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Changes in the gene expression in the inferior colliculus of the sound stimulated rats both Wistar and the strain susceptible to audiogenic seizures WAR

ABSTRACT: Using microarray analyses and subsequent verification by RT-PCR, we studied the changes in gene expression in the inferior colliculus after an ictal event in one models of audiogenic epilepsy, Wistar audigenic rat (WAR). WAR is a genetically selected strain susceptible to audiogenic seizures that was inbred in the School of Medicine of Ribeirão Preto (Brazil) beginning in 1990. This strain is a model of audiogenic idiopathic epilepsy that develops tonic-clonic generalized seizures. Genetic animal models of epilepsy are an important tool for further understanding the basic cellular mechanisms underlying epileptogenesis and for developing novel antiepileptic drugs. We conducted a comparative study of gene expression in the inferior colliculus, a nucleus that triggers audiogenic seizures, using two animal models, the Wistar audiogenic rat (WAR) and the genetic audiogenic seizure hamster (GASH:Sal). For this purpose, both models were subjected to auditory stimulation, and 60 minutes after stimulation, the inferior colliculi were collected. As a control, intact Wistar rats and Syrian hamsters were subjected to identical stimulation and tissue preparation protocols to those performed on the experimental animals.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE74150 | GEO | 2015/12/31

SECONDARY ACCESSION(S): PRJNA299177

REPOSITORIES: GEO

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Project description:Audiogenic epilepsy (AE), developing in rodent strains in response to loud sound, is widely used as the model of generalized convulsive epilepsy. The molecular and genetic mechanisms that determine the expression of AE are currently non well understood. In the present work we compared transcriptomes from the inferior and superior colliculi (corpora quadrigemina), the crucial epileptogenic midbrain zone for AE in order to identify genes associated to the AE phenotype. Transcriptomes of rats from three strains were compared: Krushinsky-Molodkina (KM) strain (100% AE-prone); Wistar outbred rats (with no AE proneness) and "0" strain, selected from F2 KMxWistar hybrids for the lack of AE. It is shown that KM strain gene expression profile have a number of characteristic differences from those of Wistar and "0" strains. In particular, KM has increased expression of a number of genes involved in positive regulation of the MAPK signaling cascade, as well as genes, responsible for positive regulation of apoptotic processes. The next characteristic difference between the KM strain from Wistar and "0" is a multiple increase in the expression level of the Ttr gene, which is known to be associated with family amyloid polyneuropathy in humans. Further, the KM strain showed a significant decrease in the expression of the Msh3 gene involved in the DNA mismatch repair system, Acsm5, coding a mitochondrial acyl-CoA synthetase specific for medium chain family member 5, and in a number of genes of the oxidative phosphorylation system, and a number of some other genes. Our data confirm the complex multigenic nature of AE inheritance in rodents. A comparison with the data obtained from other AE rodent strains suggests that the convulsive phenotype could develop differently in audiogenic rat strains selected independently. Although, the finding of parallel differences in certain genes expression in AE-prone hamsters (another rodent species) indicate the common (and crucial) neurogenetic defects, leading to AE phenotype in rodents in general.

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Changes in the gene expression in the inferior colliculus of the sound stimulated rats both Wistar and the strain susceptible to audiogenic seizures WAR

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