Abstract:
:Systematic screening of many compounds in animal models led to identification of the established antiepileptic drugs (AEDs). By contrast, the newer AEDs were specifically designed to enhance an inhibitory process or to inhibit a specific excitatory pathway. However, it was later discovered that some of the designed drugs differed in their modes of action from what was envisioned. Recently, it has become apparent that all AEDs, old and new, may affect sodium and calcium channels, increase brain concentration of free gamma-aminobutyric acid (GABA), and reduce glutamate-mediated excitation by inhibiting N-methyl-D-aspartate (NMDA) and the alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors. However, not all the drugs affect all of these mechanisms. Understanding the modes of action of each drug may explain why some of them are effective in treating other neurologic and neuropsychiatric disorders. This understanding may make it possible to develop a group of neuroexcitatory amino acid transmitter antagonists with intended antiepileptogenic actions.
journal_name
Neurologyjournal_title
Neurologyauthors
Moshé SLsubject
Has Abstractpub_date
2000-01-01 00:00:00pages
S32-40; discussion S54-8issue
5 Suppl 1eissn
0028-3878issn
1526-632Xjournal_volume
55pub_type
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