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

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Related Experiment Video

Updated: Jul 1, 2026

Paradigms for Pharmacological Characterization of C. elegans Synaptic Transmission Mutants

Paradigms for Pharmacological Characterization of C. elegans Synaptic Transmission Mutants

Published on: August 18, 2008

Riluzole Restores Circuit and Behavioral Function Altered by Allele-Specific Expression-Mediated LINC02449-CPLX1

Chaoying Ni^1,2, Jin-Ming Liu^1,3, Tengfei Yang^1,2

¹Key Laboratory of Mental Health of the Ministry of Education, Guangdong-Hong Kong-Macao Greater Bay Area Center for Brain Science and Brain-Inspired Intelligence, Guangdong-Hong Kong Joint Laboratory for Psychiatric Disorders, Guangdong Province Key Laboratory of Psychiatric Disorders, Guangdong Basic Research Center of Excellence for Integrated Traditional and Western Medicine for Qingzhi Diseases, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China.

Schizophrenia Bulletin

|March 21, 2026

Summary

This summary is machine-generated.

Pharmacological intervention with Riluzole reversed synaptic and behavioral abnormalities in mice caused by altered long non-coding RNA expression linked to psychiatric disorders. This suggests Riluzole as a potential treatment for conditions involving glutamatergic imbalance.

Keywords:

CPLX1 bipolar disorder lncRNA schizophrenia

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Optogenetic Phase Transition of TDP-43 in Spinal Motor Neurons of Zebrafish Larvae

Optogenetic Phase Transition of TDP-43 in Spinal Motor Neurons of Zebrafish Larvae

Published on: February 25, 2022

Area of Science:

Neuroscience
Genetics
Pharmacology

Background:

Allele-specific expression (ASE) of long non-coding RNAs (lncRNAs) contributes to synaptic dysfunction in psychiatric disorders.
A specific lncRNA, LINC02449, shows altered expression linked to bipolar disorder and schizophrenia.
Overexpression of LINC02449-G causes social deficits and altered excitatory synaptic transmission in the medial prefrontal cortex-nucleus accumbens (mPFC-NAc) circuit.

Purpose of the Study:

To investigate if the abnormalities induced by LINC02449-G are mediated by glutamatergic hyperexcitability.
To determine if these abnormalities are pharmacologically reversible.

Main Methods:

Mice received viral vector-mediated LINC02449-G overexpression in the mPFC.
Systemic administration of Riluzole was performed.
Molecular, behavioral, and electrophysiological analyses were conducted.

Main Results:

Riluzole normalized elevated Cplx1 expression and corrected mPFC-NAc circuit hyperexcitability.
Behavioral tests showed Riluzole rescued social interaction deficits and reduced repetitive behaviors.
Electrophysiological recordings confirmed Riluzole restored normal synaptic transmission.

Conclusions:

Synaptic and behavioral abnormalities driven by ASE-regulated lncRNAs are pharmacologically reversible.
Riluzole shows promise for treating neuropsychiatric disorders with glutamatergic imbalance.
ASE-regulated lncRNAs are potential therapeutic targets for psychiatric conditions.