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. Author manuscript; available in PMC: 2012 Nov 2.
Published in final edited form as: J Neurosci. 2012 May 2;32(18):6072–6080. doi: 10.1523/JNEUROSCI.6486-11.2012

Figure 1.

Figure 1

Pharmacological and endogenous activation of D1Rs increases glutamate transmission. (A) Plot and representative traces show application of SKF81297 (SKF) increases glutamate transmission in extracellular fEPSP recordings, which is blocked by SCH23390 (SCH) treatment (SKF: 159±2%; n=10; SKF+SCH: 104±2%; n=6; p<0.0001). All traces are 10 sweep averages. (B) Plot and representative traces show application of amphetamine (AMPH) increases glutamate transmission in extracellular fEPSP recordings which is blocked by SCH treatment (AMPH: 132±4%; n=8; AMPH+SCH: 110±5%; n=7; p<0.003). (C) Plot and representative traces show AMPH application increases the total charge transfer in whole-cell voltage clamp experiments at −70mV (n=10). Resistance traces demonstrate the stability of recordings over time. (D) Plot and representative traces show prazosin and propanolol (included in all in vitro recordings) prevent a NE mediated alteration in glutamate transmission, indicating NE does not activate D1Rs (103±6% of baseline; n=3). Error bars represent SEM.