ZFIN Image: Dogra et al., 2025, Fig 8

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Figure Caption

Fig 8 Model of relationship between slc13a5 mutations, NMDA receptor signaling and zinc chelation.

Unlike in WT larvae, slc13a5 mutations in zebrafish presumably cause an increase in extracellular citrate levels that lead to zinc chelation, thereby preventing its inhibitory effect on NMDA receptors and ultimately leading to an excessive influx of calcium to the neurons, causing epilepsy. Blocking NMDA receptors and/or treatment with zinc prevents this enhanced influx of calcium into the neurons, thereby rescuing epilepsy-related phenotypes in the slc13a5 mutants.

Acknowledgments

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