PUBLICATION

Oral gabapentin suppresses pentylenetetrazole-induced seizure-like behavior and cephalic field potential in adult zebrafish

Authors
Banote, R.K., Koutarapu, S., Chennubhotla, K.S., Chatti, K., and Kulkarni, P.
ID
ZDB-PUB-130322-36
Date
2013
Source
Epilepsy & behavior : E&B   27(1): 212-219 (Journal)
Registered Authors
Chatti, Kiranam, Kulkarni, Pushkar
Keywords
zebrafish, epilepsy, gabapentin, pentylenetetrazole, neurobehavior, cephalic field potential
MeSH Terms
  • Action Potentials/drug effects*
  • Administration, Oral
  • Amines/administration & dosage*
  • Analysis of Variance
  • Animals
  • Anticonvulsants/administration & dosage*
  • Brain/drug effects
  • Brain/physiopathology*
  • Cyclohexanecarboxylic Acids/administration & dosage*
  • Disease Models, Animal
  • Dose-Response Relationship, Drug
  • Locomotion/drug effects
  • Male
  • Pentylenetetrazole/toxicity
  • Seizures/chemically induced
  • Seizures/drug therapy*
  • Time Factors
  • Zebrafish
  • gamma-Aminobutyric Acid/administration & dosage*
PubMed
23466252 Full text @ Epilepsy Behav.
Abstract

We report the effect of orally administered gabapentin (GBP) on pentylenetetrazole (PTZ)-induced seizure-like activity in adult zebrafish. Zebrafish were pretreated with vehicle or GBP using a novel method of precise oral administration, followed by an intraperitoneal administration of PTZ. Behavioral assessment was carried out using locomotion-based video-tracking analysis and seizure score assignment using visual observation. Cephalic field potential recordings of the zebrafish brain were conducted using an electrical data acquisition system. Orally administered GBP significantly suppressed the seizure-like locomotor activity and strong slow-wave (~ 3 Hz) activity in the cephalic field potential caused by PTZ. This work is the first report of the activity of an orally delivered anticonvulsant in adult zebrafish. Our study provides behavioral and physiological evidence in support of an adult zebrafish model for studying seizures including excitotoxic brain injury and a novel in vivo framework for the evaluation of pharmacological modulators of epilepsy.

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