Related Experiment Video
Updated: Mar 23, 2026

Long-term Potentiation of Perforant Pathway-dentate Gyrus Synapse in Freely Behaving Mice
Published on: November 29, 2013
Changes in Synaptic Transmission and Long-term Potentiation Induction as a Possible Mechanism for Learning Disability
Ghasem Mosayebi1, Mohammad Reza Soleyman1, Mostafa Khalili1
1Department of Microbiology and Immunology, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran.
Purpose:
Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system. It has been shown that memory deficits is common in patients with MS. Recent studies using experimental autoimmune encephalomyelitis (EAE) as an animal model of MS have shown that indicated that EAE causes hippocampal-dependent impairment in learning and memory. Thus far, there have been no in vivo electrophysiological reports describing synaptic transmission in EAE animals. The aim of the present work is to evaluate the synaptic changes in the CA1 region of the hippocampus of EAE rats.
Methods:
To evaluate changes in synaptic transmission in the CA1 region of the hippocampus of EAE rats, field excitatory postsynaptic potentials (fEPSPs) from the stratum radiatum of CA1 neurons, were recorded following Schaffer collateral stimulation.
Results:
The results showed that EAE causes deficits in synaptic transmission and long-term potentiation (LTP) in the hippocampus. In addition, paired-pulse index with a 120 msec interstimulus interval was decreased in the EAE group. These findings indicate that EAE might induce suppression in synaptic transmission and LTP by increasing the inhibitory effect of GABAB receptors on the glutamate-mediated EPSP.
Conclusions:
In conclusion, influence of inflammation-triggered mechanisms on synaptic transmission may explain the negative effect of EAE on learning abilities in rats.
Insights
Experimental autoimmune encephalomyelitis (EAE) in rats impairs hippocampal synaptic transmission and long-term potentiation (LTP), potentially explaining memory deficits in multiple sclerosis (MS) models.
Area of Science:
- Neuroscience
- Immunology
- Pathophysiology
Background:
- Multiple sclerosis (MS) is a central nervous system inflammatory disease.
- MS commonly causes memory deficits.
- Experimental autoimmune encephalomyelitis (EAE) models MS and impairs hippocampal learning and memory.
Purpose of the Study:
- To investigate in vivo electrophysiological changes in synaptic transmission.
- To evaluate synaptic plasticity in the CA1 region of the hippocampus in EAE rats.
Main Methods:
- Recording field excitatory postsynaptic potentials (fEPSPs) in the CA1 region of EAE rat hippocampi.
- Stimulating Schaffer collaterals and recording from stratum radiatum neurons.
- Analyzing synaptic transmission and long-term potentiation (LTP).
Main Results:
- EAE significantly impairs synaptic transmission and LTP in the hippocampus.
- A decrease in paired-pulse index at 120 msec interstimulus interval was observed in EAE rats.
- Findings suggest EAE suppresses synaptic transmission and LTP via enhanced GABAB receptor inhibition of glutamate-mediated EPSPs.
Conclusions:
- Inflammation-driven mechanisms in EAE negatively impact synaptic transmission.
- These synaptic changes likely contribute to the observed learning impairments in EAE rats.
- This study provides the first in vivo electrophysiological evidence of synaptic dysfunction in EAE.
More Related Videos
04:55A Stably Established Two-Point Injection of Lysophosphatidylcholine-Induced Focal Demyelination Model in Mice
Published on: May 11, 2022
05:44Author Spotlight: Creating a Versatile Experimental Autoimmune Encephalomyelitis Model Relevant for Both Male and Female Mice
Published on: October 13, 2023
Related Concept Videos
Long-term Potentiation
Long-term Potentiation
Hebbian LTP
LTP can occur when...
Long-term Depression
Long-term Depression
Calcium Ion Concentration Mechanism
If over...