Though GABAergic neurotransmission has been found to be most directly affected by the mutations underlying Dravet's syndrome, scientists have explored the potential of other neurotransmitters rescuing the phenotype, relieving mutant zebrafish larvae of epileptic seizures. One of the neurotransmitters that has shown some promise is serotonin (5-hydroxytryptamine). It's been revealed that increasing serotonin levels can reduce epileptic locomotor activity and brain activity. As such, the drug fenafluramine was identified to be capable of targeting serotonin recetor subtypes, acting as agonists for those subtypes and allowing serotonergic neurotransmission. However, this drug does not restore the sodium channels lost in GABAergic neurons. While this drug is effective at targeting the right subtypes, it does have some co-morbidities. It happens to target the serotonin-2B receptor subtype, which leads to cardiac hypertrophy. This has made the drug unfit for use as an effective treatment against Dravet's syndrome.
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