Abstract:
PURPOSE:This study evaluated topiramate (TPM) antagonism of glutamate receptors activated by kainate. METHODS:The ability of TPM (3-30 microM) to attenuate kainate (300 microM)-activated cobalt (Co2+) flux through nonselective cation channels permeable to Co2+, Mn2+, and Ca2+ into cultured cerebellar granule neurons [9-14 days in vitro (div)] was investigated. Results were compared with those obtained with the non-N-methyl-D-aspartate (non-NMDA) antagonist 6,7-dinitroquinoxalone-2,3-dione (DNQX) (10 microM). RESULTS:Topiramate produced a concentration- and time-dependent inhibition of Co2+ uptake into cerebellar granule cells cultured 9-11 div. Inhibition was evident at 10 microM, and complete inhibition was observed at 30 microM. Maximal inhibition of Co2+ uptake required pretreatment with TPM for > or =30 minutes before stimulation by kainate. The effect of 30 microM TPM on Co2+ uptake was similar to that of 10 microM DNQX. However, TPM, unlike DNQX, did not affect kainate-evoked Co2+ uptake into older neurons (i.e., 13-14 div). CONCLUSIONS:These results provide additional support for an antagonistic effect of TPM on some types of alpha-amino-3-hydroxy-5-methylisoxazole-4-proprionic acid (AMPA) and/or kainate receptors, and specifically suggest that TPM interacts with a Ca2+-permeable non-NMDA receptor that is developmentally regulated. This observation may provide insight into the molecular biology underlying the pathophysiology of seizure disorders and antiepileptic drug resistance.
journal_name
Epilepsiajournal_title
Epilepsiaauthors
Skradski S,White HSdoi
10.1111/j.1528-1157.2000.tb02171.xsubject
Has Abstractpub_date
2000-01-01 00:00:00pages
45-7issue
S1eissn
0013-9580issn
1528-1167journal_volume
41pub_type
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