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Related Concept Videos

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.
Hebbian LTP
LTP can occur when presynaptic neurons...

Neuroplasticity

Neuroplasticity

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.

Plasticity

Plasticity

Plasticity is the property where an object loses its elasticity and undergoes irreversible deformation, even after the deformation forces are eliminated. If a material deforms irreversibly without increasing stress or load, then this is called ideal plasticity. For example, when a force is applied to an aluminum rod, it changes its shape, but it does not return to its original shape once the force is removed. Plastic deformation or ductility is thus a permanent deformation or change in the...

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.

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.
Calcium Ion Concentration Mechanism
If over time, all...

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Related Experiment Video

Updated: May 12, 2026

3D Modeling of Dendritic Spines with Synaptic Plasticity

3D Modeling of Dendritic Spines with Synaptic Plasticity

Published on: May 18, 2020

Drug-evoked synaptic plasticity: beyond metaplasticity.

Meaghan C Creed¹, Christian Lüscher

¹Department of Basic Neuroscience, Rue Michel-Servet 1, University of Geneva, 1211 Geneva, Switzerland.

Current Opinion in Neurobiology

|April 11, 2013

Summary

Cocaine alters brain circuits, creating lasting changes that may drive addiction. Targeting synaptic activity in the nucleus accumbens (NAc) could reverse these drug-induced behavioral changes.

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Ex Vivo Optogenetic Interrogation of Long-Range Synaptic Transmission and Plasticity from Medial Prefrontal Cortex to Lateral Entorhinal Cortex

Published on: February 25, 2022

Area of Science:

Neuroscience
Addiction Research
Molecular Biology

Background:

Addictive drugs, like cocaine, induce synaptic plasticity in brain regions such as the ventral tegmental area (VTA) and nucleus accumbens (NAc).
These neuroplastic changes are thought to underlie the cellular mechanisms of addiction.
Initial alterations in synaptic transmission can lead to later, more extensive remodeling of neural circuits.

Purpose of the Study:

To investigate the persistent synaptic and cellular changes in the NAc following cocaine exposure.
To explore the potential of manipulating NAc synaptic activity to reverse drug-induced behavioral alterations.

Main Methods:

Electrophysiological recordings in VTA and NAc.
Behavioral assessments following cocaine administration.
Molecular analyses of synaptic proteins.

Main Results:

Cocaine exposure induced persistent changes in excitatory transmission in the VTA, lasting for days.
These initial changes facilitated later remodeling in the NAc.
Prolonged cocaine exposure resulted in specific, enduring synaptic and cellular alterations in the NAc, correlating with behavioral changes.

Conclusions:

Synaptic plasticity in the VTA and NAc is a key cellular correlate of cocaine addiction.
The NAc undergoes significant remodeling following chronic cocaine use, contributing to addiction-related behaviors.
Targeting synaptic activity within the NAc offers a potential therapeutic strategy to reverse the effects of addictive drugs.