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Antiabsence effects of safranal in acute experimental seizure models: EEG and autoradiography
Hamid R Sadeghnia1, Miguel A Cortez, Dick Liu
1Department of Pharmacology, Mashhad University of Medical Sciences, Mashhad, Iran.
Purpose:
We examined the effect of safranal, a constituent of Crocus sativus, in acute experimental animal models of generalized absence seizures.
Methods:
the effect of acute systemic administration of safranal on latency to seizure onset as well as spike and wave discharches (SWD) duration following pharmacologically-induced absence seizures was investigated in wildtype mice. We further characterized its effects on the GABAergic system through the regional modification of [3H] flunitrazepam, a benzodiazepine agonist binding site and [3H] CGP54626A, a GABAB receptor antagonist binding site in mouse brain.
Results:
The systemic administration of safranal resulted in a significant and dose-dependent attenuation in experimental absence seizures elicited by either gamma-butyrolactone (GBL), baclofen (BAC) or low doses of GABAA receptor antagonists; pentylenetetrazole (PTZ), picrotoxin (PTX) and bicuculline (BMC). After a single intraperitoneal administration of safranal (291 mg/kg), no changes in baseline electrocorticographic (ECoG) recording were observed, however, a significant decrease in [3H] flunitrazepam binding was seen in the cortex (33.16%, p<0.001), hippocampus (27.36%, p<0.01) and thalamus (29.91%, p<0.01) of mouse brain, while the [3H] CGP54626A binding did not show any modification in the same brain regions.
Conclusion:
These data indicate that there is an antiabsence seizure property in safranal and its effect may be due to modifications on the benzodiazepine binding sites of the GABAA receptor complex.
