Linked from

The 49 pages that link to Neuromuscular junction, each with the reason it gives.

• Action potentialRelated: A motor-neuron spike triggers transmission that can produce a muscle-fiber action potential.

• Skeletal muscleRelated: Motor neurons initiate contraction by releasing acetylcholine at this specialized synapse.

• AcetylcholineRelated: Acetylcholine is the transmitter that normally initiates skeletal-muscle activation there.

• ElectromyographyRelated: Disorders at this junction can alter electrical responses measured by specialized EMG.

• SynapseBroader topic: It is a well-studied synapse whose target is a muscle cell rather than another neuron.

• Motor controlBroader topic: This junction converts neural output into signals that trigger muscle contraction.

• Myasthenia gravisBroader topic: This is the site where myasthenia gravis antibodies impair nerve-to-muscle signaling.

• AcetylcholinesteraseRelated: Dense acetylcholinesterase activity there prevents persistent muscle stimulation.

• Motor neuronRelated: Motor neurons release acetylcholine here to initiate muscle-fiber excitation.

• Amyotrophic lateral sclerosisRelated: Motor-neuron loss reduces the neural input that normally activates muscles.

• Nicotinic acetylcholine receptorRelated: Muscle-type nicotinic receptors at this junction initiate muscle-fiber depolarization.

• Botulinum toxinBroader topic: This is the main site where the toxin interrupts muscle activation.

• Motor unitBroader topic: Each fiber in a unit receives the neuron’s signal through this specialized synapse.

• ElapidaeBroader topic: Many elapid neurotoxins block signaling at this junction, producing weakness or paralysis.

• Synaptic transmissionBroader topic: It is a well-characterized case in which neuronal transmission reliably activates another cell type.

• Muscle weaknessBroader topic: Impaired transmission here can prevent a muscle from responding fully to nerve signals.

• PralidoximeRelated: Acetylcholinesterase inhibition at this junction can cause weakness and paralysis.

• Excitation-contraction couplingRelated: It supplies the muscle-fiber electrical excitation that precedes intracellular coupling.

• TetrodotoxinRelated: Tetrodotoxin can prevent nerve impulses from reaching this site and activating muscle.

• BotulismBroader topic: Botulinum toxin disrupts signaling at this interface.

• Cholinergic crisisBroader topic: Disrupted signaling here explains fasciculations, weakness, and respiratory-muscle failure.

• SarcopeniaBroader topic: Changes at this connection can impair muscle activation and contribute to weakness.

• Somatic nervous systemRelated: This is where somatic motor output activates muscle.

• TetanusRelated: Uninhibited motor neurons drive repeated signals to muscles through these junctions.

• Nerve agentBroader topic: Excess acetylcholine at this synapse causes twitching, weakness, and paralysis.

• Spinal muscular atrophyRelated: Motor-neuron dysfunction weakens signaling across this connection.

• AnticholinergicRelated: Nicotinic receptor blockade here can impair skeletal muscle activation.

• Electric organRelated: Electric organs evolved from excitable tissues whose activity is controlled by motor neurons.

• Lower motor neuronRelated: This is the contact point where a lower motor neuron's signal reaches muscle.

• Bernard KatzNarrower topic: Katz investigated transmitter release at this accessible model synapse.

• Claude BernardRelated: Curare experiments helped locate the poison’s action between nerve and muscle.

• Synaptic cleftBroader topic: Its cleft transmits the neural signal that initiates muscle contraction.

• MyopathyCompared with: Disorders here can mimic myopathy but disrupt nerve-to-muscle signaling instead of muscle tissue.

• MuscleBroader topic: It is the neural control point that initiates skeletal muscle activity.

• BatrachotoxinRelated: Disrupted electrical signaling affects communication between motor nerves and muscles.

• Muscular systemBroader topic: It is where voluntary motor commands reach skeletal muscles.

• SarcolemmaRelated: At this specialized contact, neural signals trigger electrical activity in the sarcolemma.

• Blue-ringed octopusRelated: Tetrodotoxin’s interruption of nerve signals can prevent muscles, including respiratory muscles, from working.

• SomanRelated: Acetylcholine overload at these junctions contributes to weakness and paralysis.

• Henry Hallett DaleRelated: Dale’s acetylcholine research helped explain how motor nerves trigger muscle contraction.

• MyologyRelated: It is the main link between neural commands and skeletal muscle activation.

• AtonyRelated: Disrupted signaling here can prevent skeletal muscles from maintaining normal tone.

• BungarusRelated: Krait neurotoxins can prevent signals from reaching muscles at this junction.

• Conium maculatumRelated: Poison hemlock’s interference with nerve-to-muscle signaling can cause progressive weakness and paralysis.

• Human musculoskeletal systemRelated: Signals at this junction initiate the muscle activation needed for movement.

• Muscle cellRelated: It is the usual site where a nerve signal initiates skeletal muscle-cell excitation.

• Musculoskeletal and Neural Physiological PhenomenaRelated: It converts neural output into the signal that initiates muscle contraction.

• Skeletal muscle crampBroader topic: Signals crossing this junction initiate the contractions that cramps prolong.

• StrychnineNarrower topic: Strychnine acts upstream of this junction, increasing motor-neuron output to muscles.