Molecular Basis of Synaptic Plasticity I

<p>They completely block LTP (C)</p> Signup and view all the answers

<p>Increased calcium influx through L-type Ca2+ channels (C)</p> Signup and view all the answers

<p>The structural alterations of synapses due to learning (D)</p> Signup and view all the answers

<p>Calcium permeable AMPARs (B)</p> Signup and view all the answers

<p>Tetanus stimulation (D)</p> Signup and view all the answers

<p>Large Ca2+ influx into the presynaptic terminal (A)</p> Signup and view all the answers

<p>It serves as a coincidence detector (C)</p> Signup and view all the answers

<p>Release of 5-HT onto the sensory neuron (D)</p> Signup and view all the answers

<p>Abrogation of LTP in Mossy Fibers (C)</p> Signup and view all the answers

<p>It stimulates the production of cAMP (D)</p> Signup and view all the answers

<p>Inhibition of presynaptic vesicle release (D)</p> Signup and view all the answers

<p>It enhances synaptic transmission (A)</p> Signup and view all the answers

<p>Siphon touch (C)</p> Signup and view all the answers

<p>It can last for days or even weeks. (D)</p> Signup and view all the answers

<p>Conditioned stimuli can be strengthened through LTP when paired with unconditioned stimuli. (D)</p> Signup and view all the answers

<p>They facilitate postsynaptic strengthening during synaptic activity. (C)</p> Signup and view all the answers

<p>LTD protocols reverse prior conditioning effects. (B)</p> Signup and view all the answers

<p>The mechanism of LTP suggests a causal link to memory storage. (B)</p> Signup and view all the answers

<p>Both auditory and visual stimuli. (D)</p> Signup and view all the answers

<p>To strengthen synaptic connections in specified pathways. (A)</p> Signup and view all the answers

<p>It is involved in auditory processing linked to conditioned stimuli. (C)</p> Signup and view all the answers

<p>It enhances the actions of NSF to prevent removal of GluA2. (B)</p> Signup and view all the answers

<p>PKA-mediated activation of CREB for structural changes. (A)</p> Signup and view all the answers

<p>It ensures PKMζ is constitutively active without external signals. (C)</p> Signup and view all the answers

<p>Tetanic stimulation. (D)</p> Signup and view all the answers

<p>Activation of NMDA receptors and subsequent Ca2+ influx. (C)</p> Signup and view all the answers

<p>By activating local translation of mRNA. (C)</p> Signup and view all the answers

<p>It increases the local translation of PKMζ mRNA. (C)</p> Signup and view all the answers

<p>The clustering of new AMPA receptors on postsynaptic membranes. (D)</p> Signup and view all the answers

<p>Decreased conductance at positive potentials (C)</p> Signup and view all the answers

<p>GluA1, GluA3, and GluA4 (C)</p> Signup and view all the answers

<p>GluA2-lacking AMPARs (C)</p> Signup and view all the answers

<p>Erases fear memories in various species (B)</p> Signup and view all the answers

<p>Promotion of the synaptic response through increased calcium permeability (A)</p> Signup and view all the answers

<p>Schiller et al., Nature 2010 (C)</p> Signup and view all the answers

<p>Promotes the switch to synaptic cp-AMPARs (A)</p> Signup and view all the answers

<p>By the ratio of positive to negative slope conductance (B)</p> Signup and view all the answers

<p>Prevents GluA1 from being phosphorylated (A)</p> Signup and view all the answers

<p>Absence of GluA2 subunit (B)</p> Signup and view all the answers

<p>NMDAR-dependent long-term depression (LTD) (A)</p> Signup and view all the answers

<p>Promotes phosphorylation at S845 (A)</p> Signup and view all the answers

<p>Influences their permeability to calcium ions (C)</p> Signup and view all the answers

<p>It contributes to the consolidation of fear memories (A)</p> Signup and view all the answers

<p>They are involved in the bidirectional regulation of synaptic strength. (A)</p> Signup and view all the answers

<p>cp-AMPARs lacking GluA2 (A)</p> Signup and view all the answers

<p>It plays a role in long-term depression processes. (A)</p> Signup and view all the answers

<p>Limits AMPAR recycling to GluA2-containing AMPARs (B)</p> Signup and view all the answers

<p>S845 (D)</p> Signup and view all the answers

Long-term potentiation; a strengthening of synaptic transmission.

Different forms of LTP exist, each involving distinct cellular and molecular mechanisms.

Movement of AMPA receptors, impacting post-synaptic cell sensitivity to neurotransmitters.

Initial phase of LTP; short-term strengthening.

Later phase; long-term strengthening; gene expression changes.

LTP that strengthens synaptic transmission at the presynaptic terminal.

Type of synapse, often used as a model for presynaptic LTP.

A high-frequency stimulation protocol used to induce LTP.

A significant increase in calcium ions entering the presynaptic terminal of a neuron.

A complex that activates in response to high calcium levels, starting a cascade of events.

Protein Kinase A (PKA) is activated as a result of the previous step in the cascade.

Higher levels of glutamate, a neurotransmitter, are released into the synapse.

A learning process where two stimuli are linked together to produce a learned response.

Enhancement of neurotransmitter release from the presynaptic neuron.

A stimulus that triggers an action potential (AP) in a sensory neuron.

Stimulus triggering serotonin (5-HT) release, enhancing cAMP production.

A longer-lasting form of LTP (long-term potentiation) that involves structural changes in the synapse, triggered by calcium influx and activation of protein kinases.

A short-term form of LTP primarily caused by the activation of AMPA receptors, leading to calcium influx and increased synaptic strength.

A constitutively active protein kinase C isoform that maintains LTP by preventing AMPA receptor removal from the synapse.

A type of glutamate receptor that plays a role in early LTP and synaptic transmission.

The process that keeps an enhanced synaptic connection over time.

The entry of calcium ions into a neuron, often triggered by NMDA receptor activation and leading to biological changes, such as in LTP.

Physical alterations to the synapse, such as the addition of new receptors or synapses, that are part of the long-term strengthening of a synapse during Late LTP.

An important transcription factor that gets activated in late LTP; which can change gene expression and thus the making of more proteins to help in neuron communication.

LTP (Long-Term Potentiation) is a process that strengthens synaptic connections and may be causally linked to memory formation.

Experimentally pairing specific stimuli with a response to study how LTP affects memory by controlling neural pathways with light.

A learned response to a stimulus after repeated pairing with another stimulus.

Experiments suggest a potential cause-and-effect relationship between LTP and the formation of certain types of memories.

A stimulus paired with a stronger, triggering reaction (foot shock) to study LTP's role in memory.

Strengthening of the connection between nerve cells following a stimulus.

Protocol used to reverse experience-dependent synaptic changes for studying memory.

The efficiency at which one neuron communicates with another.

AMPA receptors that allow calcium ions to pass through the channel, often involved in synaptic plasticity and learning.

The ability of the nervous system to change and adapt in response to experiences.

The process of strengthening a memory trace when it is retrieved or reactivated.

Different protein components that make up AMPA receptors, affecting their function and properties.

AMPA receptors missing the GluA2 subunit, affecting their conductance at positive potentials.

Learning to associate a neutral stimulus with a fearful event.

Changes in the strength of synaptic transmission at the postsynaptic neuron.

A measure of asymmetry in the current-voltage relationship across a membrane, comparing current at positive and negative potentials.

The ability of a synapse to allow ions to flow across the membrane.

The updating of a retrieved memory by a new experience.

Glutamate receptors without GluA2 subunit, involved in synaptic plasticity.

Protein that limits AMPAR recycling, influencing synaptic CP-AMPARs.

Strengthening of a synapse, increasing responsiveness.

Stabilizes GluA1 homomers, making them live longer on the surface.

Linked to LTD (Long-term Depression), removing CP-AMPARs.

Dampens Amygdala Transmission by removing synaptic CP-AMPARs.

GluA1 replaced Ser845 with Ala, blocking reconsolidation.

Weakening of synaptic transmission.

The ability of synapses (connections between neurons) to strengthen or weaken over time.

Adding a phosphate group to a protein, changing its properties.