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. Author manuscript; available in PMC: 2016 Sep 24.
Published in final edited form as: Neuroscience. 2015 Jul 23;304:161–175. doi: 10.1016/j.neuroscience.2015.07.052

Figure 7. Systemic nicotine acts through α6-containing nAChRs to enhance AMPA receptor function in VTA DA neurons.

Figure 7

A) Experimental design. α6L9S mice were injected (i.p.) with nicotine at the indicated dose. Sixty minutes after nicotine injection, mice were used to prepare brain slices for patch clamp recording in VTA DA neurons. AMPAR currents were elicited by locally puffing AMPA onto the cell body of the recorded neuron and recording inward currents in voltage clamp mode.

B) A dose of nicotine (0.03 mg/kg) similar to the dose used to elicit locomotor activation in α6L9S mice is sufficient to enhance AMPAR currents in VTA DA neurons. Representative AMPA-evoked currents from α6L9S and nonTG mice injected with the indicated dose of nicotine are shown.

C) Quantification of AMPA-evoked current responses in VTA DA neurons from α6L9S and nonTG mice injected with the indicated dose of nicotine. Mean peak AMPA-evoked currents for each group/treatment are plotted. Mann-Whitney U-test: *p<0.05 (actual: α6L9S saline vs. nicotine 0.03 mg/kg, p=0.0293; nonTG saline vs. nicotine 0.17 mg/kg, p=0.019). (nonTG: VEH n=4; nicotine (0.03 mg/kg) n=7; nicotine (0.17 mg/kg) n=6; α6L9S: VEH n=6; nicotine (0.03 mg/kg) n=8)