25B-NBOMe, a potent designer drug that activates the serotonin-2A receptor, can cause lethal rhabdomyolysis—a severe breakdown of skeletal muscle—in zebrafish larvae. Treatment with 25B-NBOMe reduced survival, impaired movement, and disrupted muscle structure, as shown by changes in birefringence and immunostaining for dystroglycan and myosin heavy chain. This rhabdomyolysis was blocked by the 5-HT_2A receptor antagonists ritanserin and aripiprazole, but not by antagonists for other serotonin receptors, indicating a 5-HT_2A-dependent mechanism. The 25B-NBOMe-treated zebrafish provides a useful animal model for studying rhabdomyolysis and screening potential therapies.
The designer drug 25B-NBOMe, a potent agonist of the serotonin-2A (5-HT2A) receptor, causes lethal rhabdomyolysis in zebrafish larvae. Treatment with 25B-NBOMe reduced survival and locomotion, and altered skeletal muscle birefringence and immunostaining for dystroglycan and myosin heavy chain, consistent with rhabdomyolysis. This effect was blocked by the 5-HT2A receptor antagonists ritanserin and aripiprazole, but not by antagonists of other serotonin receptors, indicating a 5-HT2A-dependent mechanism. The 25B-NBOMe-treated zebrafish provides a useful model for studying rhabdomyolysis and screening therapeutic drugs.