animals were anaesthetized with ether before being stunned and double-pithed. The preparations were pinned to a translucent chamber and superfused with (m): NaCl 113.0, KCl 2.5, CaCl 2 0.2, NaHCO 3 3.0, and MgCl 2 4.0. The pH was 7.3 at 20.0 ± 0.3°C. The Animal Care and Use Committee of the Institute of Physiology, Czech Academy of Sciences, approved the protocol.The following drugs were used (Sigma, St Louis, MO, USA): NA, dibutyryl cAMP, adenosine 3,5-monophosphothioate (Rp-cAMP), forskolin, and 3-isobutyl-1-methylxanthine (IBMX). The drugs were added to the superfusing solution, and the measurements were started 20 min after drug applic...

show abstract

mentioning

confidence: 99%

Protein kinase A cascade regulates quantal release dispersion at frog muscle endplate

Bukharaeva

Samigullin

Nikolsky

et al. 2002

The Journal of Physiology

View full text Add to dashboard Cite

show abstract

“…Isoproterenol (isoprenaline) increases the input resistance of muscle fibres, thereby increasing the amplitude of endplate potentials. Adrenaline can have both pre‐ and postsynaptic actions (Kuba, 1970; Chen et al 1991). NA stimulates the electrogenic sodium pump and increases the resting membrane potential (Zemková et al 1985).…”

mentioning

confidence: 99%

Noradrenaline synchronizes evoked quantal release at frog neuromuscular junctions

Bukcharaeva

Kim

Moravec

et al. 1999

The Journal of Physiology

View full text Add to dashboard Cite

Noradrenaline (NA) increases synaptic efficacy at the frog neuromuscular junction. To test the hypothesis that one of the actions of NA is to shorten the period over which evoked quanta are released, we measured the latencies of focally recorded uniquantal endplate currents (EPCs). NA shortened the release period for evoked quantal release. The interval between the time when responses with minimal delay appeared and the point at which 90 % of all latencies had occurred was shortened in the presence of 1 × 10−5 M NA by about 35 % at 20 °C and by about 45 % at 8 °C. Inhibitor and agonist experiments showed that NA acts on a β‐adrenoreceptor. The better synchronization of release significantly increased the size of reconstructed multi‐ quantal EPCs. This suggests that NA facilitates synaptic transmission by making the release of quanta more synchronous. The synchronizing action of NA might potentiate neuromuscular transmission during nerve regeneration, transmitter exhaustion and other extreme physiological states where the quantal content is reduced, such as survival in cold and hibernation.

show abstract

“…Like other catecholamines epinephrine exerts its pharmacologic effect by the generation of cyclic AMP, a well described second messenger. Experimental evidence points to ATP and its derivatives modulating neuromuscular transmission [ 9 , 12 , 13 ]. Whether these mechanisms might have played a role in the observation reported in this case cannot be clarified.…”

Section: Discussionmentioning

confidence: 99%

Small doses of epinephrine prolong the recovery from a rocuronium-induced neuromuscular block: a case report

2018

BMC Anesthesiol

View full text Add to dashboard Cite

BackgroundDuring anaesthesia it is not uncommon to administer epinephrine in patients blocked by non-depolarizing muscle relaxants. However, there are few reports on possible interaction of epinephrine with neuromuscular transmission in humans.Case presentationAn otherwise healthy 74-yr-old man underwent transurethral resection of a benign prostatic hyperplasia under total intravenous anaesthesia. Because of repeated drop in heart rate and blood pressure the patient received in total three bolus of epinephrine 5 μg, respectively. Each time this small dose of epinephrine intensified a rocuronium-induced neuromuscular block verified by acceleromygraphy. Further anaesthetic course was uneventful.ConclusionsIn this case reported here small doses of intravenously administered epinephrine markedly prolonged a rocuronium-induced neuromuscular block. Given the widely used co-administration of epinephrine and muscle relaxants possible adrenergic interference with neuromuscular transmission would have implications for daily anaesthetic practice.

show abstract

Transduction of the modulatory effect of catecholamines at the mammalian motor neuron terminal

Cited by 12 publications

References 43 publications

Protein kinase A cascade regulates quantal release dispersion at frog muscle endplate

Protein kinase A cascade regulates quantal release dispersion at frog muscle endplate

Noradrenaline synchronizes evoked quantal release at frog neuromuscular junctions

Small doses of epinephrine prolong the recovery from a rocuronium-induced neuromuscular block: a case report

Contact Info

Product

Resources

About