Tiagabine exerts an anti-epileptogenic effect in amygdala kindling epileptogenesis in the rat
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Cited by (32)
Divergent effects of levetiracetam and tiagabine against spontaneous seizures in adult rats following neonatal hypoxia
2018, Epilepsy ResearchCitation Excerpt :The identification of fundamentally different anti-seizure medications has previously required fundamentally different seizure models. For example, both levetiracetam (LEV) and tiagabine (TGB) are ineffective in the MES model, but were identified based on their efficacy in the amygdala kindling model of seizures (Dalby and Nielsen, 1997a, 1997b; Klitgaard et al., 1998; Löscher and Hönack, 1993). The difference in drug efficacy in these preclinical models is likely related to fundamental differences in the seizures generated in each model: the MES model engages brainstem networks mediating tonic seizures while the amygdala kindling model engages forebrain seizure networks more typical of complex partial seizures.
Pharmacological and histological characterisation of nicotine-kindled seizures in mice
2005, NeuropharmacologyCitation Excerpt :In several pre-clinical studies, LEV shows a distinct profile in that it blocked kindling development as well as kindled seizures, but was ineffective in maximal seizure tests in naïve animals e.g. maximal electroshock (MES) and PTZ-induced seizures (Gower et al., 1992; Klitgaard et al., 1998; Loscher et al., 1998). TGB mediates its anticonvulsive effects through selective inhibition of the GABA transporter-1 (GAT-1) (Dalby and Nielsen, 1997; Dalby, 2000). Tiagabine has been shown to inhibit amygdala kindling as well as several types of acute seizures in naïve animals (Dalby and Nielsen, 1997; Nielsen et al., 1991).
Anticonvulsant effects of LY456236, a selective mGlu1 receptor antagonist
2005, NeuropharmacologySelective suppression of hippocampal region hyperexcitability related to seizure susceptibility in epileptic El mice by the GABA-transporter inhibitor tiagabine
2002, Brain ResearchCitation Excerpt :Tiagabine (TGB) is a selective inhibitor of the GABA transporter, and may prolong the dwell time of GABA in the synaptic cleft. Therefore, the antiepileptic effects of TGB have been examined in animal models [4,5,18,22,23] and in some types of epilepsy in humans (reviewed in Ref. [15]) by systemic administration. However, the mechanisms responsible for TGB activity on epileptogenesis in each epilepsy model remain unclear.