title: Antiepileptic drugs prevent changes in adenosine deamination during acute seizure episodes in adult zebrafish.
abstract: Adenosine is an endogenous modulator of brain functions, which presents anticonvulsant properties. In addition, its levels can be increased during neural injury. The modulation of extracellular adenosine levels by ectonucleotidase and adenosine deaminase (ADA) activities may represent a key mechanism in the control of epileptogenesis. In the present study, we investigated the effects of acute seizure episodes and antiepileptic drug (AED) treatments on ectonucleotidases and ADA activities in adult zebrafish brain. Our data have demonstrated that pentylenetetrazole (PTZ)-induced seizures did not alter ATP, ADP, and AMP hydrolysis in brain membrane fractions. However, there was a significant increase on ecto-ADA and soluble ADA activities in PTZ-treated animals immediately after a clonus-like convulsion and loss of posture, which are typical behavioral changes observed in Stage 3. Furthermore, our results have demonstrated that AED pretreatments prevented the stimulatory effect promoted by PTZ exposure on ADA activities. The PTZ and AED treatments did not promote alterations on ADA gene expression. Interestingly, when exposed to PTZ, animals pretreated with AEDs showed longer latency to reach the clonus-like seizure status, which is an effect that matches the suppression of the increase of ADA activity promoted by the AEDs. These data suggest that the adenosine deamination could be involved in the control of seizure development in zebrafish and may be modulated by AED treatments.
authors.affiliation: Laboratório de Neuroquímica e Psicofarmacologia, Departamento de Biologia Celular e Molecular, Programa de Pós-Graduação em Biologia Celular e Molecular, Faculdade de Biociências, Pontifícia Universidade Católica do Rio Grande do Sul, Avenida Ipiranga, 6681, 90619-900 Porto Alegre, RS, Brazil.
authors.forename: Anna Maria
authors.initials: AM
authors.lastname: Siebel
authors.forename: Angelo Luis
authors.initials: AL
authors.lastname: Piato
authors.forename: Isabel Costa
authors.initials: IC
authors.lastname: Schaefer
authors.forename: Laura Roesler
authors.initials: LR
authors.lastname: Nery
authors.forename: Maurício Reis
authors.initials: MR
authors.lastname: Bogo
authors.forename: Carla Denise
authors.initials: CD
authors.lastname: Bonan
mesh_terms: D000227:Adenine Nucleotides / Q000378:metabolism; D000241:Adenosine / Q000378:metabolism*; D000243:Adenosine Deaminase / Q000235:genetics / Q000378:metabolism; D000588:Amines / Q000494:pharmacology; D000818:Animals; D000927:Anticonvulsants / Q000494:pharmacology*; D001921:Brain / Q000187:drug effects / Q000378:metabolism; D003509:Cyclohexanecarboxylic Acids / Q000494:pharmacology; D004195:Disease Models, Animal; D005260:Female; D000077206:Gabapentin; D015870:Gene Expression / Q000187:drug effects; D008297:Male; D010433:Pentylenetetrazole / Q000633:toxicity; D010672:Phenytoin / Q000494:pharmacology; D012640:Seizures / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism*; D014635:Valproic Acid / Q000494:pharmacology; D015027:Zebrafish; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology
chemical_list: D000227:Adenine Nucleotides; D000588:Amines; D000927:Anticonvulsants; D003509:Cyclohexanecarboxylic Acids; D005680:gamma-Aminobutyric Acid; D014635:Valproic Acid; D010672:Phenytoin; D000077206:Gabapentin; D000243:Adenosine Deaminase; D000241:Adenosine; D010433:Pentylenetetrazole