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Overview of Neurotransmission: Relationship to the Action of Antiepileptic Drugs
Published in Carl L. Faingold, Gerhard H. Fromm, Drugs for Control of Epilepsy:, 2019
The effect of anticonvulsant drugs on glycine synthesis, metabolism, steady-state levels or release has apparently not been systematically investigated. However, glycine has been shown to potentiate the anticonvulsant action of diazepam and phenobarbital in kindled seizures124 and of phenobarbital, carbamazepine, and diazepam in the electroshock test in rats.125a In contrast, glycine failed to enhance the anticonvulsant action of phenytoin and valproate in the electroshock test. The mechanism by which glycine potentiates the action of anticonvulsant drugs remains unknown. There is now considerable interest in milacemide (a glycinamide derivative which elevates brain glycine) as a potential antiepileptic drug. Milacemide has been shown to have anticonvulsant effects in several experimental models of epilepsy including the audiogenic seizure.125b
Neurotransmitters and pharmacology
Published in Mark J. Ashley, David A. Hovda, Traumatic Brain Injury, 2017
Ronald A. Browning, Richard W. Clough
At the present time, there are no clinically available drugs whose mechanism of action is mediated through glycinergic neurotransmission. However, there is an experimental drug called milacemide that is believed to increase glycine levels in the brain and has been shown to have anticonvulsant effects in experimental animals. Glycinergic neurons in the brain stem and spinal cord have been shown to play a role in suppressing pain, and there is now much interest in developing inhibitors of the glycine transporter-2 (GlyT2) to treat chronic pain.167 At the present time, we have no clinically useful antiepileptic drugs that act on glycine neurotransmission.1
Efficacy and safety evaluation of safinamide as an add-on treatment to levodopa for parkinson’s disease
Published in Expert Opinion on Drug Safety, 2022
Kanako Kurihara, Takayasu Mishima, Shinsuke Fujioka, Yoshio Tsuboi
Safinamide is a drug classified as α-aminoamide, which was synthesized in the process of developing antiepileptic drugs [25,26]. Safinamide is a derivative of milacemide, a compound with reversible MAO-B inhibitory effect; therefore, the MAO-B inhibitory effect was also confirmed with safinamide. It was developed as a new anti-Parkinsonian medication with both dopaminergic and non-dopaminergic properties.