midterm 2 Flashcards
forms of short term synaptic plasticity resulting from repeated neuron stimulation
synaptic facilitation- residual calcium causes extra NT release.
synaptic depression- depletion of NT vesicles so they cant be used as fast
post tetanic potentiation- increase in efficacy due to repeated synaptic activity
augmentation- like potentiation, but much shorter and faster.
habituation
decreased response with repeated or prolonged exposure to the same stimulus.
sensitization
increased response to noxious stimulus
How does pairing siphon touch with tail shock modify the presynaptic neuron?
A facilitator neuron releases serotonin, which activates a G-protein-coupled receptor (GPCR) in the presynaptic neuron.
What is the role of serotonin in sensitization?
Serotonin activates GPCR, which stimulates adenylyl cyclase to produce cAMP, leading to activation of PKA. PKA phosphorylates a K⁺ channel, reducing its probability of opening, which prolongs depolarization in the presynaptic neuron.
Why does prolonged depolarization lead to increased neurotransmitter release?
More Ca²⁺ influx occurs due to the extended depolarization, increasing neurotransmitter release.
Why is short-term sensitization temporary?
The potassium channels eventually become dephosphorylated, and the increased neurotransmitter release returns to normal.
What molecular change converts short-term sensitization into long-term sensitization?
Persistent PKA phosphorylates CREB, a transcription factor that promotes gene expression.
What role does ubiquitin hydrolase play in long-term sensitization?
It degrades regulatory subunits of PKA, keeping PKA persistently active and sustaining phosphorylation effects.
REVIEW NMDA receptor
- Permeable to Na+, K+ and Ca2+
- Mg2+ block at resting membrane potential
- postsynaptic depolarization relieves Mg2+ block
- Requires a co-agonist glycine
- Requirement of glutamate plus depolarization
- Some Glutamatergic synapses have only AMPA/Kainate or NMDA receptors
- Most have both AMPA and NMDA
what is a silent synapse
In utero there are synapses in the brain that have only NMDA receptors and no AMPA receptors. This means the synapse could not be activated as there would be no depolarization from the AMPA receptor. The silent synapses are turned on by the addition of AMPA receptors.
What is Long-Term Potentiation (LTP)?
LTP is a long-lasting increase in synaptic strength following high-frequency stimulation of synapses.
What hippocampal pathway is involved in LTP?
The trisynaptic circuit, including CA1 pyramidal neurons and Schaffer collaterals.
How is LTP induced experimentally
A brief high-frequency train of stimuli (tetanus) results in increased EPSP amplitude.
What happens when a tetanic stimulus is applied to one pathway?
Only that pathway shows increased synaptic response; unstimulated pathways remain unchanged.
schaffer collateral and presynaptic and postsynaptic dependency
Presynaptic stimulation alone is insufficient—LTP occurs when postsynaptic depolarization coincides with presynaptic activity.
What does it mean that LTP is synapse/input specific
When LTP is induced by activating one synapse, it does not occur in another. Therefore, each of the thousands of synapses of a neuron can store information
What is Associativity in LTP?
A weak stimulus alone does not induce LTP, but if a nearby synapse is strongly stimulated simultaneously, the weakly stimulated synapse is strengthened (slug)
What receptor is required for LTP induction?
NMDA receptors for Ca influx
How does AMPA receptor trafficking contribute to LTP
1.AMPA receptors are stored in recycling endosomes.
2.Synaptotagmin, activated by Ca²⁺, inserts AMPA receptors into the synapse.
3.More AMPA receptors = Stronger postsynaptic response to glutamate.
How do kinases contribute to LTP
calcium activates CaMKII and PKC phosphorylate AMPA receptors, increasing their conductance and insertion into the synapse.
What retrograde signal strengthens the presynaptic response in LTP?
NO enhances presynaptic glutamate release
How does LTP lead to long-term structural changes?
Persistent PKA activation leads to CREB-mediated gene expression, forming new synapses.
What is the key difference between LTP and LTD regarding Ca²⁺ signaling?
LTP: Large, fast Ca²⁺ influx activates kinases.
LTD: Small, slow Ca²⁺ increase activates phosphatases, leading to AMPA receptor internalization.