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. Author manuscript; available in PMC: 2011 Sep 15.
Published in final edited form as: Neuroscience. 2010 Jun 19;169(4):1848–1859. doi: 10.1016/j.neuroscience.2010.05.052

Figure 6.

Figure 6

Representative MEA tracings from a rat receiving an injection of galantamine (3 mg/kg, i.p.), followed, 5 min later, by kynurenine (50 mg/kg, i.p.). Top two tracings: MEA signal from the glutamate-sensitive site (GluOx) and its adjacent background sentinel. The third tracing, illustrating the self-referenced (Self Ref) glutamate signal, reveals that galantamine attenuates the amplitude of the decline and the time course to values similar to those seen following 25 mg/kg kynurenine (cf. Fig. 5 and Table 1). Bottom tracing: self-referenced record from an animal that first received kynurenine (50 mg/kg, arrow) and then, 3 hrs later at the nadir of glutamate levels, galantamine (3 mg/kg, arrow). The glutamate signal gradually returns to basal values following delayed galantamine administration, suggesting that the kynurenine-induced attenuation of glutamate release is consistently mediated by α7 nAChRs.

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