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Related Concept Videos

Long-term Depression01:03

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...
Long-term Depression01:05

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 Potentiation01:25

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...
Long-term Potentiation01:35

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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Related Experiment Video

Updated: May 22, 2026

Evaluation of Synapse Density in Hippocampal Rodent Brain Slices
07:44

Evaluation of Synapse Density in Hippocampal Rodent Brain Slices

Published on: October 6, 2017

Reversible synaptic deficits in early-stage batten disease.

Masood Ahmad Wani1,2, Chloe M Hall3, Thomas Mittmann2,3

  • 1Institute of Pathophysiology, University Medical Center of the Johannes Gutenberg University Mainz, 55128, Mainz, Germany.

Journal of Translational Medicine
|May 21, 2026
PubMed
Summary

Juvenile neuronal ceroid lipofuscinosis (JNCL) involves CLN3 gene mutations, causing cognitive decline. This study shows CLN3 is vital for synaptic function and gene therapy can restore function, offering hope for treatment.

Keywords:
Batten diseaseExcitabilityGene therapyLysosomal storage diseasesLysosomesSynapse

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Single Synapse Indicators of Glutamate Release and Uptake in Acute Brain Slices from Normal and Huntington Mice
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Electroconvulsive Seizures in Rats and Fractionation of Their Hippocampi to Examine Seizure-induced Changes in Postsynaptic Density Proteins

Published on: August 15, 2017

Related Experiment Videos

Last Updated: May 22, 2026

Evaluation of Synapse Density in Hippocampal Rodent Brain Slices
07:44

Evaluation of Synapse Density in Hippocampal Rodent Brain Slices

Published on: October 6, 2017

Single Synapse Indicators of Glutamate Release and Uptake in Acute Brain Slices from Normal and Huntington Mice
08:27

Single Synapse Indicators of Glutamate Release and Uptake in Acute Brain Slices from Normal and Huntington Mice

Published on: March 11, 2020

Electroconvulsive Seizures in Rats and Fractionation of Their Hippocampi to Examine Seizure-induced Changes in Postsynaptic Density Proteins
09:07

Electroconvulsive Seizures in Rats and Fractionation of Their Hippocampi to Examine Seizure-induced Changes in Postsynaptic Density Proteins

Published on: August 15, 2017

Area of Science:

  • Neuroscience
  • Genetics
  • Molecular Biology

Background:

  • Juvenile neuronal ceroid lipofuscinosis (JNCL), also known as Batten Disease, is a childhood neurodegenerative disorder.
  • It stems from mutations in the CLN3 gene, leading to progressive cognitive decline.
  • Current treatments are limited, and the neuronal function of CLN3 remains unclear.

Purpose of the Study:

  • To investigate the role of CLN3 in neuronal function and synaptic plasticity.
  • To explore the pathomechanisms underlying cognitive impairment in JNCL.
  • To assess the potential of gene therapy for treating JNCL.

Main Methods:

  • Electrophysiological recordings (patch clamp, microelectrode arrays) in Cln3-deficient mouse models.
  • Confocal imaging to quantify dendritic spine density.
  • Adeno-associated virus (AAV)-mediated gene re-expression of CLN3 combined with optogenetics.

Main Results:

  • Loss of CLN3 impairs synaptic vesicle release and reduces synaptic strength.
  • Deficits in intrinsic neuronal excitability and network activity were observed.
  • CLN3 is essential at both pre- and postsynaptic sites for neuronal function.
  • AAV9-mediated gene therapy restored synaptic function in early-stage Cln3-deficient mice.

Conclusions:

  • CLN3 is critical for maintaining synaptic integrity and function.
  • Gene therapy can reverse established synaptic deficits in JNCL models.
  • The therapeutic window for JNCL may extend to stages with functional impairments.
  • Early synaptic deficits serve as valuable readouts for preclinical research.