Mechanisms controlling neuromuscular junction stability

Neurotransmission regulates stability of acetylcholine receptors at the neuromuscular junction.

The majority of acetylcholine receptors (AChRs) at normally innervated neuromuscular junctions are stable, with a half-life averaging about 12 d in most rodent muscles. Following denervation, the AChRs turn over much more rapidly after a lag period. The mechanism by which motor nerves normally maintain stabilization of junctional AChRs is not yet known. In order to determine whether synaptic tr...

Stathmin is required for stability of the Drosophila neuromuscular junction.

Synaptic connections can be stably maintained for prolonged periods, yet can be rapidly disassembled during the developmental refinement of neural circuitry and following cytological insults that lead to neurodegeneration. To date, the molecular mechanisms that determine whether a synapse will persist versus being remodeled or eliminated remain poorly understood. Mutations in Drosophila stathmi...

Neuromuscular Junction Effects Does Pb Produce Neuromuscular Junction Changes?

Acetylcholinesterase (AChE) inhibitors, including PB, produce acute destructive changes at the neuromuscular junction, the site of connection between nerve cells and muscle fibers, at which nerve cells signal muscles to contract. Because studies of the neuromuscular junction require microscopic inspection of muscle tissue and tests of electrical and chemical properties of the neuromuscular junc...

The neuromuscular junction disorders.

Neuromuscular junction (NMJ) disorders result from destruction, malfunction or absence of one or more key proteins involved in neuromuscular transmission, illustrated diagrammatically in fig 1. The most common pathology is antibody mediated damage or down regulation of ion channels or receptors, resulting in myasthenia gravis (MG), Lambert-Eaton myasthenic syndrome (LEMS), and acquired neuromyo...

SnapShot: Neuromuscular Junction