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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Maximal electroshock-induced seizures are able to induce Homer1a mRNA expression but not pentylenetetrazole-induced seizures

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Author(s):
Cavarsan, Clarissa F. [1] ; Matsuo, Alisson [2] ; Blanco, Miriam M. [1] ; Mello, Luiz E. [1]
Total Authors: 4
Affiliation:
[1] Univ Fed Sao Paulo, Dept Physiol, BR-04039032 Sao Paulo - Brazil
[2] Univ Fed Sao Paulo, Dept Microbiol Immunol & Parasitol, UNONEX, BR-04023062 Sao Paulo - Brazil
Total Affiliations: 2
Document type: Journal article
Source: Epilepsy & Behavior; v. 44, p. 90-95, MAR 2015.
Web of Science Citations: 3
Abstract

Objective: Homer1a is a protein that regulates metabotropic glutamate receptors involved in neural plasticity processes. Recently, we demonstrated that Homer1a mRNA is enhanced after pilocarpine-induced status epilepticus. Here, we investigated whether a single acute seizure triggered by means of pentylenetetrazole (PTZ) injection or maximal electroshock (MES) stimulation (2 different seizure models) would alter Homer1a expression in the hippocampus. Methods: Male Wistar rats subjected to the PTZ or MES model were analyzed 2 h, 8 h, 24 h, and 7 days after seizure induction. Homer1a, mGluR1, and mGluR5 mRNA expression levels in hippocampal extracts were analyzed by quantitative PCR. Results: Quantitative PCR revealed Homer1a overexpression at 2 h after MES-induced tonic-clonic seizures compared to control, but the overexpression did not remain elevated after 8 h. Pentylenetetrazole-induced seizures, in contrast, were not able to change Homer1a mRNA expression. No differences were observed at these time points after seizures for mGluR1 and mGluR5 mRNA expression in any of the models. Significance: Our data indicate that the levels of Homer1a mRNA were transiently increased only after MES induced tonic-clonic seizures (and not after PTZ-induced seizures). We suggest that Homer1a expression may be dependent on seizure intensity or on specific brain circuit activation. We suggest that Homer1a may contribute to counteract hyperexcitability processes. (C) 2015 Elsevier Inc. All rights reserved. (AU)