Publications by authors named "Polina O Bogacheva"

This review focuses on the recently discovered specific action of two classical endocannabinoids (ECs), 2-arachidonoylglycerol (2-AG) and arachidonoyl ethanolamide (AEA), in the case of their synthesis and degradation in skeletal muscles; in other words, this review is dedicated to properties and action of the myoendocannabinoid (myoEC) pool. Influence of this pool is considered at three different levels: at the level of skeletal muscles, motor synapses, and also at the level of the whole organism, including central nervous system. Special attention is paid to the still significantly underestimated and intriguing ability of ECs to have positive effect on energy exchange and contractile activity of muscle fibers, as well as on transmitter secretion in motor synapses.

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The effects of brain-derived neurotrophic factor (BDNF) processing by-products (proBDNF and BDNF prodomain) on the activity of mouse neuromuscular junctions (NMJs) were studied in synapses formed during the reinnervation of extensor digitorum longus muscle (m. EDL) and mature synapses of the diaphragm. The parameters of spontaneous miniature endplate potentials (MEPPs) and evoked endplate potentials (EPPs) were analyzed in presence of each of the BDNF maturation products (both - 1 nM).

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We used an intracellular microelectrode technique to study the mechanisms of action of two isoforms (human and rat) of calcitonin gene-related peptide (CGRP) on the evoked and spontaneous quantal secretion of acetylcholine (ACh) in mouse diaphragm motor synapses. Recordings of miniature endplate potentials (MEPPs) and evoked multiquantal endplate potentials (EPPs) in a cut neuromuscular preparation showed that CGRP increased the amplitude of EPPs without influencing their quantal content. Both isoforms of CGRP in a wide range of concentrations (1nM-1μM) provoked a similar considerable increase in MEPPs amplitude in a dose-dependent manner (up to 150-160% compared to control) without changing their frequency, rise-time, and decay.

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