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. Author manuscript; available in PMC: 2018 Feb 8.
Published in final edited form as: Neuropharmacology. 2017 Apr 15;121:69–78. doi: 10.1016/j.neuropharm.2017.04.023

Figure 1. MEA design, signal transduction scheme, in vitro calibration, and representative placement.

Figure 1

(A): Four platinum recording channels near the tip of the MEA allow for the detection and isolation of glutamate within a single brain sub-region (see Burmeister and Gerhardt, 2001 for further detail on self-referencing); (B): Glutamate is detected in vivo when a glutamate molecule (Glu) contacts the platinum surface (PT) coated with glutamate oxidase (Gluox; see Rutherford et al., 2007) and is oxidized to the reporting molecule hydrogen peroxide (H2O2). The oxidation of H2O2 generates a current that is proportional to the concentration of glutamate at the surface of the MEA; (C): In vitro calibrations of the MEA are conducted immediately before implantation into the PFC. The solid line tracing is from the glutamate-sensitive (Gluox) recording channel, and the dashed tracing is from the sentinel background channel. Arrows correspond to the addition of ascorbic acid (AA, 500 μL), glutamate (glut, 3 × 40 μL), dopamine (DA, 40 μL), and H2O2, (40 μL) into the stirred calibration beaker. Current (nAmp) is depicted along the y-axis, and time (sec) along the x-axis. The successive additions of glutamate (20 μM/aliquot) produce a linear increase on Gluox, but not sentinel channels. Important for self-referencing, the Gluox and sentinel channels respond equally to every addition, except glutamate; (D): The cartoon and the corresponding photomicrograph depict the desired target location for both the MEAs (between the prelimbic (PrI) and infralimbic (IL) cortices) and infusion cannulae (within the nucleus accumbens shell). Arrows indicate the ventral termination of the MEA, guide, and infusion cannula within the respective photomicrographs. NAcc: Nucleus accumbens core; CC: Corpus callosum; aca: anterior commissure; NAcSh: Nucleus accumbens shell.