PUBLICATION

PTZ-induced seizures inhibit adenosine deamination in adult zebrafish brain membranes

Authors
Siebel, A.M., Piato, A.L., Capiotti, K.M., Seibt, K.J., Bogo, M.R., and Bonan, C.D.
ID
ZDB-PUB-110920-5
Date
2011
Source
Brain research bulletin   86(5-6): 385-9 (Journal)
Registered Authors
Bonan, Carla Denise
Keywords
adenosine, adenosine deaminase, ectonucleotidases, seizures, pentylenetetrazole, zebrafish
MeSH Terms
  • Adenosine/metabolism*
  • Adenosine Deaminase/metabolism
  • Animals
  • Brain/anatomy & histology*
  • Brain/metabolism*
  • Convulsants/pharmacology*
  • Deamination
  • Pentylenetetrazole/pharmacology*
  • Pyrophosphatases/metabolism
  • Seizures/chemically induced*
  • Seizures/physiopathology*
  • Zebrafish
PubMed
21907764 Full text @ Brain Res. Bull.
Abstract
Adenosine exerts neuromodulatory functions with mostly inhibitory effects, being considered an endogenous anticonvulsant. The hydrolysis of ATP by ectonucleotidases is an important source of adenosine, and adenosine deaminase (ADA) contributes to the regulation of this nucleoside concentration through its deamination. In this study, we tested the effect of pentylenetetrazole (PTZ)-induced seizures on ectonucleotidases and ADA activities in adult zebrafish brain. Our results have demonstrated that PTZ treatments did not alter ectonucleotidases and ADA activities in membranes and soluble fraction, respectively. However, ecto-ADA activity was significantly decreased in brain membranes of animals exposed to 5 mM and 15 mM PTZ treatments (22.4% and 29.5%, respectively) when compared to the control group. Semiquantitative RT-PCR analysis did not show significant changes after the PTZ exposure on ADA gene expression. The decreased adenosine deamination observed in this study suggests a modulation of extracellular adenosine levels during PTZ-induced seizures in zebrafish.
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