Evgeny E Nikolsky

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Acetylcholinesterase (AChE) is an enzyme that hydrolyses the neurotransmitter acetylcholine, thereby limiting spillover and duration of action. This study demonstrates the existence of an endogenous mechanism for the regulation of synaptic AChE activity. At the rat extensor digitorum longus neuromuscular junction, activation of N-methyl-d-aspartate (NMDA)(More)
In this study we demonstrate expression of the N-methyl-D-aspartate receptor NR1 subunit in the rat neuromuscular junction of skeletal muscles of different functional types (extensor digitorum longus, soleus, and diaphragm muscles) using fluorescence immunocytochemistry. Electron microscopic immunocytochemistry has shown that the NR1 subunit is localized(More)
The kinetics of the phasic synchronous and delayed asynchronous release of acetylcholine quanta was studied at the neuromuscular junctions of aging rats from infant to mature animals at various frequencies of rhythmic stimulation of the motor nerve. We found that in infants 6 (P6) and 10 (P10) days after birth a strongly asynchronous phase of quantal(More)
The effects of high-frequency nerve stimulation (10-100 Hz) on the kinetics of evoked acetylcholine quanta secretion from frog motor nerve endings were studied. The amplitude and temporal parameters of uni- and multiquantal endplate currents were analysed to estimate the possible changes in the degree of synchrony of quantal release. The frog neuromuscular(More)
4 In the space flight environment and in models of the effects of weightlessness on Earth, the functional unloading of skeletal muscles leads to the development of the soocalled hypogravity syndrome expressed, in particular, in a number of morphological and funcc tional changes in the neuromuscular system. The characteristic features of this syndrome(More)
334 The cytoskeleton carries out many functions in cells of the nervous system, including synaptic formaa tion and function. Actin microfilaments, microtuu bules (MTs), and intermediate filaments are the main components of the cytoskeleton of motor axon termii nals. Microfilaments form a network and are often linked to the presynaptic membrane and its(More)
283 Acetylcholine entering the synaptic cleft from choo linergic nerve endings after depolarization by the action potential not only causes generation of postsynn aptic potential, but also modulates the intensity of the release of subsequent portions of the neurotransmitter, activating presynaptic autoreceptors [1]. Effects of endogenous acetylcholine are(More)
Experiments on frog neuromuscular junctions have demonstrated that asynchrony of the acetylcholine quantal release forming the multi-quantal evoked response at high-frequency synaptic activity is caused, in particular, by a decrease in velocity of the action potential propagation along the non-myelinated nerve endings, which is mediated by activation of the(More)
There is some evidence that glutamate (Glu) acts as a signaling molecule at vertebrate neuromuscular junctions where acetylcholine (ACh) serves as a neurotransmitter. In this study, performed on the cutaneous pectoris muscle of the frog Rana ridibunda, Glu receptor mechanisms that modulate ACh release processes were analyzed. Electrophysiological(More)
Acetylcholine (ACh), released from axonal terminals of motor neurons in neuromuscular junctions regulates the efficacy of neurotransmission through activation of presynaptic nicotinic and muscarinic autoreceptors. Receptor-mediated presynaptic regulation could reflect either direct action on exocytotic machinery or modulation of Ca2+ entry and resulting(More)