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. Author manuscript; available in PMC: 2022 Apr 26.
Published in final edited form as: ACS Chem Neurosci. 2022 Mar 21;13(7):946–958. doi: 10.1021/acschemneuro.1c00715

Figure 3:

Figure 3:

A. The left panel shows the effects of intrastriatal perfusion of 10 μM escitalopram on dopamine (DA; top, red), 3-methyltyramine (3-MT; middle, pink), and serotonin levels (5-HT; bottom, blue). Only basal 5-HT (blue) was significantly increased after escitalopram administration (right). B. Representative chromatograms (DA; 1), 3-methyltyramine (3-MT; 2), and serotonin levels (5-HT; 3) from a Chrimson-transfected mouse under basal conditions (gray) and during perfusion of the selective serotonin reuptake inhibitor (SSRI) escitalopram (green). Peak 3 showed a large increase in response to local delivery of the SSRI suggesting that this peak was serotonin. A standard containing 500 pM dopamine (peak 1) and serotonin (peak 3) is shown in black. C. The left panel shows the effects of systemic administration of tolcapone, a catechol-O- methyltransferase (COMT) inhibitor on dopamine (DA; top, red), 3-methyltyramine (3-MT; middle, pink), and serotonin levels (5-HT; bottom, blue). The enzyme COMT converts dopamine to 3-MT. Only 3-MT (pink) was significantly reduced after tolcapone administration (right). D. Representative chromatograms (DA; 1), 3-methyltyramine (3-MT; 2), and serotonin levels (5-HT; 3) after the intrastriatal perfusion of 50 nM 3-MT (red) vs. a basal dialysate sample from the same control mouse (gray). Reverse dialysis of 3-MT confirms peak 2 as 3-MT. A standard containing 5 nM dopamine (peak 1), 3-MT (peak 2), and serotonin (peak 3) is shown in black. Data in C are means ± SEMs. **P<0.01. A peak sometimes appearing between peaks 1 and 2 was not responsive to optical stimulation or high K+ perfusion, therefore, we did not attempt to identify this peak.