Fig. 2
G1-induced cLTP involves a postsynaptic expression mechanism, and is dependent on NMDA, but not GABA, receptors. A Plot of pooled data illustrating the effects of 10 nM G1 (15 min) on synaptic transmission at TA-CA1 synapses. B Corresponding plot of the pooled paired pulse ratio (PPR) against time for the experiments shown in A. The effects of G1 were not associated with any change in PPR, indicating a postsynaptic expression mechanism. C–F Plots of pooled data illustrating the effects of G1 (10 nM; 15 min) on synaptic transmission in juvenile hippocampal slices. Activation of NMDA receptors was involved as G1 failed to increase synaptic efficacy in the presence of the NMDA receptor antagonist, D-AP5 (50 µM; C). D, E The ability of G1 to induce cLTP was blocked by inhibition of GluN2A subunits with NVP-AAM0077 (D), but was not altered by the GluN2B antagonist, ifenprodil (E). F G1-induced cLTP was independent of GABAergic inhibition as the effects of G1 were unaffected in the presence of GABAA and GABAB receptor antagonists, picrotoxin and CGP55845, respectively