Skip to main content
. Author manuscript; available in PMC: 2008 Nov 28.
Published in final edited form as: J Neurosci. 2008 May 28;28(22):5762–5771. doi: 10.1523/JNEUROSCI.0575-08.2008

Figure 1.

Figure 1

Gabapentin dose-dependently increases basal GABAergic transmission in CeA from non-dependent rats through a GABAB receptor-related mechanism. A: Concentration-response relationship for gabapentin (10, 25, 50 and 75 μM) enhancement of mean IPSC amplitudes in CeA neurons, expressed as percent of control (number of cells for the four doses: 3, 5, 8, and 4 respectively). The logistic curve, plotted by Origin Software (Microcal), using y = (A1 – A2)/{1 + (x/xo)*p + A2), gives an apparent EC50 (dashed line) of 27 μM gabapentin for IPSC enhancement. Parameters of the logistic curve were set at: upper asymptote fixed at 140% and lower at 100%. Rate was fixed at 4.0, with “center” unfixed. Error bars = S.E.M., *p < 0.05. B: Gabapentin (50 μM) superfusion for 10 min significantly (p < 0.05) increased the mean amplitudes of evoked GABA-IPSCs without (solid circles; n = 8), but not with (solid squares; n = 5) co-application of 1 μM CGP 55845A (CGP), a GABAB receptor antagonist. Note that CGP completely blocked the gabapentin-induced enhancement of IPSCs. Insert: Representative recordings of evoked IPSCs. Superfusion of GABAA and GABAB receptor blockers completely blocked these IPSCs. C: Gabapentin (50 μM) significantly (*p < 0.05) decreased the mean PPF of IPSCs only in the absence of CGP. Mean (± s.e.m) of paired-pulse ratio expressed as IPSC2/IPSC1.