Skip to main content
. Author manuscript; available in PMC: 2014 Aug 1.
Published in final edited form as: Nat Neurosci. 2013 Jun 30;16(8):1094–1100. doi: 10.1038/nn.3445

Figure 6.

Figure 6

NMDARs regulate evoked action potential firing under mPFC-to-NAcore inputs from alcohol-drinking but not naive rats. A ten-pulse train (20 Hz) of mPFC-ChR2-evoked EPSPs was stimulated every 10 s to evoke action potential firing; neurons were depolarized to about −55 mV (alcohol, −56.7 ± 2.5 mV; naive, −54.1 ± 2.9 mV; P = 0.491) with the patch amplifier to allow EPSPs to evoke ∼5 action potentials. (a,b) Traces (a) and time courses (b) from individual neurons showing AP5 inhibition of firing evoked by mPFC-to-NAcore ChR2 stimulation in neurons from alcohol-drinking but not naive rats. Each point represents the average of the six sweeps in that minute. Tick marks under firing traces in a indicate ChR2 stimulation. Firing does not completely track the timing of ChR2 stimulation, which likely reflects the strong potassium channel–mediated after hyperpolarization in NAcore neurons. (c) AP5 decreased firing in neurons from alcohol-drinking but not naive rats. Because of variability in firing across time, we averaged the firing across 4 min before AP5 administration (“basal”) and averaged the firing across the minutes 4–7 of AP5 exposure (“AP5”), as firing tended to run down in all cells after this point. For b, firing was normalized to the basal firing value. Tukey post hoc *P < 0.05. Error bars indicate s.e.m.