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Long-term Potentiation

Long-term Potentiation

Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.

Long-term Potentiation

Long-term Potentiation

Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
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Neuroplasticity

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Neuroplasticity reflects the brain's remarkable capacity to adapt and evolve, responding dynamically to learning, experiences, or injury by reorganizing its neural circuitry. This reorganization involves creating new neural connections and refining old ones through a series of biological processes that contribute to the brain's lifelong development and adaptability.

Chemical Synapses

Chemical Synapses

Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...

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Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...

Long-term Depression

Long-term Depression

Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
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3D Modeling of Dendritic Spines with Synaptic Plasticity

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Published on: May 18, 2020

Synaptic AMPA receptor composition in development, plasticity and disease.

Jeremy M Henley¹, Kevin A Wilkinson¹

¹School of Biochemistry, Centre for Synaptic Plasticity, Biomedical Sciences Building, University of Bristol, Bristol BS8 1TD, UK.

Nature Reviews. Neuroscience

|April 16, 2016

Summary

The roles of individual AMPA receptor (AMPAR) subunits in trafficking are being re-evaluated. This review explores subunit assembly, trafficking, and function in neurological health and disease.

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Area of Science:

Neuroscience
Molecular Biology
Cellular Biology

Background:

AMPA receptors (AMPARs), composed of GluA1-4 subunits, are critical for fast excitatory neurotransmission.
Subunit composition traditionally dictates AMPAR trafficking, crucial for synaptic plasticity and neuronal stress responses.
Recent findings challenge the strict subunit dependence of AMPAR trafficking.

Purpose of the Study:

To critically review the known, uncertain, and unknown roles of individual AMPAR subunits in receptor assembly and trafficking.
To re-evaluate the prevailing view on subunit-dependent AMPAR trafficking.
To discuss the impact of subunit composition on AMPAR function in physiological and pathological conditions.

Main Methods:

Literature review and synthesis of existing research on AMPAR subunit composition and trafficking.
Analysis of studies investigating AMPAR assembly, surface expression, and synaptic localization.
Discussion of evidence supporting and refuting subunit-dependent trafficking mechanisms.

Main Results:

The precise role of individual subunits (GluA1-4) in determining AMPAR trafficking dynamics remains debated.
Evidence suggests that factors beyond subunit composition may significantly influence AMPAR trafficking.
Understanding these roles is crucial for comprehending synaptic plasticity and neurological disorders.

Conclusions:

A reappraisal of AMPAR subunit-dependent trafficking is necessary.
Further research is needed to elucidate the complex interplay between subunits, trafficking, and function.
Clarifying these mechanisms is vital for developing therapeutic strategies for neurological diseases.