Description
Title: Structure and Function of the Neuromuscular Active Zone in Lambert-Eaton Myasthenic Syndrome and Healthy States
Abstract: For many years, the mouse neuromuscular junction (NMJ) has served as a model synapse for the investigation of neurotransmission in both normal and pathological conditions of the NMJ. These neuromuscular nerve terminals’ active zones, which are highly organized structures, are where neurotransmission from them occurs (AZs). The likelihood of acetylcholine release during individual action potentials and the properties of short-term plasticity during brief, high frequency trains of action potentials are controlled within AZs by the interactions between voltage-gated calcium channels and docked synaptic vesicles. Not only for healthy synapses, but also to better understand the pathophysiology of neuromuscular diseases, it is crucial to comprehend these relationships. We are particularly interested in Lambert-Eaton myasthenic syndrome (LEMS), an autoimmune condition in which the NMJ’s neurotransmitter release declines and results in severe muscle weakness. The reduction in neurotransmission in LEMS has traditionally been attributed to the removal of presynaptic voltage-gated calcium channels by antibody-mediated means. Recent experimental data and AZ computer simulations, however, suggest that pathological effects in the active zone and the properties of chemical transmitters are significantly influenced by disruptions in the normally highly organized active zone structure and perhaps autoantibodies to other presynaptic proteins.
Keywords: active zone; neuromuscular junction; Lambert-Eaton myasthenic syndrome; computational modeling
Paper Quality: SCOPUS / Web of Science Level Research Paper
Subject: Biomolecules
Writer Experience: 20+ Years
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