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The metabotropic glutamate receptor 5 (mGluR5) is a promising treatment target for psychiatric disorders due to its modulatory effects on glutamate transmission. Using [ 11 C]ABP688, we previously showed that the rapidly acting antidepressant ketamine decreases mGluR5 availability. The mGluR5 radioligand [ 18 F]FPEB offers key advantages over [ 11 C]ABP688; however, its suitability for drug challenge studies is unknown. We evaluated whether [ 18 F]FPEB can be used to capture ketamine-induced effects on mGluR5. Seven healthy subjects participated in three [ 18 F]FPEB scans: a baseline, a same-day post-ketamine, and a 24-h post-ketamine scan. The outcome measure was V T / f P , obtained using a two-tissue compartment model and a metabolite-corrected arterial input function. Dissociative symptoms, heart rate and blood pressure increased following ketamine infusion. [ 18 F]FPEB V T / f P  decreased by 9% across the cortex after ketamine infusion, with minimal difference between baseline and 24-h scans. Compared to our previous work using [ 11 C]ABP688, the magnitude of the ketamine-induced change in mGluR5 was smaller using [ 18 F]FPEB; however, effect sizes were similar for the same-day post-ketamine vs. baseline scan (Cohen’s d = 0.75 for [ 18 F]FPEB and 0.88 for [ 11 C]ABP688). [ 18 F]FPEB is therefore able to capture some of the effects of ketamine on mGluR5, but [ 11 C]ABP688 appears to be more suitable in drug challenge paradigms designed to probe glutamate transmission.

Measuring the effects of ketamine on mGluR5 using [18F]FPEB and PET

Measuring the effects of ketamine on mGluR5 using [¹⁸F]FPEB and PET