Rapid retrograde regulation of transmitter release at the NMJ. Issue 4 (August 2018)

• Record Type: Journal Article
• Authors: Ribchester, Richard R; Slater, Clarke R
• Is Part Of: Current opinion in physiology. Issue 4(2018)
• Page Start: 82
• Page End: 87
• Publication Date: 2018-08
• Subjects: Physiology -- Periodicals; Physiological Phenomena; Periodical; Fulltext; Internet Resources; Periodicals; 571
• DOI: 10.1016/j.cophys.2018.06.007
• Languages: English
• ISSNs: 2468-8673

Abstract

Highlights: Neuromuscular junctions transmit signals from nerve to muscles to control contraction. Neuromuscular junctions are good at maintaining their own function. Muscles exert retrograde effects on the nerves that innervate them. Blocking transmitter receptors causes increased release of transmitter from the nerve. Self-regulation is often unable to overcome the bad effects of disease. Abstract : Numerous regulatory processes act to ensure effective signal transmission at neuromuscular junctions (NMJs). In the disease myasthenia gravis (MG), the muscle response to transmitter is impaired but transmitter release from the nerve is enhanced. Recently evidence has emerged of a rapid (seconds to minutes) form of retrograde regulation of release, known as 'homeostatic plasticity' (HP). At mouse and Drosophila NMJs HP can be triggered by mimicking MG by blocking some of the postsynaptic transmitter receptors. Whether HP accounts for the increased release in MG is unclear, as is the identity of any natural trigger of HP, the retrograde signal, or the target of the signal. Better knowledge of HP might suggest better ways of treating some forms of NMJ disorder.