Somatic Motor System

• Levels of Motor Control (Direct Pathway)

  • Cerebral cortex
  • Brain stem
  • Spinal cord

  
• Cerebral cortex


  • Primary motor cortex, premotor cortex, supplementary motor area project directly to spinal cord via corticospinal tract as well as indirectly via brain stem
  • Premotor and supplementary motor areas important for planning and co-ordinating complex movements
  • Both areas receive projections from posterior parietal and prefrontal association cortex

  
• Brain stem


  • Uses visual and vestibular information to modulate spinal motor circuits in control of posture
  • Also, eye and head movement nuclei

  
• Spinal cord


  • Reflexes: alternating activity of flexion and extension during locomotion
• Levels of Motor Control (Indirect Pathway)

  • Cerebellum
  • Basal Ganglia

  
• Cerebellum


  • Improves accuracy of movement by comparing descending motor commands with incoming proprioceptive information
  • Acts on the brain stem and the cortical motor areas
  • A general movement command from cerebrum leaves details of execution to subcortical (especially cerebellar) mechanisms

  
• Basal Ganglia


  • All functions not clearly known
  • Necessary for initiation of movement (disabled in Parkinson's disease)
  • Role in planning and programming movements
• Corticospinal Tract


  • Originates in the precentral gyrus, the premotor and supplementary motor areas (anterior to the precentral gyrus), and the postcentral gyrus of each cerebral hemisphere
  • Continues through the pons to the ventral surface of the medulla from the ventral surface of the midbrain within the cerebral peduncles
  • Right and left corticospinal tracts decussate at the level of the caudal medulla forming the decussation of the pyramids
  • Crossing over fibers become the lateral funiculi forming the lateral corticospinal tract
  • The lateral corticospinal tract is involved in control of limb muscles
  • Most tract fibres terminate on interneurons to indirectly influence motor neurons
  • Some also terminate directly on motor neurons
  • A few fibers do not decussate at the caudal medulla but continue in a ventral ipsilateral position to form the medial corticospinal tract carrying fibers from the ipsilateral cerebral cortex involved in control of axial and trunk muscles, predominantly by way of interneurons

  
• Corticobulbar (Direct)


  • The corticobulbar tract innervates motor neurons of the brainstem, i.e. cranial nerve nuclei 5, 7, and 12, and the nucleus ambiguus
  • The corticobulbar tract innervation is primarily bilateral
  • Corticobulbar innervation of nuclei of CN VII is bilateral for the upper face motor neurons but exclusively contralateral for the motor neurons of the lower face

  
• Indirect Pathways


  • The superior colliculus (tectum) receives axons from the optic tract and projects to the contralateral spinal cord via the tectospinal tract
  • The vestibular complex is involved in the control of balance and influences spinal cord motor neurons
  • The medial reticular formation (MRF) integrates a variety of sensory inputs and commands from the cortex and projects the integrated commands (e.g. postural adjustment) to the spinal cord via the reticulospinal tract
  • The red nucleus, which receives input from motor cortex, projects to the spinal cord via the rubrospinal tract

  
• Medial tracts


  • The tectospinal tract, the medial and lateral vestibulospinal and reticulospinal tracts, and the anterior corticospinal tract
  • Descend in the medial, ventral white matter of the spinal cord and terminate in the medial regions of the ventral horns where motor neurons that innervate axial and proximal limb musculature are located
  • Involved in reflex postural adjustments and maintenance of balance

  
• Lateral tracts


  • The lateral corticospinal and rubrospinal tracts
  • Involved in limb movements
• Spastic paralysis


  Damage to upper motor neurones causes spastic paralysis on the opposite side of the body: decreased or absent muscle tone, muscle is limp or flaccid, no voluntary action of innervated muscles
• Neuromuscular junction


  • Branches from one lower motor neurone innervate many muscle fibres; each muscle fibre is innervated by one neurone
  • Axon of neurone terminates in a synaptic bulb
  • The region adjacent to synaptic end bulbs is the motor endplate
  • When the action potential reaches the end bulb, synaptic vesicles dump their acetylcholine (ACh) into synaptic cleft
  • ACh binds to muscle ACh receptors; this opens gated ion channels and Na+(Sodium) flows into membrane
  • Influx of Na+ triggers muscle action potential; after a series of events, the muscle fibre contracts (twitch)

  
• Synaptic Vesicles


  • Neurotransmitters are released into the synaptic cleft via exocytosis from synaptic vesicles
  • At the neuromuscular junction small clear core vesicles transport small molecule neurotransmitters that are synthesised locally in the presynaptic terminals
  • Finalised neurotransmitter vesicles are bound to the presynaptic membrane
  • When an action potential propagates down the motor axon and arrives at the axon terminal, it causes a depolarisation of the axon terminal and opens calcium channels
  • This causes the release of the neurotransmitters via vesicle exocytosis
  • Vesicles are recycled after exocytosis & this is known as the synaptic vesicle cycle
  • Recycled vesicle membranes are stored in a reserve pool until they are needed again for release of more neurotransmitter
• Readily releasable pool of synaptic vesicles

  • Upon activation these are released emptying their entire contents into the synaptic cleft
  • This is called quantal release of transmitter from synaptic vesicles
  • However, during high frequency stimulation of nerve and therefore muscle, this ready supply of vesicles is depleted, and the size of the endplate potential (EPP) is reduced
  • For this not to occur, a fine balance between repletion and depletion has to be maintained – and is done at frequencies lower than 30Hz
• Quantal release


  Release of transmitter in whole numbers, first described by Sir Bernard Katz of UCL for which he won the Nobel Prize in 1970
• Synaptic vesicles of acetylcholine


  • Clear core synaptic vesicles with a diameter of 30 nm
  • Each acetylcholine vesicle contains approximately 5000 acetylcholine molecules
  • The vesicles release their entire quantity of acetylcholine, and this causes miniature end plate potentials (MEPPs) to occur which are less than 1mV in amplitude and not enough to reach threshold
• Miniature End Plate Potentials (MEPPs)

  • The small (~0.4mV) depolarisations of the postsynaptic terminal caused by the release of a single vesicle into the synaptic cleft
  • Neurotransmitter vesicles containing acetylcholine collide spontaneously with the nerve terminal and release acetylcholine into the neuromuscular junction even without a signal from the axon
  • These small depolarisations are not enough to reach threshold and so an action potential in the postsynaptic membrane does not occur
• End Plate Spikes


  • Spontaneous action potentials or end plate spikes may occur, in normal striated muscle without any stimulus
  • Small end plate spikes have a negative onset without signal propagation and large end plate spikes resemble motor unit potentials (MUPs)
  • Caused by the proprioceptors within the muscle – called muscle spindles
• End Plate Potentials (EPPs)

  • MEPPs are additive and lead to a greater depolarisation of the postsynaptic membrane and become end plate potentials (EPPs)
  • When EPPs cause the membrane to reach threshold, voltage gated ion channels in the postsynaptic membrane open causing an influx of sodium ions and a sharp spike depolarising spike which in its turn causes a muscle action potential to occur and propagate down the postsynaptic membrane leading to muscle contraction
  • EPPs are not action potentials but they trigger action potentials
• Muscle Action Potential


  1. Threshold is reached as MEPPs are added together to raise the membrane potential to -60 mV

  2. Voltage gated channels open causing rapid sodium influx ions making the membrane potential positive

  3. Potassium efflux equals sodium influx when the peak is reached

  4. During repolarisation, sodium channels inactivate and a net influx of potassium ions

  5. This causes the membrane potential to drop down to its resting membrane potential of -100mV

  6. Hyperpolarisation occurs because the slow-acting potassium channels take longer to inactivate, and the membrane gradually returns to resting

  7. The membrane remains unresponsive to any stimulation during the action potential phase – prior to hyperpolarisation being reached: the absolute refractory period

  8. During the hyperpolarisation period, and during the relative refractory period, stronger stimulation may evoke a subsequent action potential

  9. On completing the action potential cycle at the neuromuscular junction, ACh is cleared out of the synaptic cleft by AChE or acetylcholine esterase

  10. If neurotransmitters are not cleared away from the synaptic cleft, continued action potential propagation occurs resulting in muscle rigor
• Myasthenia Gravis


  • An autoimmune disease in which patients develop antibodies against nicotinic ACh receptors
  • The amplitudes of MEPPs and EPPs are reduced (since there will be less depolarization for the same amount of released ACh) and the muscle membrane may not be depolarized sufficiently to fire an action potential
  • Treatment is to give an acetylcholinesterase inhibitor to prolong and increase the action of ACh at the available receptors and to restore the muscle action potential