期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 22, 期 9, 页码 -出版社
MDPI
DOI: 10.3390/ijms22094611
关键词
synaptic transmission; neuromuscular junction; adrenergic drugs; adrenoreceptors; acetylcholine quantal release; acetylcholine receptor
资金
- Russian Science Foundation [18-15-00046]
- government assignment for FRC Kazan Scientific Center of RAS
- Russian Science Foundation [18-15-00046, 21-15-28015] Funding Source: Russian Science Foundation
Adrenoceptor activators and blockers are commonly used in the clinical treatment of cardiovascular, pulmonary, and neurodegenerative diseases by regulating neurotransmission at the neuromuscular junction. Understanding the molecular mechanisms of these drugs may lead to the development of highly effective and well-tolerated sympathomimetics for treating various neurodegenerative diseases with synaptic defects.
Adrenoceptor activators and blockers are widely used clinically for the treatment of cardiovascular and pulmonary disorders. More recently, adrenergic agents have also been used to treat neurodegenerative diseases. Recent studies indicate a location of sympathetic varicosities in close proximity to neuromuscular junctions. The pressing question is whether there could be any effects of endo- or exogenous catecholamines on cholinergic neuromuscular transmission. It was shown that the pharmacological stimulation of adrenoceptors, as well as sympathectomy, can affect both acetylcholine release from motor nerve terminals and the functioning of postsynaptic acetylcholine receptors. In this review, we discuss the recent data regarding the effects of adrenergic drugs on neurotransmission at the neuromuscular junction. The elucidation of the molecular mechanisms by which the clinically relevant adrenomimetics and adrenoblockers regulate quantal acetylcholine release from the presynaptic nerve terminals and postsynaptic sensitivity may help in the design of highly effective and well-tolerated sympathomimetics for treating a number of neurodegenerative diseases accompanied by synaptic defects.
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