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. Author manuscript; available in PMC: 2019 Jun 1.
Published in final edited form as: Neuropharmacology. 2018 Mar 20;135:297–307. doi: 10.1016/j.neuropharm.2018.03.022

Figure 3.

Figure 3.

GLT-1a overexpression attenuates glutamate release during cocaine-primed reinstatement but is not sufficient to attenuate reinstatement. Cocaine intake (A), active lever presses during self-administration (B), inactive lever presses during self-administration (C) and lever presses on the previously active lever during the first twelve days of extinction (D) did not differ between groups later assigned to receive AAV-GFAP-GLT-1a or AAV-GFAP-eGFP. GLT-1a overexpression did not attenuate cocaine-primed reinstatement of cocaine-seeking (E). Glutamate efflux in the NAc was observed during the reinstatement of cocaine seeking for both groups (F). Area under the curve analysis of efflux during the full 90 minutes of cocaine-primed reinstatement test was reduced in rats receiving AAV-GFAP-GLT-1a compared to rats receiving AAV_GFAP-eGFP (G). Placement of microdialysis probes (H). (I). Immunohistochemistry for the hexa histidine tag on the AAV-GFAP-GLT-1a and GFAP in the same slice and the overlay of his and GFAP immunoreactivity reveals probe placement within the area of GLT-1a overexpression.* = p<0.05 compared to extinction. # = p<0.05 compared to AAV-GFAP-eGFP.