Karsten K. Madsen

TL;DR: The development of tiagabine selectively inhibiting the GABA transporter GAT1 constitutes a proof of concept that the GABA transporters are interesting drug targets in the context of antiepileptic drugs, and it is suggested that the betaine-GABA transporter BGT1 should receive particular interest in this context.

TL;DR: A greater understanding is provided of the role that each of the aforementioned metabolic processes plays in controlling excitatory and inhibitory neurotransmission and how their use will hopefully facilitate the development of safer and more efficacious therapies for the treatment of epilepsy and other neurological disorders.

TL;DR: It is found that removal of Glu by astrocytic transporters triggers an elevation in the extracellular level of GABA, which represents a direct link between inhibitory and excitatory neurotransmission and may function as a negative feedback combating intense excitation in pathological conditions such as epilepsy or ischemia.

TL;DR: Analysis of the anti‐convulsant effect of the GAT2/3 inhibitor SNAP‐5114 in the Frings audiogenic seizure‐susceptible mouse alone, and in combination with tiagabine and EF1502 suggests that the combined inhibition of GAT1 and BGT‐1 may afford some advantage over inhibiting either transporter alone.

TL;DR: The present results do not support a role for BGT1 in the control of seizure susceptibility and cannot provide a mechanistic understanding of the synergism that has been previously reported with tiagabine and EF1502.