Differential expression of synaptic vesicle protein 2A after status epilepticus and during epilepsy in a lithium-pilocarpine model

Synaptic vesicle protein 2A (SV2A) has become an attractive target of investigation because of its role in the pathophysiology of epilepsy; SV2A is expressed ubiquitously throughout the brain in all nerve terminals independently of their neurotransmitter content and plays an important but poorly def...

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Bibliographic Details
Published in:Epilepsy & behavior 2018-11, Vol.88, p.283-294
Main Authors: Contreras-García, Itzel Jatziri, Pichardo-Macías, Luz Adriana, Santana-Gómez, César Emmanuel, Sánchez-Huerta, Karla, Ramírez-Hernández, Rogelio, Gómez-González, Beatriz, Rocha, Luisa, Mendoza Torreblanca, Julieta G.
Format: Article
Language:English
Subjects:
Animals
Disease Models, Animal
Gene Expression
Hippocampus - drug effects
Hippocampus - metabolism
Lithium Chloride - toxicity
Lithium-pilocarpine
Male
Membrane Glycoproteins - biosynthesis
Membrane Glycoproteins - genetics
Nerve Tissue Proteins - biosynthesis
Nerve Tissue Proteins - genetics
Neurons - drug effects
Neurons - metabolism
Pilocarpine - toxicity
Rats
Rats, Wistar
Status epilepticus
Status Epilepticus - chemically induced
Status Epilepticus - genetics
Status Epilepticus - metabolism
SV2A protein
Temporal lobe epilepsy
VGAT
VGLUT 1
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Summary:Synaptic vesicle protein 2A (SV2A) has become an attractive target of investigation because of its role in the pathophysiology of epilepsy; SV2A is expressed ubiquitously throughout the brain in all nerve terminals independently of their neurotransmitter content and plays an important but poorly defined role in neurotransmission. Previous studies have shown that modifications in the SV2A protein expression could be a direct consequence of disease severity. Furthermore, these SV2A modifications may depend on specific changes in the nerve tissue following the induction of epilepsy and might be present in both excitatory and inhibitory terminals. Thus, we evaluated SV2A protein expression throughout the hippocampi of lithium-pilocarpine rats after status epilepticus (SE) and during early and late epilepsy. In addition, we determined the γ-aminobutyric acid (GABA)ergic or glutamatergic nature associated with SV2A modifications. Wistar rats were treated with lithium-pilocarpine to induce SE and subsequently were shown to present spontaneous recurrent seizures (SRS). Later, we conducted an exhaustive semi-quantitative analysis of SV2A optical density (OD) throughout the hippocampus by immunohistochemistry. Levels of the SV2A protein were substantially increased in layers formed by principal neurons after SE, mainly because of GABAergic activity. No changes were observed in the early stage of epilepsy. In the late stage of epilepsy, there were minor changes in SV2A OD compared with the robust modifications of SE; however, SV2A protein expression generally showed an increment reaching significant differences in two dendritic layers and hilus, without clear modifications of GABAergic or glutamatergic systems. Our results suggest that the SV2A variations may depend on several factors, such as neuronal activity, and might appear in both excitatory and inhibitory systems depending on the epilepsy stage. •SV2A and VGAT increase in somatic layers of hippocampus during status epilepticus.•SV2A modifications depend on neuronal activity and pathophysiological changes.•SV2A is not modified in the hippocampus during early epilepsy.•SV2A increases in the hippocampus during late epilepsy in some glutamatergic layers.•SV2A modifications depend on the epilepsy stage.
ISSN:1525-5050
1525-5069
DOI:10.1016/j.yebeh.2018.08.023