Sumatriptan reduces severity of status epilepticus induced by lithium–pilocarpine through nitrergic transmission and 5‐HT1B/D receptors in rats: A pharmacological‐based evidence

• Published in: Fundamental & clinical pharmacology 2021-02, Vol.35 (1), p.131-140
• Main Authors: Eslami, Faezeh, Rahimi, Nastaran, Ostovaneh, Aysa, Ghasemi, Mehdi, Dejban, Pegah, Abbasi, Ata, Dehpour, Ahmad Reza
• Format: Article
• Language: English
• Subjects: 5‐HT1B/1D receptors; Animal models; Animal tissues; Epilepsy; Headache; Inflammation; Lithium; Lithium chloride; Migraine; Mortality; Nitric oxide; Nitric-oxide synthase; Pentylenetetrazole; Pharmacology; Pilocarpine; rat; Receptors; Rodents; Seizures; status epilepticus; Sumatriptan; Tumor necrosis factor; Tumor necrosis factor-TNF; tumor necrosis factor‐alpha (TNF‐α)
• ISSN: 0767-3981; 1472-8206
• DOI: 10.1111/fcp.12590

Status epilepticus (SE) is a life‐threatening neurologic disorder that can be as both cause and consequence of neuroinflammation. In addition to previous reports on anti‐inflammatory property of the anti‐migraine medication sumatriptan, we have recently shown its anticonvulsive effects on pentylenetetrazole‐induced seizure in mice. In the present study, we investigated further (i) the effects of sumatriptan in the lithium–pilocarpine SE model in rats, and (ii) the possible involvement of nitric oxide (NO), 5‐hydroxytryptamin 1B/1D (5‐HT1B/1D) receptor, and inflammatory pathways in such effects of sumatriptan. Status epilepticus was induced by lithium chloride (127 mg/kg, i.p) and pilocarpine (60 mg/kg, i.p.) in Wistar rats. While SE induction increased SE scores and mortality rate, sumatriptan (0.001‐1 mg/kg, i.p.) improved it (P