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. 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 2.

Figure 2

Halorhodopsin inhibition of mPFC- and INS-to-NAcore inputs reduced quinine-resistant alcohol intake. (a) Halorhodopsin (eNpHr3.0) activation in mPFC-to-NAcore terminals significantly reduced intake, relative to that in the absence of laser stimulation, of alcohol adulterated with 10 or 30 mg l−1 quinine but not quinine-free alcohol. (b) Laser stimulation had no effect on alcohol intake in control rats infected with EYFP in mPFC-to-NAcore terminals. (c) To compare laser stimulation of halorhodopsin versus EYFP in mPFC terminals, we calculated the difference in intake between laser stimulation and no stimulation under six conditions: halorhodopsin + 10 or 30 mg l−1 quinine, halorhodopsin + no quinine, EYFP + 10 or 30 mg l−1 quinine, EYFP + no quinine. Laser stimulation only decreased alcohol intake with halorhodopsin + quinine. (d) Inhibiting mPFC-to-NAcore terminals did not alter intake of saccharin (sacc) ± quinine (quin). (e) Halorhodopsin inhibition of INS-to-NAcore terminals significantly reduced intake of quinine-adulterated alcohol (30 mg l−1 quinine) but not quinine-free alcohol. (f) Laser stimulation of INS-to-NAcore terminals had no effect in EYFP-infected rats. (g) Difference scores. Laser stimulation of INS-to-NAcore terminals decreased alcohol intake only with halorhodopsin + quinine. Tukey post hoc *P < 0.05. Error bars indicate s.e.m.