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. Author manuscript; available in PMC: 2014 Apr 10.
Published in final edited form as: Neuron. 2013 Apr 10;78(1):81–93. doi: 10.1016/j.neuron.2013.02.011

Figure 5. Glutamate mediates the psychosis-associated pattern of hippocampal hypermetabolism induced by acute ketamine administration.

Figure 5

(A) As shown by in vivo recording of extracellular glutamate efflux performed under the same conditions as for the imaging shown in Figure 3, acute ketamine administration (30mg/kg) resulted in increases in evoked extracellular glutamate in CA1 and subiculum (SUB), and not in entorhinal cortex (EC) or dentate gyrus (DG). * p < 0.05 relative to EC.

(B) The time course of the effect of acute ketamine administration in the CA1 (red line) vs. entorhinal cortex (EC; black line).

(C) Pre-treatment with the mGluR2/3 agonist LY379268 (10mg/kg) blocked the evoked extracellular glutamate response within the CA1 subfield.

(D) Relative to saline pre-treatment, pre-treatment with mGluR2/3 agonist LY379268 (10mg/kg) blocked the evoked rCBV response, with a trend for also reducing basal rCBV as measured at “Time 0” (prior to the ketamine challenge).

Data for panels A–D are represented as mean ± SEM. See also Figure S2.