Figure 1. The enhanced tonic GABAA current in TC neurons of rat and mouse genetic models of typical absence seizures results from a malfunction in the GABA transporter GAT-1.

Figure 1The enhanced tonic GABAA current in TC neurons of rat and mouse genetic models of typical absence seizures results from a malfunction in the GABA transporter GAT-1

A1. Current traces from TC neurons of postnatal day (P) 14 and 17 non-epileptic control (NEC) and GAERS rats indicate the presence of a tonic GABAA current which is revealed as a shift in baseline current following the focal application of 100 μM gabazine (GBZ, white bars). The amplitude of the tonic current is about two-fold larger in GAERS compared to NEC at P17. A2. Tonic current in NEC and GAERS at the indicated postnatal days. A3. Tonic GABAA current in stargazer (stg) (P19-21) and lethargic (lh) (P27-30) mice and respective control age-matched littermates (Lit). B. Comparison in P18-21 NEC and GAERS (1), and in P19-21 stargazer (stg) mice and littermates (Lit) (2) of the effects of blocking GAT-1 alone (by 10 μM NO711), GAT-3 alone (by 20 μM SNAP5114), and GAT-1 and GAT-3 together (NO + SNAP) on tonic GABAA current amplitude of TC neurons. A2 and A3: * p<0.05, ** p<0.01 and *** p<0.001, mutant vs. non-mutant animals. B1 and B2: * p<0.05, ** p<0.01 and *** p<0.001, mutant vs. non-mutant animals under control conditions; + p<0.05, $ p<0.01 and # p<0.001, drug vs. non-drug for each strain. (A-D: reproduced with permission from Cope et al., 2009, ©Nature Publishing Group).

From: GABA-A Receptor Function in Typical Absence Seizures

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Jasper's Basic Mechanisms of the Epilepsies [Internet]. 4th edition.
Noebels JL, Avoli M, Rogawski MA, et al., editors.
Copyright © 2012, Michael A Rogawski, Antonio V Delgado-Escueta, Jeffrey L Noebels, Massimo Avoli and Richard W Olsen.

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