block 6- CPG Flashcards
what are the basic units of motor control?
-reflexes .e.g knee jerks
-involuntary
simple reflexes to fixed acion patterns
Simple Reflexes:
Fast, stereotypic responses to external stimuli.
Fixed Action Patterns (FAPs):
More complex behaviours are triggered by specific stimuli.
Example: Egg retrieval in geese and gulls.
Other Examples of FAPs:
Courtship behaviours.
Gaping and pecking responses in young birds.
features of FAPs
Innate and species-typical behaviors.
Triggered by sign stimulus or releaser (specific stimulus).
Once triggered, FAPs are carried out to completion.
Hypothesises for the control of FAP’s
-hypotheis 1 : FAP’s generated by a sequence of reflexes =e.g. reflex for 1 acts are a stimulus for the second reflex and so on. see imaine if needed (S1= reflex 1= S2= reflex 2) and so on untion FAP generated
-hypotheis 2: stimulus activates the central pattern generator which generates a sequences of motor behaviours
Arguments for the central pattern generation hypothesis
- during egg retrieval behavior still carries on after stimulus is removed- suggests that behavioural sequence is generated centrally and not by a reflex chain
possible mechanisms for central pattern generation
- found in studys which use locomotion as it’s a simpler action to study
-1:we have a pacemaker neurone cell which controls rhythmic activity
-2: Rhythmic activity is generated via the interactions of the neurons with each other. (emergent network property)
The pacemaker model
Pacemaker / Intrinsic Oscillator:
Generates rhythmic activity in motoneurons.
Imposes a rhythm on neural circuits that control stereotyped behaviors (e.g., walking, courtship displays).
Opposing Phases of Activity:
Rhythmic motor patterns involve two opposing phases (e.g., flexion and extension during movement).
Pacemaker controls which neurons are active and which are inactive at different times.
Mechanisms for Opposing Phases:
Post-Inhibitory Rebound (PIR):
After a neuron is inhibited, it “rebounds” to become active once inhibition stops.
Spontaneous Activity:
Some neurons spontaneously fire without external input, contributing to the rhythm.
Constant Excitation:
Some neurons receive constant excitation, maintaining a steady level of activity.
How It Works:
Pacemaker creates alternating phases of activity and inactivity in motoneurons.
Neurons active during inactive phases are driven by PIR, spontaneous activity, or constant excitation.
half-centre model
-two neurones coupled by inhibitory synaspses
-when activated produces stable oscillations(rhythm)
-if the flexor gets activated the extendor is inhibited and vice versa therefore only one side is active at a time. The mechanism of Post-Inhibitory Rebound (PIR) helps the cycle continue, as Neuron A will rebound and become active after Neuron B has inhibited it, and vice versa.
So, to keep the oscillation going, the inhibitory effect needs to reduce gradually, allowing each neuron to take turns being active.
Mechanisms to Reduce Inhibition:
To allow this alternating pattern to continue smoothly, certain mechanisms come into play:
Fatigue: Neurons become less responsive to inhibition over time due to fatigue, allowing them to respond less strongly to the inhibitory signal. This enables the rebound effect when the inhibition is removed.
Adaptation: Over time, neurons can adapt to constant inhibitory input, meaning they adjust their response to it and start firing more readily when the inhibition is removed.
Progressive Self-Inhibition: This is where a neuron may reduce its own inhibitory influence, essentially allowing itself to be more easily activated after being inhibited, helping to sustain the rhythm.
clione limacia
Clione Limacina – A Simple Model System for Swimming Behavior
Clione Limacina is a simple organism used to study swimming behavior and neural control.
The “wings” of the Clione are actually modified feet from a snail, and they play a key role in swimming.
Clione Swimming Behavior:
The swimming consists of two alternating phases:
Dorsal Flexion (D-phase) – The body bends upwards.
Ventral Flexion (V-phase) – The body bends downwards.
cliones CNS
Clione’s CNS is made up of only a few thousand neurons.
These neurons are clustered in a small number of central ganglia.
Cerebral ganglia: Involved in higher processing.
Pleural ganglion: Coordinates swimming movements.
Pedal ganglion: Involved in controlling movement.
Intestinal ganglion: Associated with digestive function but also involved in swimming.
Swimming Central Pattern Generator (CPG):
The swimming behavior is controlled by a Central Pattern Generator (CPG) located in the Cerebral Ganglia and Pleural Ganglia.
Cliones experimental evidence
Electromyography (EMG) recordings from the left and right wings show the alternating patterns of swimming (D-phase and V-phase).
Experiments show that:
Pleural & Intestinal Ganglia Removed: Swimming activity still occurs, indicating that these ganglia are not essential for the basic swimming pattern.
Cerebral Ganglia Removed: Swimming is disrupted, showing that the cerebral ganglia are crucial for swimming control.
Pedal Ganglia Disconnected: This also affects swimming, confirming its role in coordinating swimming movements.
identification of swin motoneurons
Backfilling Method: A technique used to identify neurons with axons in a specific nerve.
Place the cut end of the nerve into a dye.
The dye is taken up by axons and travels back to the cell body.
Mapped neurons can then be impaled with intracellular electrodes to record their activity.
motoneurones in cliones
There are about 40 swim motoneurons in total.
Two large motoneurons:
-when one neurone is active 1A the other is inhibited (2A)
1A: Innervates the dorsal wing.
2A: Innervates the ventral wing.
Smaller motoneurons innervate specific areas of the wing.
iniactivation of motor neurones
Inactivation of Motoneurons:
Inactivating individual motoneurons does not affect the overall swimming rhythm as expected.(if you suppress the activity of one side of the neurone the other side is not also suppressed and so that pattern is still generated in simple terms)
Even photoinactivating all motoneurons does not interrupt the basic swim rhythm.
in concussion:
- Swim motoneurons are not involved in generating the swim rhythm only for contracting muscles
swin interneurones
No peripheral processes (cannot be identified by backfilling). completely contained within the central nervous system
Identified by intracellular electrodes: Look for neurons active in phase with motoneurons.
-inactivation of interneurons e.g. via hyperpolarisation is sufficient to inactive swin rhytms
clione swim interneurons
Two Groups of Swim Interneurons:
Group 7: Active during D-phase of swimming
Group 8: Active during V-phase.
Interneuron Connections:
Interneurons in Group 7 and Group 8 are connected by inhibitory synapses e.g. activation of group 7 inhibits group 8.
Interneurons in the same group are electrically coupled.
Swim interneurons fire on rebound from inhibition (post-inhibitory rebound).
neuroanatomy of the tadpole
-eight types of spinal neurons
including: motoneurons and commissural interneurons = connect the left and right side of the spinal cord together
-decending interneurons = descend along the spinal cord
-dorsolateral interneurons
-dorsolateral commisural interneurons
-Rohon-beard neurons
-spinal cord is very small= 100 micrometers
how to record swim mototneurons in tadpoles?
-motoneurons show rhythmic activity in response to brief tail stimulus so you stimulate the tail
-but you use a neuromuscular blocker so the muscle can’t contact as if they start to actually swim you can’r record however the psinal cord is still active
-what you find is depolarisation of the motor neurones which triggers action potential which you can see in the recordings
-activity of left and right motoneurones alternates ( when the left side has an action potential the right side isn’t excited vice versa)=This causes the body to bend side-to-side – the classic swimming motion
basic swimming in tadpoles explained
Three Neuron Types Needed for Basic Swimming Rhythm:
dINs (descending interneurons)
cINs (commissural interneurons)
mns (motoneurons)
(In the diagram, d = dIN, m = motoneuron, c = cIN)
🔑 Shared Features of These Neurons:
They all:
Fire one action potential per swim cycle.
Are tonically excited (held in a depolarized, ready-to-fire state).
Receive inhibition halfway through the cycle (called mid-cycle inhibition), to help alternate sides.
🧠 Forming a Half-Centre Oscillator:
The neurons are arranged in two groups (left and right sides).
Commissural interneurons (cINs) send inhibitory signals across to the other side, creating the alternation.
This setup forms a half-centre oscillator: each side inhibits the other, causing rhythmic alternation.
activation of swim CPG
-1. Sensory Input:
The skin of the tadpole is covered in free nerve endings.
These are connected to Rohon-Beard (RB) neurons — specialized sensory neurons.
🧬 Rohon-Beard (RB) neurons:
Located in the dorsal spinal cord.
Their axons run longitudinally (along the length of the body).
They detect mechanical stimulation (like touching the tail).
🔹 2. Activation of Interneurons:
RB neurons send excitatory signals to:
Dorsolateral (dl) interneurons
Dorsolateral commissural (dlc) interneurons
These interneurons are sensory relay cells.
🔹 3. Activation of Swim CPG:
The dl and dlc interneurons excite the CPG neurons (like dINs, cINs, motoneurons).
This initiates the rhythmic swimming activity.
head to tail swimming in tadpoles
When a tadpole swims, its body bends in a wave-like pattern, starting from the head and moving toward the tail.
This is called a traveling wave of muscle contractions.
🔌 Motoneuron Activation:
This bending is driven by motoneuron activity.
The signal doesn’t activate the whole body at once — it spreads gradually, from head to tail.
🔬 Experimental Evidence:
In the isolated spinal cord, you can still observe this head-to-tail pattern.
Electrodes placed at different points along the spinal cord show that motoneuron firing happens slightly later as you move farther down (caudally).
This delay per distance is measured in milliseconds per millimeter (ms/mm).
📈 What it shows:
This progressive delay means motoneuron activity travels like a wave, allowing the tadpole to produce smooth, coordinated swimming movements.
hypothesis as why the wave activity in tadpoles propogates from head to tail?
Hypothesis 1: Single Oscillator with Variable Delays
Idea: There’s one central CPG (central pattern generator) at the front (rostral end).
The same signal travels down to more caudal (rear) segments, taking longer to reach them.
🛑 Why it’s unlikely:
The tadpole’s CPG is distributed—not located in one place.
Even isolated spinal cord segments can independently produce rhythmic swim-like activity.
➤ Conclusion: This hypothesis doesn’t fit what we know about the system.
💡 Hypothesis 2: Chain of Unitary Oscillators (More Likely)
Idea: The spinal cord contains a series of small CPGs, like linked mini-oscillators, one per segment.
Each segment has its own rhythm-generating CPG.
A leading oscillator (usually in the rostral part) sets the pace for the rest.
A gradient exists: rostral (head) CPGs oscillate faster than caudal (tail) ones.
This causes the wave of activity to move from head to tail in a coordinated fashion.
- this is the best explained hypothesis
Rostral-caudal delay?
The spinal cord has a difference in how excitable the neurons are, from head to tail — neurons near the head are more easily activated than those near the tail (rostral-caudal)
-Rostral motoneurons:
Are more depolarised during swimming.
-Receive stronger mid-cycle inhibition
manipulating excitability in caudal segents
-predicted to change the rostral-caudal delay
-lutamate is the excitatory neurotransmitter driving swimming.
Applying drugs to caudal segments:
🔹 NMDA (a glutamate agonist):
Increases excitability.
Reduces or reverses the delay — caudal segments may activate earlier.
🔹 AP5 (a glutamate antagonist):
Decreases excitability.
Increases the rostral-caudal delay — activity moves more slowly tailward.
in conclusion How is activity in unitary oscillators coordinated?
Coordination between unitary oscillators relies on a gradient of excitability, fine-tuned by neurotransmitter action
longitudunal gradients in axon distribution
Highest numbers of axons originate from:
Dorsolateral commissural interneurons (dlc)
Dorsolateral ascending interneurons (dca)
Descending interneurons (dIN)
Concentration is highest at rostral end of spinal cord and gets less and less as you go along
➔ Supports rostral-caudal excitability gradient
-the more axons you have
lamprey swim CPG
Lamprey swimming involves rhythmic, undulatory body movements coordinated along the spinal cord.
The swim rhythm is generated by a central pattern generator (CPG) with a half-centre oscillator structure.
The spinal cord functions as a chain of unitary oscillators, each segment capable of generating rhythm.
Even when isolated, spinal segments can produce rhythmic activity — but overall rhythm slows down.
Phase lag per segment remains consistent, preserving the head-to-tail wave even if rhythm is slower.
Glutamate (via NMDA receptors) is the key excitatory neurotransmitter in rhythm generation.
Changing NMDA levels in different spinal regions can reverse or split the direction of the wave:
Equal NMDA → normal rostral-caudal wave (forward swim).
High NMDA caudally → caudal-rostral wave (backward swim).
High NMDA in the middle → waves go both rostrally and caudally.
This supports the leading oscillator hypothesis: the fastest oscillator sets the rhythm and coordinates the rest
kinematic anaylsis of walking
Walking is a coordinated activity, and we can think of it as a repetitive “step cycle” that involves two main parts:
Stance (Support) Phase:
This is when your foot is in contact with the ground, supporting your body weight.
The leg moves from the front (anterior) to the back (posterior) of your body.
During this phase, the leg is also helping to push the body forward (propulsive force).
Swing (Transfer) Phase:
After the stance phase, the leg lifts off the ground and swings forward, moving from the back (posterior) to the front (anterior).
This phase gets the leg ready to land again.
Walking is not like a simple swinging motion, like a pendulum. It involves the hip, knee, and ankle joints all working together in a controlled way to make sure that the leg moves smoothly and efficiently.
speed related changes in step cycle
When walking speed changes, the body adjusts in different ways:
Moderate Speed Changes:
Stance Phase: The biggest change happens in how long the foot stays on the ground (stance phase). This is where the duration of time spent with your foot planted changes when you walk faster or slower.
Swing Phase: There is a smaller change in how long the leg swings through the air before it touches the ground.
-When you change speed significantly, the coordination between limbs also changes.
neuronal control of walking
-Each limb is controlled by its own controller. There is evidence in both humans and animals
-various gaits (pattern of coordination) are controlled by a single neuronal network. again evidence
-Even though each limb has its own “controller,” all of these “controllers” are connected and work together through a single network of neurons in the brain and spinal cord. This network coordinates the movements of the limbs to produce different gaits or patterns of movement
location of neuronal networks for walking
The basic neuronal network for walking is located in the spinal cord, posterior brainstem, and cerebellum, rather than in the higher brain regions. This was shown through transection experiments, where cutting the spinal cord at the superior colliculus level still allowed cats to walk, though in a machine-like manner. However, when the spinal cord was severed at more caudal level(lower levels), spontaneous walking did not recover. This demonstrated that the lower brainstem and spinal cord are crucial for locomotion, and the Mesencephalic Locomotor Region (MLR) is key for initiating walking
Function of MLR
The Mesencephalic Locomotor Region (MLR) plays a key role in controlling muscle force and limb coordination during walking, but it doesn’t directly control the frequency of the step cycle. This was shown in two experiments:
When the MLR was stimulated at a constant level while the treadmill speed decreased, the step cycle frequency also decreased, showing that the MLR does not regulate cycle frequency.
When the MLR was stimulated at increasing levels while keeping treadmill speed constant, there was an increase in force and a change in gait pattern, but no change in cycle frequency.
In conclusion, MLR activity influences muscle force and limb coordination, but not the frequency of the walking cycle. its control by the feedback cycle
Role of the sponal cord in walking
in low spinal cats (cats with transections of the spinal cord in the thoracic region), stepping movements can still occur when the cat is placed on a treadmill and supported by body weight. However, the movements are weak and poorly coordinated. The strength and coordination of these movements can be improved by applying clonidine, an α2-noradrenergic receptor agonist. This suggests that the limb controller for walking is located in the spinal cord, but the weak movements result from insufficient excitatory drive. The spinal cord’s lumbosacral enlargement( This enlargement occurs in the lower part of the spinal cord, in the lumbar (lower back) and sacral (pelvic) regions. The reason this area is enlarged is that it contains a high concentration of motor neurons that control the muscles of the legs.) is likely involved in these movements
do mammals need sensory feedback for walking?
-Even without sensory feedback, the spinal cord can still produce rhythmic activity for stepping.
This suggests that the spinal cord has the capacity to generate walking movements without needing continuous sensory input.
-Sensory feedback is not required for the spinal cord to generate rhythmic stepping activity, meaning that the spinal cord has an intrinsic ability to control stepping, likely due to central pattern generators (CPGs) within the spinal cord.
one rhytm-multiple CPGS
- refers to the idea that even though each part of the body has its own CPG, they work together through coordination to produce one overall rhythmic movement, like the coordinated action of the limbs during walking.
-Destruction of grey matter in specific spinal cord regions (L3/L4 + L6/L7) still allows for rhythmic activity, indicating that local oscillatory networks (CPGs) in the spinal cord control stepping.
This shows that individual CPGs can work together as part of a larger rhythm generator, with L5 still capable of generating rhythmic activity.
neuronal elements of Limb CPG
Identifying Limb CPG Neurons:
Limb CPGs can be identified using techniques like activity-dependent labeling, genetic approaches, and electrophysiology.
Only about 0.1% of spinal cord neurons are part of the CPG.
Models for Limb CPG – Contribution of Endogenous Bursters
Endogenous Bursting Neurons (Hb9 interneurons):
Some neurons have endogenous bursting properties that help generate rhythmic activity, especially during locomotion.
At the start of locomotion, rhythmic activity is generated by network interactions.
During slow locomotion, it’s a combination of network interactions and pacemaker activity.
During fast locomotion, rhythmic activity is mainly driven by pacemaker activity.
Organisation of Mammalian Limb CPGs
CPGs for Individual Joints:
There are individual spinal CPGs for each joint and muscle group, which combine to create a limb CPG.
Limb CPGs interact to coordinate overall limb movement.
These limb CPGs are activated by commands from the brainstem and higher control centers.
