Mechanisms of Long-Term Potentiation and Memory Formation(2)

LTP

Long-term potentiation; enhances synaptic strength.

CaMKII

Calcium/calmodulin-dependent kinase involved in LTP.

Early LTP

Lasts 1-2 hours; no protein synthesis needed.

Late LTP

Lasts days; requires RNA and protein synthesis.

NMDA Receptors

Glutamate receptors crucial for LTP induction.

Calmodulin

Calcium-binding protein activating CaMKII.

HFS

High-frequency stimulation inducing LTP.

AMPARs

AMPA receptors; increase synaptic efficacy.

NMDAR1

Subunit of NMDA receptor; essential for LTP.

Glutamate

Neurotransmitter activating NMDA and AMPA receptors.

Coincidence Detection

NMDA receptors require simultaneous signals for activation.

Calcium Influx

Ca2+ entry through NMDA receptors during LTP.

CNQX

Antagonist for non-NMDA receptors (AMPA, Kainate).

APV

NMDA receptor antagonist inhibiting LTP.

Spatial Learning

Cognitive process impaired by NMDAR1 knockout.

RNA Transcription

Required for late LTP and long-term memory.

Protein Synthesis

Necessary for late LTP and memory consolidation.

Heteromeric NMDA Receptors

Formed by different NMDA subunits.

Gating Mechanism

Mg2+ blocks ion flow in NMDA receptors.

Postsynaptic Depolarization

Removes Mg2+ block, allowing Ca2+ entry.

Actinomycin

Inhibits RNA transcription affecting memory.

Anisomycin

Inhibits protein translation affecting memory.

D-serine

Co-agonist for NMDA receptor activation.

GluN Subunits

Diverse NMDA receptor components affecting function.

Input Specificity

LTP occurs only at stimulated synapses.

Intracellular Ca2+

Calcium ions that increase during LTP activation.

Associativity

LTP at subthreshold synapses with concurrent stimulation.

Ca2+/calmodulin

Complex that activates CaMKII after calcium influx.

Autophosphorylation

Self-phosphorylation of CaMKII for persistent activation.

GluR1 phosphorylation

CaMKII phosphorylates GluR1 to enhance AMPAR conductance.

Slot hypothesis

Mechanism explaining AMPAR trapping at synapses.

TARP stargazin

Protein that anchors AMPARs at synapses.

CaMKII-T286A mutant

Mutant lacking LTP due to CaMKII dysfunction.

Morris Water Maze

Test assessing spatial learning and memory.

Exocytosis of AMPARs

Process of AMPARs being inserted into the membrane.

PSD95

Protein that anchors AMPARs at postsynaptic density.

Ca2+ entry

Calcium influx triggering LTP signaling pathways.

CaMKII holoenzyme

Complex of 12 subunits forming CaMKII structure.

Kinase domain

Region in CaMKII responsible for phosphorylation activity.

Linker region

Connects hub domain and kinase domain in CaMKII.

C-terminal domain

Hub domain facilitating subunit organization in CaMKII.

Calcium signaling

Cellular communication mechanism involving calcium ions.

Proteolysis

Breakdown of proteins, influencing synaptic changes.

Microtubule motors

Proteins aiding in transport within neurons.

Conductance increase

Enhanced ion flow through AMPA receptors during LTP.