ACS chemical neuroscience, 7(3), 316-326 (2016-01-08)
Although the antiepileptic properties of α-substituted lactams, acetamides, and cyclic imides have been known for over 60 years, the mechanism by which they act remains unclear. I report here that these compounds bind to the nicotinic acetylcholine receptor (nAChR) and
Inhibition of T-type Ca(2+) channels has been proposed to play a role in the therapeutic action of succinimide antiepileptic drugs. Despite the widespread acceptance of this hypothesis, recent studies using rat and cat neurons have failed to confirm inhibition of
British journal of pharmacology, 100(4), 807-813 (1990-08-01)
1. Currents evoked by applications of gamma-aminobutyric acid (GABA) to acutely dissociated thalamic neurones were analysed by voltage-clamp techniques, and the effects of the anticonvulsant succinimides ethosuximide (ES) and alpha-methyl-alpha-phenylsuccinimide (MPS) and the convulsants tetramethylsuccinimide (TMS), picrotoxin, pentylenetetrazol (PTZ), and
Pharmacokinetics of N-desmethylmethsuximide in pediatric patients.
M V Miles et al.
The Journal of pediatrics, 114(4 Pt 1), 647-650 (1989-04-01)
Serum protein binding of desmethyl-methsuximide (DM-MSM) in serum from 23 patients on polytherapy were determined using ultrafiltration and high-performance liquid chromatography. Desmethyl-methsuximide, The active metabolite of methsuximide (MSM), was found to have a moderate protein binding ranging between 45% and
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