Epilepsy is a chronic disorder of the brain characterised by recurrent seizures. Around 1-2% of the world’s population are affected, with many sufferers exhibiting or developing resistance to drug therapy. Animal models have played a significant role in shaping our understanding of the neural mechanisms that underpin epilepsy; however current acute seizure models have a range of limitations. The physiological complexity and ready availability of larval zebrafish affords an ideal vertebrate model for high throughput screening of seizurogenic compounds. 4 days post fertilisation (dpf) zebrafish have a complex nervous system (~105 neurons) and seizure-like behaviours can be elicited by a range of known convulsant molecules. Here we investigate the utility of a lower vertebrate, the zebrafish (Danio rerio), to explore patterns of neural activity provoked by a variety of pharmacological treatments known to generate neural network hyperexcitability in mammals. All procedures were in accordance with current UK legislation. Intact 4 dpf zebrafish were immobilised by continuous exposure to 4 mM tubocurarine and fixed and positioned dorsal side up in 1 % low melting point agarose. Single glass micropipette (3-5 MΩ) recordings from the optic tectum were used to investigate both spontaneous and light-evoked local field potentials. In such recordings exposure to a range of convulsant molecules revealed distinct phenotypic profiles of each drug depending on their target. Further to single electrode study, a novel experimental set up was employed using 4 shank 16 channel silicon probes inserted across the zebrafish brain. These enabled us to measure a matrix of central nervous system activity, and also permitting single unit recording in vivo. 5 mM pentylenetetrazol elicited low frequency synchronous activity (~0.4 Hz, n=3) typical of a GABAergic modulatory response. In contrast, 1 mM 4AP application resulted in a loss of spontaneous synchronous activity and the appearance of higher frequency activity (~2.0 Hz, n=3). The overall power (mV2) of neural activity was increased in response to addition of selective KCC2 blocker, VU0463271, at a concentration of 1 µM (P<0.01, n=3, paired t test). Epileptiform activity recorded from layer ΙΙ of the mouse medial entorhinal cortex in vitro, permitted evaluation of the suitability of this model for studying epilepsy. Inter-ictal events recorded in response to CNS active drugs were qualitatively very similar in both preparations. Electrophysiological recording in zebrafish permits measurement of local patterns of neural activity, where differences in phenotypic activity can be observed across a range of different convulsants. We propose this experimental model can aid in gaining better understanding of drug-associated hyperexcitability in vivo.