Zebrafish as a Simple Vertebrate Organism for Epilepsy Research

Baraban, Scott C.

doi:10.1007/978-1-60327-263-6_4

Cited by 5 publications

(5 citation statements)

References 79 publications

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“…On the other hand, we found a good correlation between our EEG data and those reported by Baraban and colleagues [5], [25], [26], despite differences in protocol, namely: 1) PTZ concentration (15 mM PTZ, Baraban; 20 mM PTZ, our study), 2) Strains used (TL, Baraban; Ekkwill, our study), 3) Timing of drug application (PTZ added before AED, Baraban; AED added before PTZ, our study), and 4) Type of EEG parameter/s evaluated (spike amplitude, Baraban; number and duration of epileptiform discharges, our study). The single difference we observed was in the case of ETS.…”

Section: Discussionsupporting

confidence: 89%

Validation of the Zebrafish Pentylenetetrazol Seizure Model: Locomotor versus Electrographic Responses to Antiepileptic Drugs

et al. 2013

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Zebrafish have recently emerged as an attractive in vivo model for epilepsy. Seven-day-old zebrafish larvae exposed to the GABAA antagonist pentylenetetrazol (PTZ) exhibit increased locomotor activity, seizure-like behavior, and epileptiform electrographic activity. A previous study showed that 12 out of 13 antiepileptic drugs (AEDs) suppressed PTZ-mediated increases in larval movement, indicating the potential utility of zebrafish as a high-throughput in vivo model for AED discovery. However, a question remained as to whether an AED-induced decrease in locomotion is truly indicative of anticonvulsant activity, as some drugs may impair larval movement through other mechanisms such as general toxicity or sedation. We therefore carried out a study in PTZ-treated zebrafish larvae, to directly compare the ability of AEDs to inhibit seizure-like behavioral manifestations with their capacity to suppress epileptiform electrographic activity. We re-tested the 13 AEDs of which 12 were previously reported to inhibit convulsions in the larval movement tracking assay, administering concentrations that did not, on their own, impair locomotion. In parallel, we carried out open-field recordings on larval brains after treatment with each AED. For the majority of AEDs we obtained the same response in both the behavioral and electrographic assays. Overall our data correlate well with those reported in the literature for acute rodent PTZ tests, indicating that the larval zebrafish brain is more discriminatory than previously thought in its response to AEDs with different modes of action. Our results underscore the validity of using the zebrafish larval locomotor assay as a rapid first-pass screening tool in assessing the anticonvulsant and/or proconvulsant activity of compounds, but also highlight the importance of performing adequate validation when using in vivo models.

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Section: Discussionsupporting

confidence: 89%

Validation of the Zebrafish Pentylenetetrazol Seizure Model: Locomotor versus Electrographic Responses to Antiepileptic Drugs

et al. 2013

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“…These observations are further corroborated by genetic studies using interneuron‐deficient transgenic mice suggesting that particular gene defects affect specific interneuronal development, resulting in seizures (Jones‐Davies et al ., 2009). In general, these studies infer that the loss of interneurons has a negative impact on the balance of overall neuronal circuitry, which has been challenged by other research groups who suggest that specific interneuronal loss results in the preservation of lateral inhibitory circuits (Buckmaster and Jongen‐Relo, 1999).…”

Section: Introductionmentioning

confidence: 99%

Cannabidiol exerts antiepileptic effects by restoring hippocampal interneuron functions in a temporal lobe epilepsy model

Khan

Shekh‐Ahmad²,

Khalil³

et al. 2018

British J Pharmacology

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Background and PurposeA non‐psychoactive phytocannabinoid, cannabidiol (CBD), shows promising results as an effective potential antiepileptic drug in some forms of refractory epilepsy. To elucidate the mechanisms by which CBD exerts its anti‐seizure effects, we investigated its effects at synaptic connections and on the intrinsic membrane properties of hippocampal CA1 pyramidal cells and two major inhibitory interneurons: fast spiking, parvalbumin (PV)‐expressing and adapting, cholecystokinin (CCK)‐expressing interneurons. We also investigated whether in vivo treatment with CBD altered the fate of CCK and PV interneurons using immunohistochemistry.Experimental ApproachElectrophysiological intracellular whole‐cell recordings combined with neuroanatomy were performed in acute brain slices of rat temporal lobe epilepsy in in vivo (induced by kainic acid) and in vitro (induced by Mg2+‐free solution) epileptic seizure models. For immunohistochemistry experiments, CBD was administered in vivo (100 mg·kg−1) at zero time and 90 min post status epilepticus, induced with kainic acid.Key ResultsBath application of CBD (10 μM) dampened excitability at unitary synapses between pyramidal cells but enhanced inhibitory synaptic potentials elicited by fast spiking and adapting interneurons at postsynaptic pyramidal cells. Furthermore, CBD restored impaired membrane excitability of PV, CCK and pyramidal cells in a cell type‐specific manner. These neuroprotective effects of CBD were corroborated by immunohistochemistry experiments that revealed a significant reduction in atrophy and death of PV‐ and CCK‐expressing interneurons after CBD treatment.Conclusions and ImplicationsOur data suggest that CBD restores excitability and morphological impairments in epileptic models to pre‐epilepsy control levels through multiple mechanisms to reinstate normal network function.

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“…The sequencing of the entire ZF genome has revealed that 70% of the proteins encoded by human genes are related to genes found in ZF, while 84% of the ZF genes are known to be associated with human diseases [32]. The nervous system of the ZF is simple, with individual elements (glutamatergic excitatory neurons and GABAergic inhibitory neurons) [33]. Decui et al [34] have recently presented data that reveal that micronized resveratrol can prevent pentylenetetrazole (PTZ)-induced seizure in epilepsy, whereas results by Mazumder et al [35] have suggested that the anticonvulsant action of the phosphatidylinositol-3-kinase inhibitor LY294002 can be highly potential against PTZ-induced convulsions.…”

Section: Zf As Model For the Experimental Simulation Of Neurological Disordersmentioning

confidence: 99%

Zebrafish as an experimental model for the simulation of neurological and craniofacial disorders

et al. 2022

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Zebrafish have gained momentum as a leading experimental model in recent years. At present, the zebrafish vertebrate model is increasingly used due to its multifactorial similarities to humans that include genetic, organ, and cellular factors. With the emergence of novel research techniques that are very expensive, it is necessary to develop affordable and valid experimental models. This review aimed to highlight some of the most important similarities between zebrafish and humans by emphasizing the relevance of the first in simulating neurological disorders and craniofacial deformity.

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Zebrafish as a Simple Vertebrate Organism for Epilepsy Research

Cited by 5 publications

References 79 publications

Validation of the Zebrafish Pentylenetetrazol Seizure Model: Locomotor versus Electrographic Responses to Antiepileptic Drugs

Validation of the Zebrafish Pentylenetetrazol Seizure Model: Locomotor versus Electrographic Responses to Antiepileptic Drugs

Cannabidiol exerts antiepileptic effects by restoring hippocampal interneuron functions in a temporal lobe epilepsy model

Zebrafish as an experimental model for the simulation of neurological and craniofacial disorders

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