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. Author manuscript; available in PMC: 2016 May 1.
Published in final edited form as: Trends Neurosci. 2015 Apr 14;38(5):279–294. doi: 10.1016/j.tins.2015.03.003

Figure 3. Stress decreases AMPAR-mediated excitation and GluA1 expression at temporoammonic to CA1 cell synapses and chronic fluoxetine reverses these effects.

Figure 3

A. Field excitatory postsynaptic potentials (fEPSPs) are recorded in stratum lacunosum moleculare in response to stimulation of the temporoammonic (TA) pathway in Mg2+-free saline, allowing dissection of AMPAR- and NMDAR-mediated components. AMPAR-mediated transmission was reduced over a range of stimulation intensities after chronic unpredictable stress (red) compared to unstressed rats (blue). Quantification of AMPA:NMDA ratios (B) and GluA1 protein (C) reveals that the selective decrease in AMPAR-mediated transmission is due to decreased GluA1 expression. Administration of fluoxetine for three weeks to stressed rats restored both AMPA:NMDA ratios and GluA1 expression. Modified with permission from Kallarackal et al., 2013 [72].