PUBLICATION

Forebrain glutamate uptake and behavioral parameters are altered in adult zebrafish after the induction of Status Epilepticus by kainic acid

Authors
Mussulini, B.H.M., Vizuete, A.F.K., Braga, M., Moro, L., Baggio, S., Santos, E., Lazzarotto, G., Zenki, K.C., Pettenuzzo, L., Rocha, J.B.T., de Oliveira, D.L., Calcagnotto, M.E., Zuanazzi, J.A.S., Burgos, J.S., Rico, E.P.
ID
ZDB-PUB-180424-1
Date
2018
Source
Neurotoxicology   67: 305-312 (Journal)
Registered Authors
Burgos, Javier S.
Keywords
Behavior, GFAP, Glutamate Uptake, Kainic Acid, Key-words, S100B, Zebrafish
MeSH Terms
  • Age Factors
  • Animals
  • Glutamic Acid/metabolism*
  • Kainic Acid/toxicity*
  • Locomotion/drug effects*
  • Locomotion/physiology
  • Male
  • Prosencephalon/drug effects
  • Prosencephalon/metabolism*
  • Status Epilepticus/chemically induced*
  • Status Epilepticus/metabolism*
  • Zebrafish
PubMed
29680360 Full text @ Neurotoxicology
Abstract
The development of new antiepileptic drugs is a high-risk/high-cost research field, which is made even riskier if the behavioral epileptic seizure profile is the unique approach on which the development is based. In order to increase the effectiveness of the screening conducted in the zebrafish model of status epilepticus (SE), the evaluation of neurochemical markers of SE would be of great relevance. Epilepsy is associated with changes in the glutamatergic system, and glutamate uptake is one of the critical parameters of this process. In this study therefore, we evaluated the levels of glutamate uptake in the zebrafish brain and analyzed its correlation with the progression of behavioral changes in zebrafish at different times after the administration of kainic acid 5 mg/kg). The results showed that the zebrafish suffered with lethargy while swimming for up to 72 h after SE, had reduced levels of GFAP cells 12 h after SE, reduced levels of S100B up to 72 h after SE, and reduced levels of glutamate uptake in the forebrain between 3 h and 12 h after SE. The forebrain region of adult zebrafish after SE is similar to the neurochemical limbic alterations that are seen in rodent models of SE. This study demonstrated that there is a time window in which to use the KA zebrafish model of SE to explore some of the known neurochemical alterations that have been observed in rodent models of epilepsy and epileptic human patients.
Genes / Markers
Figures
Show all Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping