MOTOR SYSTEM – Muscle, LMC, Spinal cord mechanisms of control

- Motion around a certain joint creates a mechanical effect such that each successive joint is disturbed and must be stabilized

- To localize lesion in motor system is presence of absence of weakness

-Upper motor neurons (UMNs)lower motor neurons (LMNs), NMJ, Muscle fiberspresent weakness if damaged (motor cortex  muscles)

- Motor cortex gets input form basalganglia (via thalamus), cerebellum (via thalamus), and other cortical areas; Damage to one of these does not result in weakness, but produces disorders of the quality of movement

2. – A muscle is innervated by several hundred LMNs (cell bodies in anterior horn of spinal cord)

- A motoneuron, with its axon and all the muscle fibers that it innervates is called a motor unit

- Each muscle fiber innervated by single LMN and has a single NMJ

- AP along LMN reaches nerve terminal at NMJcalcium ions enter nerve terminal due to depolarization and Ach is released from the nerve terminal

- Ach binds its receptor on surface of muscle fiber depolarizationAP along full length of myofiber (both directions)

-As AP spreads along surface of myofiber, it travels into T-tubules (transverse tubules)  long invaginations of plasma membrane into the myofiber

- T-tubules aligned along junction between A-band and I-band; T-tubules are closely apposed to sarcoplasmic reticulum (SR). Two cistern of SR associated with single T-tubules triad.

- At each triad, voltage-gated calcium channels in T-tubule membrane are coupled to a different class of calcium channel in SR channel

- AP in the T-tubule causes release of Ca2+ from SR  rise in [Ca2+] causes activation of sarcomeres and contraction of myofiber

- One AP in LMN caused one AP in each of the muscle fibers it innervates

1. EMG – electrodes detect sum of electrical activity of active muscle fibers; APs of each muscle fiber belonging to a single motor unit add up to produce a compound AP (EMG records a sum of compound APs)

Myopathic disease

- Muscle fiber dysfunction  no APs in muscle fibers  fewer surviving muscles in each motor unit that can generate an AP amplitude of EMG record is reduced

Neurogenic disease

- Damage to LMN has abnormal findings

- fibrillations spontaneous contractions of individual muscle fibers (small spikes on EMG record); small potential, low frequency; fibrillations arise from increased expressions of Na and Ca channels in denervated muscles  nearby intact fibers activated previously and residual ionic currents cause depolarization in adjacent denervated fibers (with increased channels)

-fasciculations spontaneous activation of motor units (spontaneous activation of LMN involving Ach); visible as twitching; can be abolished by Ach blocker and induced by AchAse blocker;

- EMG can detect Giant units abnormally large compound APs (show when voluntary movements are attempted); occurs due to sprouting: motoneurons die and lose innervation of muscle fibers  nearby intact motoneurons make new collateral branches and send those branches to innervate vacant slots ondenervated musclesurviving motor units include more muscle fibers recorded compound AP increases in seize

Hyperactive reflexes  UMN lesion (motor cortex of CST)

Normal or reduced reflexes LMN or muscle lesion (including NMJ); to distinguish between LMN and muscle look at EMG (fibrillations, fasciculation, etc.  LMN, reduced amplitude  muscle if constant weakness or NMJ if fluctuating weakness)

3. Automatic functions of spinal cord – automatic regulation of muscle force

Types of motor units

Motor Unit Type / Motoneurons Properties / Muscle Fiber Properties / Histological Type of muscle fiber
Slow twitch (S) / Small, slow conducting axons / Low force, slow contraction, fatigue-resistant, oxidative metabolism / Type I (smallest)
Fast-twitch, fatigue resistant (FR) / Medium size, moderate-fast conducting / Moderate-high forces, fast contraction, fatigue-resistant / Type IIa (medium size)
Fast-twitch, fatigable (FF) / Large, fast-conduction / High force, fast contraction, fatigable / Type IIb (largest)

- Properties of motoneurons match properties of muscle fibers they innervate

- Muscles contain a mixture of the 3 types of motor units

4. How muscle force is increased – 1) increase number of motor units activated, 2) increase discharge rates of already firing motor units

Rule #1 – Fixed order of recruitment according to size principle; smallest motoneurons activated first, and successively larger motoneurons activated as more force needed; S  FR  FF

- Smaller motoneuron has fewer parallel ion channels and has a higher total cell input resistance

- Larger motoneuron has more parallel ion channels and has a lower total cell input resistance

- according to V=IR (I is constant as the CST UMN); R is high in small motoneurons and low in large motoneurons

- V of the small LMN is higher, and V of the large LMN is lower; small motoneurons will reach threshold first, and the large motoneurons will reach threshold later

Rule #2 – fixed sequence for firing rate of motoneurons; when first activated, a motoneuron may fire at 10 Hz; when it receives more excitation is will increase its firing up to 25 Hz

- Increasing the discharge rate of an already active unit increases its force output until it reaches maximum force (tetany)

- Both rules lead to increases in force that are smooth

5. - A network of interneurons responsible for generating an automatic rhythmical movement is called central pattern generator (CPG); CPGs are in the spinal cord and brainstemfor respiration, chewing, swallowing, and locomotion

- once a CPG is activated it can product the complex muscle instruction by its own subroutine; does not need descending cortical input or sensory feedback

- A CPG reduces the amount of planning that the nervous system at other levels need; A CPG established the timing signals and basic motor pattern at a lower level; cortical areas and sensory feedbackmodulate these elementary instructions

Locomotor central pattern generator – network of interneurons residing in spinal cord; most unconscious and automatic part of the motor system (like walking)

- capability for rhythmical stepping after cord transection and deafferentation; CPG is dependent on descending influences; the locomotor CPG provides timing instructions for alternating activity in flexor and extensor muscles at each joint of the leg: hip, knee, ankle

- locomotor CPG requires sensory sources and cortical, higher motor center sources: cutaneous sense, position sense, and force feedback from limbs

6. Reflexes during walking – the network of spinal cord circuitry for reflexes must interact with the circuitry for the locomotor CPG

- If the dorsum of the foot is pinched during the swing phase of locomotion withdrawal response in which flexor muscles of the stimulated leg are activated foot is drawn up and away for stimulus

- If the dorsum of the foot is pinched during the stance phase of locomotion (leg is accepting body’s weight) extensor muscles are activated to produce an extension response in the standing leg to move away from the stimulus

7. Brainstem – CPGs for breathing, chewing, and swallowing; receive sensory and corticalinput to adapt the basic instructions for the functional and environmental context

Respiration – nuclei in pons/medulla; two medullary centers  a dorsal and ventral respiratory group in reticular formation, pons, and medullatiming instructions to inspiratory and expiratory muscles;

- output of two respiratory centers activates trigeminal, facial, glossopharyngeal, vagus, and hypoglossal nerve (and spinal input to diaphragm via phrenic nerve and intercostals, abdominal muscles)

- neurons in respiratory groups include pacemaker neurons spontaneous rhythmical oscillations  APs to quiet to APs; CPG provides alternating EPSPs and IPSPs to respiratory motoneurons

- breathing requires sensory and corticalinput to respiratory CPG

- chemoreceptors, pulmonary stretch receptors and muscle spindles, provide sensory feedback about blood gases and muscle work to regulate breathing muscle pattern

- cortical inputnecessary for adjusting breathing pattern to hold breath, whistle, talk.

Chewing – repetitive jaw opening and closing; initial prep phase food from anterior to posterior of mouth; reduction phase food is torn and crushed to form bolus

- the CPG for chewing isolated to gigantocellular reticular nucleus in reticular formation in medial pons/medulla to motoneurons (trigeminal and facial)

-sensory and cortical inputs sculpt the rhythmical jaw movements into everyday patterns of chewing; muscle spindleinformation (trigeminal mesencephalic nucleus) for jaw closure muscles modifies timing of switch from jaw opening to jaw closing; feedback from pressure sensors in teeth modify force and timing of chewing (jaw closure); cortical input involved in modulating chewing pattern

Swallowing – three phase: oral, pharyngeal, and esophageal;

Pharyngeal phage:

1. Hyoid bone elevated and moved anteriorly

2. Larynx is adducted

3. Soft palate elevated

4. Pharynx is constricted

5. Esophageal sphincter is relaxed

- Muscles receive alternating excitatory and inhibitory input t p produce sequenced EMG pattern producing these steps

- CPG in nucleus of Solitary tract and dorsal motor nucleus (X)  LMN (nucleus ambiguus)

- CN X (Superior laryngeal nerve)  on-switch for pharyngeal CPG (activated by cortical or sensory input)

- sensory/cortical info; chemoreceptors at dorsum of tongue, epiglottis, pharynx walls carries with V3, IX, and X modify duration of EMG and force of muscle contractions of swallowing pattern; cortical areas voluntary swallowing