Neuromuscular Unit
Fast interactions with the environment: objective of neurons.
Large effective unit: response to motor command from our brain → action
Ventral Horn (Anterior Horn/Anterior Horn Cell) of Spinal cord: houses thousand of motor neurons
motor neuron (in ventral horn) → axon → branching → NMJ → Effector Muscle
Q: How many muscle fibers can one neuron command?
Branches in axon terminals:
limitation due to electrical properties and arrangement of Na+ → limit branch
Reliability on one single neuron is not effective.
Small Motor Units:
Large Motor Units: up to 1000 fibers
Motor Unit
smallest functional unit of neuromuscular unit
single motor neuron → projects axon with branches → innervate multiple muscle fibers within the same muscle
Each muscle fiber is innervated by a single motor neuron
Fine Motor Muscles: smaller motor unit (ex. hand, fewer number of innervated muscle fibers
Coarse Motor Muscles: larger motor unit (ex. thigh)
Why?: we need many computational units to control fine movement.
Anterior Horn Cells
Ventral root merge with dorsal root → Spinal Nerve?
One root supply many muscles
One muscle supplied by many roots
Peripheral Nerve
smallest circle = single neuron
Grouped together: Fascicle
Large Peripheral nerve: many fascicles
Layers:
Endoneurium: loose connective tissue that lies between each neuron in the fascicle.
Perineurium: dense type of connective tissue that covers each fascicle
Epineurium: loose connective tissue that covers the peripheral nerve (outermost)
Vasa nervorum
Types of Peripheral Nerve: classified by Axon size correlates with function (see slide 10,11)
A alpha: large diameter with myelin.
A beta: large but secondary to A alpha: sensory axons that receive many sensory stimulus: touch, pressure, vibration, proprioception but not pain prick and temp.
C: very small and unmyelinated.
Responsible for autonomic neurons
Axon that serves pain prick and temperature : C fiber
Differe nt types of axons have different velocities: up to 100 m/s (large), small velocity around 3 - 10 m/s.
Gamma motor neuron: controls muscle tone Passive resting small contractions within muscles (slight contract)
Alpha vs. Gamma Motor Neuron
Alpha
Type 1: slow twitch, Type 2: fast twitch
Type 2 larger > 1 because requires more force exertion in a single movement
How many synapse in a muscle fiber? Only One
Physiology and Electrophysiology of NMJ: see slide 16 → 19 (SOS)
(18.) Quanta = molecules
EPP = End Plate Potential is caused by Acetylcholine bind with receptor → Na+ influx into cell → Grated Potential: depends on amount of Sodium influx through acetykcholine receptors (not all or none like action potential), if a threshold is reached → action potential in muscle membrane is induced.
Why does muscle membrane require action potential? Action potential can send long signals without decrease → send signal deeply into T-tubule in muscular cell: activate fibers → muscle contraction
End plate potential: although reduced, is still higher than the threshold that generates action potential → continuous action potential generation
5 molecules of acetylcholine → produce 1 mV of EPP
15 mV of EPP is the threshold required to → Action Potential
Myasthenia Gravis
Lambert-Eaton Mysathenic Syndrome
Acetylcholine in synaptic cleft reduced from 200 to 20 from the very beginning.
T-Tubule:
tube invaginate down to sarcoplasmic reticulum: special organelles in muscle that stores Calcium, sarcolemma. → activates Calcium release in Sarcoplasmic reticulum (elaborate more on the process) something about DHPR → Ryanodine Receptor RYR → ???
Excitation Contraction Coupling
Cross-bridge formation: calcium binds to troponin C → change in troponin-tropomyosin conformation → tropomyosin moves → cleft, leaves binding sites exposed → myosin attaches head to exposed binding site.
Sliding FIlament Theory: Myosin head touch with actin → Pi is removed → Pwer stroke: Actin gets pulled towards middle of sarcomere → ADP released → New ATP binds to myosin head → unbinding of myosin and actin → cocking of myosin head → start over
Relaxation: reduction of calcium (calcium reflux back into sarcoplasmic reticulum depends on concrentration of Calcium ion) → troponin can not stroke acti anymore even with ATP NOT related to ATP depletion.
What happens if ATP is depleted but not Calcium? → Cramping (excessive use of muscle): ATP completely depleted → can NOT unbind myosin head out of actin → contraction.
What defines force of contraction?
Temporal Summation: “Tetany”: every single motor unit can gradually increase the force by itself.
Spatial Summation: “Recruitment”
Neuromuscular Unit Pathology
Differentiate between upper and lower motor neuron lesions:
Upper: primary motor cortex: pyramidal
Whys does cell body lesion → Atrophy? Muscles require neurotrophic factor produced by cell body from neurons for muscle to survive, Once muscle lacks these factors → slowly die off.
Atrophy & Fasciculations can be used to differentiate
Symptoms and Manifestations of NMJ Disorders:
Pre-synaptic disorders:
Lambert-eaton syndrome (LEMS)
• Persistent chronic progressive weakness with significant improvement on brief exercise
• Affect proximal muscles (esp. lower exrtemities) with early sparing oculo-bulbar muscles
• Hyporeflexia (improved with exercise), hypotonia
• Autonomic dysfunction as well
Botulism
Acute weakness from the intoxication (12-36 hours)
Affect all muscles from oculobulbar to respiratory muscles (if severe, leading to death)
Autonomic dysfunction
Post-synaptic disorders
Myasthenia Gravis
Progressive intermittent weakness with ‘fatigability’/’fluctuated’ pattern (diurnal variation : strong in the morning, weaker in the afternoon)
Affect the oculo-bulbar muscles and proximal muscles.
Normal reflex
Only Weakness
Clinical Correlations: see case discussion