Int Neurourol J.  2016 Mar;20(1):26-32. 10.5213/inj.1632514.257.

Changes in Synaptic Transmission and Long-term Potentiation Induction as a Possible Mechanism for Learning Disability in an Animal Model of Multiple Sclerosis

• Mosayebi G
• Soleyman M
• khalili M
• Mosleh M
• Palizvan M

• KMID: 2173124
• DOI: http://doi.org/10.5213/inj.1632514.257

Abstract

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.

Keyword

Encephalomyelitis, Autoimmune, Experimental; Hippocampus; Long-term Potentiation; Paired Pulse Index

MeSH Terms

Animals*
Central Nervous System
Demyelinating Diseases
Encephalomyelitis, Autoimmune, Experimental
Excitatory Postsynaptic Potentials
Hippocampus
Humans
Learning Disorders*
Learning*
Long-Term Potentiation*
Memory
Memory Disorders
Models, Animal*
Multiple Sclerosis*
Neurons
Rats
Synaptic Transmission*