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LO: Describe each of the components of the somatic motor system
The somatic motor system controls voluntary muscle movement and consists of:
Skeletal muscles: the effectors that produce movement
Alpha motor neurons: located in the ventral horn of the spinal cord; directly synapse on muscle fibers to initiate contraction
release ACh
A single alpha motor neuron innervates MANY muscle fibers
Alpha motor neurons receive input from upper motor neurons in the motor cortex and from sensory neurons in the periphery
Excitation of this neuron ALWAYS causes contractions due to the release of ACh at the NMJ
Descending motor pathways: tracts from the brain that carry movement commands to spinal motor neurons
Interneurons: located in the spinal cord; help integrate sensory feedback and coordinate motor output
LO: Demonstrate flexion & extension and describe how muscles coordinate these movements
Flexion: movement that decreases the angle between bones
Extension: movement that increases the angle between bones
Antagonist pairs
when one muscle contracts, the opposing muscle relaxes (reciprocal inhibition)
Coordination occurs through alpha motor neuron activation and spinal interneurons
Muscles
they pull, they don’t push
muscle contraction occurs due to the release of ACh
Motor neurons controlling flexors lie dorsal to extensors
Motor neurons controlling axial muscles lie medial to those controlling distal muscles
LO: Identify axial, proximal and distal muscles
Axial Muscles
located along the trunk and head; maintain posture and balance
Proximal muscles
controls movement of shoulders, elbows, pelvis, and knees
Distal muscles
controls hands, feet, fingers, and toes
responsible for fine motor control and manipulation
LO: Summarize key features of alpha motor neurons
Alpha Motor Neurons (AKA Lower Motor Neurons - LMN)
found in the ventral horn of the spinal cord (upper motor neurons in the primary motor cortex)
Only the LMN directly triggers muscle contraction through the release of ACH at the NMJ
Three inputs
dorsal root ganglion cells with axons that innervate a specialized sensory apparatus embedded within the muscle known as muscle spindle
Descending input from the upper motor neurons in the brain (motor cortex& brain stem)
interneurons in the spinal cord
Segmental Organization
neurons innervating the same muscle are grouped together in longitudinal columns across several spinal segments
Distribution:
medial ventral horn: controls axial muscles
intermediate ventral horn: controls proximal muscles
lateral ventral horn: controls distal muscles
LO: Compare the terms motor unit and motor neuron pool
Motor unit
LMN & all muscle fibers it innervates (LMNs control the activity of many fibers)
Motor neuron pool
all alpha MN that innervates a single muscle
LO: Summarize how the force of muscle contraction is controlled in a finely graded fashion
The CNS finely controls muscle force through three mechanisms
Adjusting firing rate of motor neurons
each action potential from an alpha motor neuron release ACh at the NMJ, triggering a twitch
sustained contractions require a continuous stream of action potentials
higher firing rates cause temporal summation of twitches, increasing muscle tension and producing smoother, stronger contracts
thus, the frequency of motor neuron firing directly controls the strength and smoothness of contraction
Recruiting additional synergistic motor units
Motor Unit - one alpha motor neuron and all the muscle fibers it innervates
by recruiting more motor units, total muscle tension increases
Motor unit size
large units (leg muscles) have about 1000 fibers per neuron causing coarse movements and a large force
small units (finger muscles) have 3 fibers per neurons causing fine, precise control
Muscles with many small motor units allow finer control by the CNS
Recruiting motor units from smallest to largest
motor units are activated from smallest to largest
small alpha MN are easily excited by brain signals due to their geometry and physiology
ordered recruitment allows for fine control under light loads and a gradual increase in force as load increases
Known as Size Principle (Henneman)
LO: Compare the different types of muscle fibers and motor units
Slow motor units (I)
slowly-fatiguing red fibers
contain slow-twitch (Type I) muscle fibers
fibers are red due to high myoglobin and mitochondria content
produce slow, steady, weak contractions, but resist fatigue
used for endurance and postural control
Fatigue-resistant fast fibers (IIa)
white fibers with moderate strength and fast contractions
contain fast-twitch oxidative (Type IIa) fibers
generate moderately strong, fast contractions
resistant to fatigue
used for repetitive movements like walking or swimming
Fast fatigable fibers (IIb)
fastest, strongest white fibers, but rapidly fatiguing
contain fast-twitch glycolytic (Type IIb) fibers
generate the strongest, fastest contractions
fatigue quickly during sustained activity
used for brief, powerful movements
LO: Describe the process of excitation-contraction coupling
Excitation
an action potential occurs in an alpha motor neuron axon
ACh is released by the axon terminal of the alpha motor neuron at the NMJ
Nicotine receptor channels in the sarcolemma open, and the postsynaptic sarcolemma depolarizes
Voltage-gated sodium channels in the sarcolemma open and an action potential is generated in the muscle fiber, which sweeps down the sarcolemma and into the T tubules
Depolarization of the T tubules causes Ca2+ release from the SR
Contraction
Ca2+ binds to troponin
Tropomyosin shifts position and myosin binding sites on actin are exposed
Myosin heads bind actin
Myosin heads pivot
An ATP binds to each myosin head and it disengages from actin
The cycle continues as long as Ca2+ and ATP are present
Relaxation
As EPSPs end, the sarcolemma and T tubules return to their resting potentials
Ca2+ is sequestered by the SR by an ATP-driven pump
Myosin binding sites on actin are covered by tropomyosin
LO: Describe the molecular basis of muscle contraction
Sarcomere Structure
basic contractile unit between two Z lines
thin filaments (actin) anchored to Z lines; thick filaments (myosin) in between
Contraction = thin filaments slide past thick, shortening the sarcomere (sliding filament model)
Key Proteins
Actin: has myosin-binding sites
Myosin: uses ATP to bind, pivot, and pull actin
Tropomyosin: blocks binding sites at rest
Troponin: binds Ca2+, moves tropomyosin to expose actin sites
Cross-Bridge Cycle
Ca2+ bind troponin —> exposes actin sites
Myosin binds actin —> power stroke moves thin filament
ATP binds myosin —> detaches from actin
ATP hydrolyzed —> myosin re-cocks for next cycle
repeats while Ca2+ & ATP are present
Role of Calcium
released from sarcoplasmic reticulum upon excitation
triggers contraction via troponin - tropomyosin shift
pumped back into SR by ATP-driven pump for relaxation
Energy Use
ATP required for: cross-bridge cycling, detachment, and Ca2+ reuptake
without ATP —> myosin remains bound —> stiffness
LO: Diagram the knee jerk reflex
Knee Jerk Reflex
tendon beneath your knee cap briefly stretches the quadriceps of your thigh, which then reflexively contract and cause your leg to extend
Muscle Spindle
stretch receptor, specialized muscle fibers
group la axons encircle (detection of muscle length-stretch)
la axon
detect muscle length
sensory receptor for proprioception
proprioception - sense of how our body is positioned and moving in space
thickest and most muelinated = fast conduction
synapse on alpha motor neurons & interneurons in spinal cord
Monosynaptic
only 1 synapse between sensory neuron and alpha motor neuron
LO: Discuss the role of interneurons, reciprocal inhibition, and reflexes when you step on a tack
When You Step on a Tack
Interneurons in the spinal cord connect sensory and motor neurons, coordinating reflexes through excitatory or inhibitory signals.
Reciprocal inhibition: contraction of one muscle group is paired with relaxation of its antagonist via inhibitory interneurons.
Flexor withdrawal reflex: painful stimulus activates nociceptors → excitatory interneurons → flexor muscles contract to withdraw the limb.
Crossed-extensor reflex: opposite leg’s extensor muscles activate while flexors are inhibited to maintain balance.
Together, these spinal reflexes allow rapid withdrawal from pain while stabilizing posture without cortical input.
LO: Describe the components of the motor control hierarchy in terms of anatomy and function
Anatomy and Function
Overview
Upper motor neurons in the cortex control lower motor neurons in the spinal cord to produce voluntary movement.
Hierarchy of Control
Strategy (highest): Neocortex & basal ganglia — decide movement goals.
Tactics (middle): Motor cortex & cerebellum — plan and coordinate muscle activity.
Execution (lowest): Brainstem & spinal cord — activate motor neurons and adjust posture.
Sensorimotor Integration
Sensory feedback guides and refines movement at all levels.
Descending Pathways
Lateral: Controls voluntary distal movement.
Ventromedial: Controls posture and balance.
Example
Stepping on a tack quietly shows cortical (upper motor neuron) control overriding reflexive spinal (lower motor neuron) actions.
LO: Compare and contrast the lateral pathways and ventromedial pathways
Lateral Pathways
Includes: Corticospinal and Rubrospinal tracts
Function: Control voluntary, precise, and fractionated movements of distal muscles (hands, fingers).
Anatomy: Fibers decussate in the medulla (pyramidal decussation) → control the contralateral side of the body.
Damage: Loss of fine motor control; slower, less accurate voluntary movements.
Ventromedial Pathways
Includes: Vestibulospinal, Tectospinal, Pontine Reticulospinal, Medullary Reticulospinal tracts
Function: Maintain posture, balance, and head/eye coordination; control of axial and proximal muscles.
Anatomy: Mostly bilateral projections; work together to stabilize the body and head.
Damage: Impaired balance, posture, and coordination of head and trunk movements.
LO: Predict the site or consequence of a lesion based on knowledge of the pathways and their function
Corticospinal (lateral) – Lesion → loss of fine, fractionated movements (fingers/hands); slower, less precise voluntary movement; contralateral deficit.
Rubrospinal (lateral) – Lesion → minor loss of coordination/fine motor control.
Vestibulospinal (ventromedial) – Lesion → poor balance, head stabilization problems.
Tectospinal (ventromedial) – Lesion → impaired head and eye orientation to stimuli.
Pontine reticulospinal (ventromedial) – Lesion → weakened antigravity reflexes; trouble maintaining posture.
Medullary reticulospinal (ventromedial) – Lesion → excessive rigidity; loss of reflexive posture relaxation.
LO: Describe the organization and function of the motor cortex
Primary Motor Cortex (M1 / Area 4)
Precentral gyrus; contralateral body control; somatotopic map.
Betz cells = upper motor neurons to spinal cord.
Inputs: cortical areas & thalamus.
Encodes force and direction via population coding (many neurons collectively determine movement).
Secondary Motor Areas (Area 6: PMA & SMA)
Convert action plans into movement signals (how to act).
Receive input from prefrontal & posterior parietal cortex.
Maintain movement strategies until execution.
Higher-Level Cortical Inputs
Prefrontal Cortex: decides actions & outcomes.
Posterior Parietal Cortex: sensory info about body position for planning.
Execution Hierarchy
Plan: parietal & frontal lobes
Strategy: SMA/PMA (Area 6)
Tactics: M1 → brainstem & spinal cord → voluntary movement
LO: Describe the organization and function of the posterior parietal cortex
Integrates sensory information (visual, somatosensory, vestibular) for spatial awareness and movement planning.
Works with premotor areas to transform sensory input into coordinated motor output.
LO: Explain how movements are planned by the brain
Goal-Directed Movement:
Requires knowledge of body position, plan selection, memory of plan, and execution.
Cortical Areas:
Prefrontal Cortex: Decide what to do.
Posterior Parietal Cortex: Track where the body is.
Area 6 (SMA/PMA): Convert plan into how actions are performed; hold strategies.
Primary Motor Cortex (M1): Execute tactics; send signals to brainstem/spinal cord.
Basal Ganglia Loop:
Cortex → basal ganglia → VLo (thalamus) → SMA → cortex.
Function: selection & initiation of voluntary movement.
Parkinson’s disease = impaired initiation due to dopaminergic loss.
Hierarchy Summary:
Decisions (prefrontal/parietal) → Strategy (SMA/PMA) → Tactics/Execution (M1 & descending pathways).
Loops and sensory feedback ensure coordinated, goal-directed movement.
LO: Discuss the cause of Parkinson’s disease and why it is called a basal ganglia disorder
Definition: Difficulty initiating voluntary movements due to basal ganglia dysfunction.
Symptoms: Hypokinesia, bradykinesia, akinesia, rigidity, resting tremor.
Cause: Degeneration of dopaminergic neurons in substantia nigra → less dopamine to striatum → increased thalamic inhibition → reduced SMA activation.
Treatment: L-DOPA (restores dopamine), Deep Brain Stimulation (modulates basal ganglia).
Epidemiology: ~1% of people >60; prevalence increases with age; slightly higher in males and certain regions.
Key Point: PD is a basal ganglia disorder because the basal ganglia normally select and initiate voluntary movement, and dopamine loss disrupts this.