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The positron emission tomography (PET) tracer [ 18 F]GE-179 binds to the phencyclidine (PCP) site in the open N -methyl-D-aspartate receptor ion channel (NMDAR-IC). To demonstrate that PET can visualise increased [ 18 F]GE-179 uptake by active NMDAR-ICs and that this can be blocked by the PCP antagonist S-ketamine, 15 rats had an electrode unilaterally implanted in their ventral hippocampus. Seven rats had no stimulation, five received pulsed 400 µA supra-threshold 60 Hz stimulation alone, and three received intravenous S-ketamine injection prior to stimulation. Six other rats were not implanted. Each rat had a 90 min [ 18 F]GE-179 PET scan. Stimulated rats had simultaneous depth-EEG recordings of induced seizure activity. [ 18 F]GE-179 uptake (volume of distribution, V T ) was compared between hemispheres and between groups. Electrical stimulation induced a significant increase in [ 18 F]GE-179 uptake at the electrode site compared to the contralateral hippocampus (mean 22% increase in V T , p  =   0.0014) and to non-stimulated comparator groups. Rats injected with S-ketamine prior to stimulation maintained non-stimulated levels of [ 18 F]GE-179 uptake during stimulation. In conclusion, PET visualisation of focal [ 18 F]GE-179 uptake during electrically activated NMDAR-ICs and the demonstration of specificity for PCP sites by blockade with S-ketamine support the in vivo utility of [ 18 F]GE-179 PET as a use-dependent marker of NMDAR-IC activation.

NMDA receptor ion channel activation detected in vivo with [18F]GE-179 PET after electrical stimulation of rat hippocampus

NMDA receptor ion channel activation detected in vivo with [¹⁸F]GE-179 PET after electrical stimulation of rat hippocampus