Changes in Synaptic Transmission and Long-term Potentiation Induction as a Possible Mechanism for Learning Disability in an Animal Model of Multiple Sclerosis.
- Author:
Ghasem MOSAYEBI
1
;
Mohammad Reza SOLEYMAN
;
Mostafa KHALILI
;
Masoumeh MOSLEH
;
Mohammad Reza PALIZVAN
Author Information
- Publication Type:Original Article
- Keywords: Encephalomyelitis, Autoimmune, Experimental; Hippocampus; Long-term Potentiation; Paired Pulse Index
- MeSH: 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*
- From:International Neurourology Journal 2016;20(1):26-32
- CountryRepublic of Korea
- Language:English
- 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.
