ArticleThe Journal of physiology2002
Protein kinase A cascade regulates quantal release dispersion at frog muscle endplate.
Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 54 citations in OpenAlex.
- Adrenergic Modulation of Acetylcholine Release at the Mouse Neuromuscular Junctions of Fast-Twitch Skeletal Muscle.Neurochemical research · 2025Review
- From Frog Muscle to Brain Neurons: Joys and Sorrows in Neuroscience.Physiological research · 2024Review
- Presynaptic Acetylcholine Receptors Modulate the Time Course of Action Potential-Evoked Acetylcholine Quanta Secretion at Neuromuscular Junctions.Biomedicines · 2022Review
- Adrenoceptors Modulate Cholinergic Synaptic Transmission at the Neuromuscular Junction.International journal of molecular sciences · 2021Review
- Activation of 5-HT1A Receptors Promotes Retinal Ganglion Cell Function by Inhibiting the cAMP-PKA Pathway to Modulate Presynaptic GABA Release in Chronic Glaucoma.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Bayesian analysis of the kinetics of quantal transmitter secretion at the neuromuscular junction.Journal of computational neuroscience · 2015Article
- Estimation of presynaptic calcium currents and endogenous calcium buffers at the frog neuromuscular junction with two different calcium fluorescent dyes.Frontiers in synaptic neuroscience · 2014Article
- Modeling of quantal neurotransmitter release kinetics in the presence of fixed and mobile calcium buffers.Journal of computational neuroscience · 2008Article
- Cholinergic regulation of the evoked quantal release at frog neuromuscular junction.The Journal of physiology · 2004Article
- Characteristics of calcium transient in different parts of frog nerve terminal in response to nerve impulse.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sectionsArticle
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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 (P90 = 1.25 ms); it decreased to P90 = 0.95 ms in the central part and to P90 = 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 beta1 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.
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