ANTICONVULSANT EFFECTS OF NIFEDIPINE ON MES INDUCED SEIZURES
Objective: To evaluate the anticonvulsant activity of Nifedipine against MES induced seizures.
Methods: The study was induced by techno electroconvulsometer. The animals were treated with Nifedipine (100 Î¼g/100 g i. p. and 200 Î¼g/100 g i. p.) and MES was induced 2 h after the administration of the drug, and duration of various phases was noted. Duration of THLE was taken as an index for antiepileptic activity.
Results: Nifedipine when administered in a dose of 100 Î¼g/100 g ip, did not produce any changes in any phases of the MES induced seizure. But in a dose of 200 Î¼g/100 g ip, it significantly reduced the duration of THLE.
Conclusion: Nifedipine has a significant action against MES induced seizures suggesting an important role of CCBs as future, promising antiepileptic drug.
2. Chen Y, Lu J, Zhang Y, Wu H, Liu X, Jiang Y, et al. Association between genetic variation of CACNA1H and childhood absence epilepsy. Ann Neurol 2003;54:239-43.
3. Heron SE, Khosravani H, Varela D, Bladen C, Williams TC, Newman MR, et al. Extended spectrum of idiopathic generalized epilepsies associated with CACNA1H functional variants. Ann Neurol 2007;62:560-8.
4. Liang J, Zhang Y, Chen Y, Wang J, Pan H, Wu H, et al. Common polymorphisms in the CACNA1H gene associated with childhood absence seizure in Chinese Han population. Ann Hum Genet 2007;71:325-35.
5. Bourinet E, Soong TW, Sutton K, Slaymaker S, Mathews S, Monteil A, et al. Splicing of alpha 1A subunit gene generates phenotypic variants of P-and Q-type calcium channels. Nat Neurosci 1999;2:407-15.
6. Trimmer JS, Rhodes KJ. Localization of voltage-gated ion channels in mammalian brain. Annu Rev Physiol 2004;66:477-519.
7. N Gouemo P, Yasuda R, Faingold CL. Seizure susceptibility is associated with altered protein expression of voltage-gated calcium channels subunits in inferior colliculus neurons of the genetically epilepsy-prone rat. Brain Res 2010;1308:153-7.
8. Heinemann IJ, Hamon B. Calcium and epileptogenesis. Exp Brain Res 1986;65:1-10.
9. Grifffths T, Evans MC, Meldrum BS. Intracellular sites of early calcium accumulation in the rat hippocampus during status epilepticus. Neurosc Lett 1982;30:329-34.
10. John H Menker, Raman Sarkar. Paroxysmal disorders. Text Book of childhood neurology. 5th edition; 1995. p. 724-60.
11. Speckmann EJ, Walden J, Bingmann D, Specific suppression of pentylenetetrazol-induced epileptiform discharges in CA3 neurons (hippocampal slice, guinea pig) by the organic calcium antagonists flunarizine and verapamil. Exp Brain Res 1989;39:149.
12. Desai CK, Dikshit RK, Mansuri SM, Shah UH. Comparative evaluation of anticonvulsant activity of CCBs in experimental animals. Indian J Exp Biol 1995;33:931-4.
13. Meyer FB, Anderson RE, Sundt TM. Anticonvulsant effects of dihydropyridine calcium antagonists in electrocortical shock seizures. Epilepsia 1990;31:68-74.
14. Catterall WA. Structure and function of neuronal calcium channels and their role in neurotransmitter release. Cell Calcium 1998;24:307-23.
15. Neher E, Sakaba T. Multiple roles of calcium ions in the regulation of neurotransmitter release. Neuron 2008;59:861-72.
16. Wadel K, Neher E, Sabaka T. The coupling between synaptic vescicles and calcium channels determines fast neurotransmitter release. Neuron 2007;53:563-75.
17. Spedding M. Trends Pharmacol Sci; 1987. p. 115.
18. Tringham E, Powell KL, Cain SM, Kuplast K, Mezeyova J, Weerapura M, et al. T type calcium channel blockers that attenuate thalamic burst firing and suppress absence seizures. Sci Transl Med 2012;4:12-9.