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Protein kinase A cascade regulates quantal release dispersion at frog muscle endplate
Author(s) -
Bukharaeva Ella A.,
Samigullin Dmitry,
Nikolsky Eugeny,
Vyskočil František
Publication year - 2002
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2001.012752
Subject(s) - adenylyl cyclase , protein kinase a , synapse , stimulation , receptor , chemistry , latency (audio) , neurotransmission , biophysics , microbiology and biotechnology , biology , endocrinology , medicine , neuroscience , kinase , biochemistry , engineering , electrical engineering
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 β1 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.