Antiepileptic Effects of Tiagabine, a Selective GABA Uptake Inhibitor, in the Rat Kindling Model of Temporal Lobe Epilepsy

Morimoto, Kiyoshi; Sato, Hitoshi; Yamamoto, Yoshitaka; Watanabe, Takemi; Sekiya, Hiroshi

doi:10.1111/j.1528-1157.1997.tb01478.x

Cited by 55 publications

(27 citation statements)

References 24 publications

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“…The severity and duration of convulsions in amygdala-kindled rats are reduced (4); in addition, daily treatment with TGB 10 mgkg for 10 days significantly retards the development of kindling (7). TGB also shows activity in maximal electroshockinduced seizures, bicuculline-induced seizures in rats (4), and picrotoxin-induced convulsions in mice (8).…”

Section: Animal Studies and Pharmacokineticsmentioning

confidence: 99%

Tiagabine

Schachter

1999

Epilepsia

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Summary: Tiagabine (TGB) is a recently approved antiepileptic drug (AED) that inhibits y-aminobutyric acid (GABA) reuptake into neurons and glia, a mechanism of action that is specific and unique among the AEDs. TGB is potent and has linear and predictable pharmacokinetics. It has no clinically relevant effects on hepatic metabolism or serum concentrations of other AEDs, effects on laboratory values, or interactions with common non-AEDs. TGB is effective as add-on therapy for partial seizures in patients with medically refractory epilepsy in doses ranging from 30 to 56 mg daily. Conversion to TGB monotherapy can be achieved in patients with medically refractory epilepsy, although additional controlled studies are needed to confii the efficacy of TGB as monotherapy and to establish the effective dosage range. In controlled studies, the most common adverse events of TGB are dizziness, asthenia, somnolence, accidental injury, infection, headache, nausea, and nervousness. These are usually mild to moderate in seventy and almost always resolve without medical intervention.

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Section: Animal Studies and Pharmacokineticsmentioning

confidence: 99%

Tiagabine

Schachter

1999

Epilepsia

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“…and 2.5 mg/kg, i.p., respectively. 18,19) NNC-711 and diazepam also inhibited pentetrazol-induced kindled seizure activities in mice at doses of 2 mg/kg, i.p. and 1 mg/kg, i.p., respectively; however, significant potentiation of effects of both drugs were observed in simultaneous use with AIDA in this study.…”

Section: Discussionmentioning

confidence: 99%

Anticonvulsant Effect of (RS)-1-Aminoindan-1,5-dicarboxylic Acid on Pentetrazol-Induced Kindled Seizures in Mice

Watanabe

Kaida

Takechi

et al. 2010

Biological & Pharmaceutical Bulletin

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The present study was undertaken to clarify the effect of group I metabotropic glutamate receptor (mGluR) antagonist, (RS)-1-aminoindan-1,5-dicarboxylic acid (AIDA) on pentetrazol-induced kindled seizures. The mechanism of the anticonvulsant effect of AIDA was also studied. Mice were anesthetized with pentobarbital; the electrodes and guide cannula were chronically implanted into the cortex and lateral ventricle. In order to induce kindling, pentetrazol at a dose of 40 mg/kg was injected intraperitoneally once every 48 h. Behavioral and electroencephalographic (EEG) seizures were observed for 20 min following pentetrazol administration. Intracerebroventricular (i.c.v.) injection of AIDA (1000 nmol/site) resulted in a significant inhibitory effect on pentetrazol-induced kindled seizures, and this effect was antagonized by a group I mGluR agonist, (RS)-3,5-dihydroxyphenylglycine ((RS)-3,5-DHPG). The effect of AIDA (200 nmol/site) on pentetrazol-induced kindled seizures was augmented by the simultaneous use of g g-aminobutyric acid (GABA) mimetic drugs, such as NNC-711 and diazepam. Moreover, the effect of AIDA (1000 nmol/site) on pentetrazol-induced kindled seizures was antagonized by a GABA A receptor antagonist, bicuculline and a GABA C receptor antagonist, (1,2,5,6-tetrahydropyridin-4-yl) methylphosphinic acid (TPMPA). It can be concluded that AIDA had an anticonvulsant effect on pentetrazol-induced kindled seizures, which was partially mediated by the GABAergic mechanism through GABA A and GABA C receptors.

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“…It also has been used as a mood stabilizer and in treatment of panic disorder. Tiagabine has exhibited antikindling and antianxiety effects in preclinical studies [82,83], and its anxiolytic effects have been shown across anxiety disorders [84,85•]. Tiagabine is well tolerated and may hold promise in treating PTSD via its facilitation of GABA neurotransmission [23,86,87].…”

Section: Tiagabinementioning

confidence: 99%

Antiepileptic drugs for the treatment of post-traumatic stress disorder

Berlin

2007

Curr Psychiatry Rep

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Post-traumatic stress disorder (PTSD) is a disruptive, chronic, and relatively common disorder that is often difficult to treat. Many patients with PTSD are unresponsive, have only moderate or marginal responses, or have troubling side effects to first-line serotonin reuptake inhibitor treatment. Studies suggest that antiepileptic drugs (AEDs) may be an effective treatment alternative or adjunctive treatment for the symptoms of PTSD. Recent results from case reports and open and controlled studies on the efficacy and tolerability of AEDs in PTSD are reviewed here, and their methodological limitations are discussed when relevant. AEDs shown to be effective in double-blind, placebo-controlled trials of PTSD include lamotrigine, topiramate, and tiagabine. Other AEDs that appear promising in open-label trials of PTSD include carbamazepine, valproate, gabapentin, vigabatrin, phenytoin, and levetiracetam. Stress-activated limbic kindling may be involved in the pathogenesis of PTSD. The possibility that AEDs may be effective in the treatment of PTSD due to their antikindling effect is discussed, and suggestions for future research are made.

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Antiepileptic Effects of Tiagabine, a Selective GABA Uptake Inhibitor, in the Rat Kindling Model of Temporal Lobe Epilepsy

Cited by 55 publications

References 24 publications

Tiagabine

Tiagabine

Anticonvulsant Effect of (RS)-1-Aminoindan-1,5-dicarboxylic Acid on Pentetrazol-Induced Kindled Seizures in Mice

Antiepileptic drugs for the treatment of post-traumatic stress disorder

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