week 10 locomotion Flashcards
Two Sensory Receptors in Muscle
🔴 1. Muscle Spindle
Location: Inside the muscle belly.
Function: Senses muscle length and how fast it’s changing (stretch and speed of stretch).
activates Sensory neurons:
1. Type Ia afferents: Rapid response — detect quick stretch.
2. Type II afferents: Slower — detect sustained stretch.
Connected to:
Alpha motor neurons (that cause contraction)
Gamma motor neurons (that reset the spindle’s sensitivity)
Think of it as a “stretch sensor” inside the muscle that helps maintain posture and muscle tone.
🔵 2. Golgi Tendon Organ
Location: At the junction between muscle and tendon.
Function: Senses muscle tension (force the muscle is generating).
Sensory neuron involved:
Type Ib afferent: Senses when the tendon is under too much tension.
Think of it as a “force sensor” that protects the muscle from overloading and tearing.
Q1: What are the main neural components involved in controlling locomotion? List them in order from highest to lowest level of control.
Model Answer:
Basal Ganglia – selects the type of locomotor behaviour (e.g. exploration, escape)
Mesencephalic Locomotor Region (MLR) – initiates locomotion
Reticular Formation – relays commands to spinal cord
Central Pattern Generators (CPGs) – generate the rhythm and pattern of stepping
Sensory Afferents (muscle/skin) – modulate locomotor output based on feedback
Cerebellum – compares internal commands with actual movement for coordination
Visual Cortex & Posterior Parietal Cortex – support visual adjustments in skilled locomotion
- Central Pattern Generators (CPGs)
Q2: What are central pattern generators and what role do they play in locomotion?
Model Answer:
CPGs are neural networks in the spinal cord capable of generating rhythmic motor patterns (e.g. walking) without sensory input or descending cortical input. They coordinate alternating activity in flexor and extensor muscles and left-right limbs. Located in the ventral spinal cord, especially the lumbar segments, they are modulated by supraspinal inputs (like from the MLR) and sensory feedback
CPGs are neural networks in the spinal cord that can produce rhythmic movements without needing brain input or sensory feedback.
They control the timing and coordination of muscles for walking, stepping, and other rhythmic actions (like breathing, swimming).
🧠💬 “In a nutshell”:
Your brain sends a signal like “start walking.”
The CPGs take over to generate the actual step-by-step rhythm.
This rhythm is then sent to motor neurons, which activate the muscles.
Q3: What did spinalized and decerebrate animal studies reveal about control of locomotion?
Model Answer:
Spinalized animals (cut below brainstem): can still generate stepping on a treadmill → suggests CPGs in spinal cord can function independently.
Decerebrate animals (brainstem cut at midbrain): still show spontaneous or stimulated walking → indicates MLR can initiate locomotion.
De-afferented animals (cut sensory roots): still step → proves sensory input not essential for rhythm generation, but modulates stepping.
Electrically stimulated MLR → triggers rhythmic stepping → shows it initiates CPG activity.
Q4: How do proprioceptors modulate locomotion?
Model Answer:
Muscle spindles (Ia afferents) in flexors sense stretch → trigger reflexive contraction → initiates swing phase.
Golgi tendon organs (Ib afferents) in extensors sense tension → inhibit flexors → prolong stance.
These inputs fine-tune the timing of phase transitions (stance to swing) in the gait cycle.
Q5: What is the stumble correction reflex and what does it show about sensory feedback in locomotion?
Model Answer:
A trip stimulus on the dorsum of the foot during swing causes reflex knee and hip flexion to clear the obstacle.
A stimulus on the sole during stance causes extension and resetting.
Shows how skin afferents adapt muscle activation within a step cycle to respond to the environment.
Q6: Is the cortex required for basic locomotion? What is its role?
Model Answer:
No, the cortex is not required for basic rhythmic walking (CPGs handle that). However, it is essential for skilled locomotion — e.g. avoiding obstacles. Visual input from the visual cortex and posterior parietal cortex allows visuomotor correction via the motor cortex.
Q7: How does training or injury affect CPG function?
Model Answer:
Usage and training improve CPG function by:
Strengthening synaptic connections
Enhancing intrinsic neuron properties
Injury (e.g. muscle denervation) leads to compensatory strengthening of activity in synergistic muscles.
Reflects plasticity in spinal motor circuits.
🔵 2. Golgi Tendon Organ
Location: At the junction between muscle and tendon.
Function: Senses muscle tension (force the muscle is generating).
Sensory neuron involved:
Type Ib afferent: Senses when the tendon is under too much tension.
Think of it as a “force sensor” that protects the muscle from overloading and tearing.
Dorsal vs. Ventral – What’s the Deal?
Dorsal (back) : Dorsal root / dorsal horn: Sensory (afferent) info comes in
Ventral (front): Ventral root / ventral horn: Motor (efferent) info goes out
what is locomotion
basic walking and stepping movements
🔁 1. Locomotion is rhythmic and patterned
When we walk, our muscles activate in a repeating pattern This is rhythmic motor activity — like a natural internal beat or stepping rhythm.
👶 2. It’s innate (you’re born with it)
These walking patterns are not learned from scratch.
The neural circuits for this are already present before birth, but they mature over time.
This is why babies have primitive reflexes like the stepping reflex.
🧠3. The spinal cord can generate walking
The pattern for walking doesn’t require your brain to micromanage each step.
Instead, specialized circuits in the spinal cord — called Central Pattern Generators (CPGs) — are responsible
How We Learned About Neural Control of Walking
🔹 1. Spinal Preparations (Spinalized animals)
What they did: Cut the spinal cord at the lower thoracic level.
What happened: The animal could still produce stepping movements on a treadmill.
Why it matters: Proved that rhythmic walking can come from the spinal cord alone, thanks to central pattern generators (CPGs).
How We Learned About Neural Control of Walking
🔹 2. Decerebrate Preparations
What they did: Cut at the midbrain level.
Result: Disconnected cerebral cortex, but preserved brainstem and cerebellum.
Why it matters: Locomotion could still be initiated, especially by stimulating the mesencephalic locomotor region (MLR).
🧠 Takeaway: The MLR and brainstem can trigger walking even without the cerebral cortex.
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How We Learned About Neural Control of Walking
🔹 3. De-afferented Animals
What they did: Cut the dorsal roots, removing sensory input from limbs.
Result: Animals could still walk (step).
Why it matters: Proves that sensory input is not essential to generate walking, but it can modulate or adjust it.
🧠 Takeaway: CPGs don’t need sensory input, but sensory info helps fine-tune movement.
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How We Learned About Neural Control of Walking
🔹 4. Immobilized Preparations
What they did: Blocked motor output (e.g. using a drug to block acetylcholine at the neuromuscular junction).
Result: Muscles can’t move, but neuronal activity still occurs.
Why it matters: Shows that CPGs can run internally even when the body can’t move.
🧠 Takeaway: Motor signals still get generated in the spinal cord — movement is blocked only at the final step (the muscle).
How We Learned About Neural Control of Walking
🔹 5. Neonatal Rat Preparations
What they did: Removed spinal cord from a newborn rat, put it in a bath with NMDA + serotonin.
Result: The spinal cord produced alternating bursts of activity in flexors and extensors — just like walking.
🧠 Takeaway: Proves CPGs are hardwired in the spinal cord,(CPGs exist even in newborns)
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Neuronal systems in the brain that select the behavior
(1) Basal Ganglia (BG): Selection
Function: Decides what kind of locomotion is needed (e.g. walking vs. running vs. escape).
Input from: Hypothalamus (lateral = search/food; medial = fear/escape).
Sends to: Mesencephalic Locomotor Region (MLR).
Neuronal systems in the midbrain and lower brainstem that initiate the behavior
🔷 (2) BG → MLR → Motor Cortex
BG projects to:
1. autonomic/rhythmic : MLR to initiate locomotion
(Increasing frequency of stimulation of MLR = increase speed of walking. Eventually gallop or run)
==> MLR activates the Reticular Formation (RF) in the lower brainstem.
RF projects to spinal CPGs, which generate the walking rhythm.
✅ Think: MLR = “Start button” for locomotion.
- voluntary :
Thalamus, which relays to Motor Cortex (MCtx) for voluntary control
✅ Think: Communication route from decision → action planning.
Neuronal networks in the spinal cord that generate the behaviour
- CPGs are complex spinal networks that generate rhythm and
pattern of locomotion
– With input from lower brainstem CPGs can generate rhythmic output to muscles
– Complex muscle activity can be generated without sensory input
– CPGs are entirely within the spinal cord, with interconnected rostral-caudal and
left-right networks in ventral spinal cord
– Hind limb CPG network has rostro-caudal excitability gradient (highest
excitability in rostral lumbar segments = leading segments)
