Learning & Memory Part 1 Flashcards
What are the short-term forms of synaptic plasticity that affect neurotransmitter release?
Facilitation, augmentation, and potentiation enhance neurotransmitter release, while synaptic depression reduces it.
What is synaptic depression?How is it produced experimentally?
Persistent, activity-dependent weakening of synaptic
transmission, typically due to depletion of neurotransmitter vesicles
- Produced by low-frequency stimulation of Schaffer collaterals for 10–15 minutes.
Difference vs short term and long term plasticity
Short-term plasticity: Rapid, temporary changes in synaptic strength.
Long-term plasticity: Long lasting, potentially permanent alterations in synaptic connections.
Examples of such long-lasting plasticity:
Long-term potentiation (LTP), which strengthens synaptic connections, and long-term depression (LTD), which weakens them
What characterizes long-term plasticity?
Long-term plasticity involves alterations in synaptic transmission over 30 minutes or more
Short Term Plasticity: Synaptic Facilitation
A rapid increase in synaptic strength caused by consecutive action potentials, lasting tens of milliseconds.
What is synaptic facilitation associated with?
Prolonged elevated presynaptic calcium levels following synaptic activity.
What happens at the frog neuromuscular synapse in relation to the amount of transmitter released from the presynaptic terminal?
Synaptic depression increases as more transmitter is released because repeated stimulation depletes neurotransmitter in vesicles, weakening the synaptic connection.
What happens to synaptic responses at the squid giant synapse when external calcium levels are typical?
When external calcium levels are normal, a high-frequency tetanus causes a notable decrease in synaptic signals (EPSPs), termed “depression,” at the squid giant synapse.
How do synaptic responses change when you slightly lower the external calcium concentration at the squid giant synapse?
Lowering external calcium concentration slightly at the squid giant synapse produces mixed effects on synaptic responses: some signals weaken (depression), while others strengthen (augmentation).
What occurs when you further reduce the external calcium concentration at the squid giant synapse?
Furhter decreasing the external calcium concentration at the squid giant synapse to very low levels, the weakening effect (depression) is completely eliminated, leaving only the strengthening effect (augmentation).
What form of shot-term synaptic plasticity increases neurotransmitter release and synaptic vesicle fusion with the plasma membrane for a few seconds?
Augumentation
What form of shot-term synaptic plasticity increases neurotransmitter release and synaptic vesicle fusion with the plasma membrane over a time scale of tens of seconds to minutes?
Potentiation
Short-term forms of synaptic plasticity can interact. Label the changes in EPP at the peripheral neuromuscular synapse.
1.) ______
2.) ______
3.) ______
4.) ______
facilitation (less than a millisecond), augmentation (a few seconds), depression, potentiation (tens of seconds to minutes)
What are the different processes involved in synaptic plasticity?FAD DAP
Facilitation: Rapidly boosted synaptic strength with closely timed action potentials.
Augmentation: Enhanced synaptic signals fueled by calcium ions.
Depression: Weakening of synaptic strength, like a drop.
Potentiation: Prolonged synaptic strengthening post high-frequency stimulation.
Decay of Facilitation: Gradual fading of initial facilitation.
Augmentation Decay: Reduction of augmentation over time.
Decay of Depression: Diminishing of depression effect.
Post-Tetanic Potentiation: Heightened synaptic strength post high-frequency “Tetanus”.
What model organism (with only ~18,000 neurons) is used to study synaptic plasticity?
Aplysia (sea slug)
A light touch to the _______ of an Aplysia results in ____
Siphon; withdrawal of the animal’s gill, allowing the study of stimulus responses over time.
What form of plasticity in Aplysia causes the animal to become less responsive to repeated stimulation?
Habituation
What form of plasticity in Aplysia allows the animal to generalize an aversive stimulus (such as a shock) to other non-noxious stimuli?
Sensitization (both short-term and long-term)- heightened responsiveness in response to repeated or intense stimulation.
What happens with repeated applications of tail shocks in relation to gill withdrawal behavior?
Repeated tail shocks cause prolonged sensitization of the gill withdrawal response, altering the behavior for days or weeks.
What happens in the neural circuitry during sensitization in Aplysia?
During sensitization in Aplysia, touching the siphon skin activates sensory neurons, exciting interneurons and gill motor neurons, causing the gill muscle to contract and resulting in a withdrawal response, retracting the gill.
What happens at the sensory neuron-motor neuron synapse before sensitization in Aplysia?
Activating the siphon sensory neurons causes EPSPs in gill motor neurons.
What occurs when the sensory neuron-motor neuron synapse is repetitively activated?
Synaptic depression happens, leading to a reduction in EPSPs in motor neurons.
What is the role of serotonergic modulatory interneurons in sensitization?
They enhance neurotransmitter release from sensory neurons to motor neurons, boosting EPSP in motor neurons. increasing the EPSP in motor neurons.
What is habituation in the context of synaptic transmission?
A neuron becomes less responsive to repeated stimuli, leading to reduced synaptic transmission.
What is sensitization?
Occurs when a reaction to a stimulus causes an increased reaction to a
second stimulus
Mechanism for Short-Term Sensitization
- Short-term sensitization involves serotonin binding to G-protein-coupled receptors on presynaptic terminals
- This triggers cAMP production, activation of pKA, PKA phosphorylates K+ channels, reducing their opening
- Extended presynaptic action potentials increases Ca2+ influx, increasing neurotransmitter release for short-term sensitization.
What distinguishes short-term sensitization from long-term sensitization regarding the mechanism of change?
Short-term sensitization is due to increased glutamate release from presynaptic terminals.
due to PKA.
Long-term sensitization occurs due to changes in gene exprssion, causing expression of proteins that change pKA activity and lead to changes in synapse growth
What does Habituation causes: synaptic (EXCITATION / DEPRESSION) ?
Ssynaptic depression by reducing glutamate release at the synapse between sensory and motor neurons, thus decreasing the number of available synaptic vesicles for release.
Sensitization causes synaptic (EXCITATION / DEPRESSION)
Synaptic excitation by releasing serotonin onto sensory presynaptic terminals. This enhances glutamate release between sensory and motor neurons, leading to increased firing of motor neurons.
Long-Term Sensitization Steps
- Serotonin binds to G-coupled receptors on sensory neuron terminals.
- Adenylyl cyclase stimulates cAMP production.
- cAMP binds to regulatory subunits of pKA (protien kinase A)
- Catalytic subunits of PKA are released, phosphorylating proteins, including CREB.
- CREB prompts synthesis of proteins like ubiquitin hydrolase and a trasncriptional activator protein called C/EBP.
- These changes lead to structural increases in synapses, resulting in a long-lasting enhancement of synaptic strength
CREB and C/EBP Function
Act as transcription factors, helping to turn specific genes on or off in response to various cellular signals,
What form of long-term synaptic plasticity increases synaptic strength?
long-term potentiation (LTP)
What form of long-term synaptic plasticity decreases synaptic strength?
long-term depression (LTD)
What does long-term potentiation depend on?
A trisynaptic circuit between three hippocampal elements: CA1 synapse, CA3 synapse, Schaffer collaterals (connects the two pyramidal neurons)
Which tract carries info out of the hippocampus and into the limbic system into the amygdala?
Fornex
Dentate Gyrus
Region of the hippocampus known for its high rate of neurogenesis, where new neurons are born throughout life.
Trisynaptic Circuit
Plays a critical role in memory formation and spatial navigation in the brain.
To evoke an LTP response you need to:
Stimulate the neurons with a high frequency stimulus,
What happens when LTP is induced at one synapse (pathway 1) in terms of other synapses contacting the same neuron (pathway 2)?
LTP does not automatically occur in other, inactive synapses (pathway 2) that contact the same neuron. This demonstrates the SPECIFICITY of LTP.
How can you make both sets of synapses stronger?
When you activate the weak stimulation of pathway 2 along with strong stimulation of pathway 1, it causes both sets of synapses to be strengthened
Specificity of LTP:
The specificity of LTP means that strong activity can cause LTP at an active synapse without affecting nearby inactive synapses.
Associativity Property LTP:
Weak stimulation of a synapse doesn’t induce LTP in its pathway, but when a neighboring pathway is strongly activated, both pathways are strengthened.
What occurs when depolarization happens at the NMDA channel?
Depolarization expels Mg2+ from the NMDA channel, allowing current to flow into the postsynaptic cell.
How does CaMKII (Calcium/Calmodulin-dependent protein kinase II) respond to an increase in calcium levels?
CaMKII gets activated indirectly because calcium binds to calmodulin
What happens when calmodulin binds to calcium ions?
Calmodulin undergoes a conformational change, and this calcium-calmodulin complex can then activate CaMKII.
How does a peptide blocker prevent or stop the process of LTP?
Disrupts key proteins or receptors involved in LTP, stopping the normal strengthening of neural connections.
Morris Water Test Function
Used to assess hippocampal function related to spatial navigation.
What is the impact of a mutation in the CaMKII protein in the context of this test?
It can impair the ability to learn the task effectively, showing that CaMKII is crucial for learning and memory.
What receptor(s) is/are found at silent synapses?
NMDA (only)
What receptor(s) is/are found at functional synapses?
NMDA and AMPA
What is a silent synapse known for?
A silent synapse is known for not spontaneously transmitting signals in a resting state.
How are silent synapses converted to active excitatory synapses?
Silent synapses are turned “on” when (induced by LTP) when AMPA receptors are inserted into the postsynaptic membrane, allowing it to respond to glutamate.
signaling mechanisms underlying LTP (Long-Term Potentiation): GATE-CA-CHANGE-AMP
GATE (Glutamate, Activation, Threshold, Entry):
1. Glutamate released.
2. NMDA receptors activated.
3. Calcium enters postsynaptic neuron, activating proteins like CaMKII and PKC in the cell
4. AMPA receptors inserted.
5. Synapse grows.
6. Genes activated for long-lasting changes.
What’s responsible for the late part of LTP?
The late part of LTP occurs when PKA activates the regulator CREB, which switches on genes leading to long-lasting changes in PKA activity and synapse structure.
What characterizes the initial phase of LTP?
The initial phase is a rapid and short-term strengthening of synaptic connections that occurs immediately after high-frequency stimulation
What’s responsible for the late part of LTP?
The late part of LTP occurs when PKA activates the regulator CREB, which switches on genes leading to long-lasting changes in PKA activity and synapse structure.
Explain how LTD weakens synaptic connections by making the postsynaptic neuron less responsive to signals from other neurons.
- Low Calcium Rise: Small increase in calcium (Ca2+) in postsynaptic neuron triggers process.
- Protein Phosphatases Activate: Low calcium activates protein phosphatases.
- AMPA Receptor Internalization: Protein phosphatases cause AMPA receptors to move inside neuron.
- Less Responsive: Moving AMPA receptors inside makes neuron less responsive to glutamate.
Facilitation, augmentation, and potentiation enhance neurotransmitter release and are caused by persistent actions of:
Calcium ions within the presynaptic terminal
SA: How do second messenger systems “turn off” after they have been turned on?
Enzymes such as phosphatases and phosphodiesterases facilitate turning off of second messenger cascades.
SA: Why is it crucial that Ca2+ levels are maintained at low concentrations inside the cell? What is the mechanism of action that maintains a low concentration?
Ca2+ is a second messenger, and increases in its intracellular concentration can trigger signaling cascades and other events inside the cell.
Pumping of Ca2+ into the
intracellular compartments and extracellular space maintains low levels of Ca2+ level
SA:How do the short-term forms of synaptic plasticity contribute to learning and memory?
They dynamically alter communication at chemical synapses based on recent activity, shaping how we learn and remember.
SA: What is the synaptic basis for short-term sensitization in Aplysia?
In Aplysia, short-term sensitization is based on modulatory interneurons enhancing the synaptic connections between sensory and motor neurons in the gill withdrawal circuit.
SA: What is needed for: a) the initial acquisition of LTP and
b) the maintenance of longlasting LTP?
Initial Acquisition of LTP:
- Increase in postsynaptic Ca2+
Maintenance of Long-lasting LTP:
- Increase in postsynaptic AMPA receptors with subsequent
changes in protein expression in postsynaptic cell
SA: Compare cellular mechanisms involved in LTP versus LTD
LTP (Long-Term Potentiation):
- accompanied by an Increase in postsynaptic AMPA receptors
LTD (Long-Term Depression):
- Decrease in postsynaptic AMPA receptors
SA: Why is it thought that Ca2+ levels might be involved in spike timing-dependent
plasticity (STDP)?
High postsynaptic Ca2+ levels lead to LTP when presynaptic activity comes first, while low levels result in LTD when postsynaptic potential comes first.
SA: What might LTP and epilepsy have in common?
LTP and epilepsy both involve long-term changes in neuronal circuits.
