block 7- neuronal plasticity Flashcards
learning
a chnage in behvaiour as a result of experience with specific stimulus/stimuli
memory
the storage of and ability to recall learned experiences
why do we study learning and memeory in aplysia?
“(1) its nervous system has a small number of cells…..
(2) the cells are unusually large…..
(3) many of the cells are invariant and identifiable as
unique individuals.
anatomy of aplysia
-learn for understanding
-Gill: The organ that Aplysia uses for breathing.
Siphon: A small flap of tissue that protects the gill and helps control water flow into the mantle cavity.
Mantle shelf (mantle cavity):
A protective body cavity where the gill and siphon can withdraw for safety.
Head: At the front of the body — typical in any animal.
Parapodium:
Wing-like structures on the side of the body.
Help with movement and protection.
Summary:
👉 When you touch the gill or siphon, both withdraw into the mantle cavity — this reflex was used by Kandel to study learning.
nonassociative learning
-Nonassociative learning = when a single stimulus causes a change in behavior.
❗ No associations made between different stimuli or outcomes — just one stimulus.
types of Nanoassociative
Habituation:
Response gets weaker after repeated exposure to a harmless (innocuous) stimulus.
Sensitization:
Response gets stronger after a new, strong, or painful (noxious) stimulus.
Dishabituation:
Recovery of a response that had previously been weakened by habituation, triggered by a new stimulus.
how did kandal test habituation in aplysia
Setup:
Photocell placed under gill to detect gill movement (by sensing light changes).
Procedure:
Gentle tactile stimulus to the siphon every 90 seconds.
Observation:
With repeated stimulation, the gill withdrawal response gets weaker (habituates).
Key point:
The animal “learns” that the repeated gentle touch is harmless.
how did kandal test dishabituation in Alysia
After habituation has occurred…
Procedure:
A new, strong stimulus (like touching or shocking the tail) is applied.
Observation:
The gill withdrawal response becomes strong again — it “wakes up.”
Key point:
Novel or strong stimuli can reverse habituation temporarily.
how did kandal test sensitisation in aplysia
Procedure:
Give a strong, noxious shock to the tail.
Then, lightly touch the siphon (as normal).
Observation:
Even a gentle touch now causes a stronger than normal gill withdrawal.
Key point:
A painful or strong event heightens responsiveness even to mild stimuli.
memory types in aplysia
Short-term memory:
Immediate, lasts minutes to hours.
Long-term memory:
Stored changes, lasts days or longer.
Cellular Basis:
Short-term habituation/sensitization = temporary changes in synaptic strength.
Long-term memory = structural changes at synapses (e.g., new synapse formation).
Associative learning in aplysia
Associative learning = linking different stimuli together.
Classical conditioning:
Conditioned Stimulus (CS): Innocuous stimulus (e.g., tactile stimulation of siphon).
Unconditioned Stimulus (US): Strong/noxious stimulus (e.g., tail shock).
Training Process:
Pre-training: Measure normal response to CS (siphon touch).
Training:
Paired group: CS + US given together (closely timed).
Unpaired group: CS and US given separately.
US alone: Only strong stimulus, no CS.
Test: After training, test response to CS alone.
Result:
If trained with paired CS + US, siphon stimulation alone causes exaggerated gill withdrawal.
Shows learning and memory formation (memory lasts about 4 days!).
🕰️ Timing is Critical for Learning:
Best learning happens when:
CS comes slightly before US (~0.5 seconds).
No learning happens if:
US happens before CS.
US happens too long after CS (e.g., 2 seconds later).
celular basis of short term memory in aplysia
Habituation:
Repeated tactile stimulation of the siphon → response (gill withdrawal) gets smaller (weaker).
Shows short-term habituation = reduced neurotransmitter release.
Sensitization:
Strong tail shock → next tactile stimulus to siphon causes a stronger response.
Shows short-term sensitization = enhanced neurotransmitter release
cellular basis if long term memory in aplysia
Habituation:
After repeated training across days → even the first touch on the next day shows reduced response.
Indicates long-term habituation = changes to the physical structure of synapses.
Sensitization:
After strong repeated shocks + time → increased response to siphon touch persists for days.
Indicates long-term sensitization = creation of new synaptic connections.
memory retention of time
Memory Retention over Time
After training, if you test after rest:
Short-term memory: behavior changes quickly fade.
Long-term memory: behavior changes persist even after rest periods.
Extinction:
If no more reinforcement (no more shocks/stimuli), memory gradually weakens over time.
the gill-siphon withdrawal circuit
Sensory neurons from the mantle organs connect to motor neurons that control the gill muscles.
These connections can be:
Monosynaptic – direct connection (one synapse).
Disynaptic – indirect connection via an interneuron (two synapses).
The synapses use glutamate, a chemical that helps transmit signals.
This circuit is responsible for the gill-siphon withdrawal reflex.
Learning and memory (short-term and long-term) involve changes (plasticity) in this circuit.
Glutamate release plays a key role in these changes.
how can you use electrophysiology to easiliy monitor changes in activity at the synapse ?
In studies of the gill-siphon withdrawal reflex (as in Kandel’s experiments), scientists can manipulate the circuit to study learning and memory.
They insert microelectrodes into both the sensory neuron (from the siphon) and the motor neuron (to the gill).
These electrodes are filled with a saline solution, which mimics the intracellular environment.
Inside the electrode is a silver wire that detects electrical signals (changes in voltage).
The signal is sent to an amplifier, which then displays the neuronal activity on a graph (oscilloscope or computer screen).
This setup allows researchers to observe synaptic strength, measure action potentials, and see how these change with learning (e.g., during habituation or sensitisation).
short-term habituation response to the gill-siphon circuit
-To study habituation, an electrode is placed on the siphon and used to give gentle, repetitive tactile-like stimulation.
This stimulation mimics natural touch and activates sensory neurons.
You also insert electrodes into both the sensory and motor neurons to inject current, trigger action potentials, and record responses.
By comparing the motor neuron’s response before and after repeated stimulation, you can observe synaptic changes.
What Kandel Found:
At the beginning, each stimulus to the siphon causes a consistent EPSP (excitatory postsynaptic potential) in the motor neuron.
After repetitive stimulation, the EPSPs decrease in size – this is habituation.
This shows that the synapses between the sensory and motor neurons become weaker.
On a cellular level:
Action potentials in the sensory neuron become narrower.
Voltage-gated calcium channels are open for less time, since the action potential returns to rest faster.
Less calcium enters the presynaptic terminal → less glutamate is released.
This leads to weaker activation of the motor neuron → reduced gill withdrawal.
short-term sensitization response to the gill-siphon circuit
ame setup as habituation:
Electrodes in both the sensory neuron (from the siphon) and the motor neuron (to the gill).
Gentle touch to the siphon triggers the reflex.
Responses are measured before and after sensitisation training.
To induce sensitisation, apply a strong shock to the tail (activates modulatory interneurons).
🧪 What You Do:
Test motor neuron response to a gentle siphon touch:
Before the tail shock (baseline).
After the tail shock (sensitised state).
💡 Observations:
Before Tail Shock (Baseline):
Normal sensory neuron firing.
A regular-sized EPSP in the motor neuron.
Moderate gill withdrawal.
After Tail Shock (Sensitisation):
The same gentle touch now causes:
Larger EPSP in the motor neuron.
Stronger gill withdrawal than before.
This shows that the synapse has become stronger – a facilitated response.
⚙️ Mechanism Behind Sensitisation:
The tail shock activates facilitating interneurons, which release serotonin onto the sensory neuron terminals.
Serotonin causes:
More cAMP, which activates PKA (protein kinase A).
This closes potassium channels, so the action potential lasts longer.
More calcium enters → more glutamate is released.
Stronger EPSP in the motor neuron → enhanced gill response.
evidence that serotonin mediates the sensitisation response
- ignored for now if you think you need check chatgpt or maybe towards the end
how does serontonin cause spike broadening ?
-the lecture slide picture really explain this well
-there is a rising phase : Na=/ca2+ mediates this and te fall back of action potential is what we are talking about btwe is mediated by k+ channel activation and Na+ in activation
-serotonin release causes a depression is k+ channel conductance = reduces speed of repolarisations so the action potential takes longer to fall causing broadening
-in turn increases duration of action of ca+ channels
the biochemical underlying sertonergic facillation
1) Serotonin binds to G-protein coupled
serotonin receptors located on sensory neurons.
* 2) Activates adenylyl cyclase: increased
production of cAMP in sensory neurons
* 3) cAMP activates protein kinase A
* 4) Protein kinase A phosphorylates potassium
channels: reduces potassium conductance
* 5) Sensory neuron spikes are longer
the cellular basis of associtive learning experiement?
o understand how pairing a neutral stimulus (CS = siphon touch) with a strong stimulus (US = tail shock) leads to a lasting increase in the gill withdrawal reflex — a conditioned response.
🧪 The Experiment Setup:
Record from 2 sensory neurons and 1 motor neuron using sharp electrodes.
Stimulate:
Sensory Neuron A (CS) just before a tail shock (US) → Paired
Sensory Neuron B at a different time from the tail shock → Unpaired
🔍 What They Observed:
After training:
The Paired sensory neuron (CS + US) showed a stronger synapse with the motor neuron (larger EPSP).
The Unpaired sensory neuron did not show this strengthening.
This shows that pairing is critical for synaptic changes to occur — it’s not just the shock or the touch alone.
Why Does Pairing Strengthen the Synapse?
It all comes down to how adenylyl cyclase (an enzyme in the sensory neuron) is activated:
Serotonin is released by the interneuron during the tail shock (US).
Serotonin binds to receptors on the sensory neuron terminal.
This normally activates adenylyl cyclase, which leads to cAMP production, and strengthens the synapse.
But there’s a boost when the CS (siphon stimulus) comes just before the US:
The CS (sensory neuron firing) causes calcium to enter the sensory neuron terminal.
Calcium “primes” the adenylyl cyclase, making it more responsive to serotonin.
So when serotonin arrives just after the calcium signal, the enzyme is super-activated.
This leads to more cAMP, stronger synaptic facilitation, and lasting plasticity (learning).
✅ Key Takeaway:
Timing matters — the pairing of stimuli allows a biochemical “coincidence detector” (adenylyl cyclase) to enhance synaptic strength.
This is the cellular mechanism of associative learning: the neuron “learns” the CS predicts the US.
How Serotonin Triggers Memory
Both depend on serotonin and cAMP signaling, but the duration and extent of activation lead to different outcomes:
