• Yota Fujimura, Fumihiko Yasuno, Amanda Farris, Jeih-San Liow, Marilla Geraci, Wayne Drevets, Daniel S Pine, Subroto Ghose, Alicja Lerner, Richard Hargreaves, H Donald Burns, Cheryl Morse, Victor W Pike, and Robert B Innis.
• Molecular Imaging Branch, National Institute of Mental Health, Bethesda, Maryland 20892, USA. FujimuraY@mail.nih.gov
• Biol. Psychiatry. 2009 Jul 1;66(1):94-7.

BackgroundPositron emission tomography (PET) can localize and quantify neurokinin-1 (NK(1)) receptors in brain using the nonpeptide antagonist radioligand, [(18)F]SPA-RQ. We sought to determine if patients with panic disorder have altered density of NK(1) receptors in brain because of their history of recurrent panic attacks. We also sought to determine if a drug-induced panic attack releases substance P in brain, as measured by decreased binding of [(18)F]SPA-RQ.MethodsPositron emission tomography scans with [(18)F]SPA-RQ were performed in 14 patients with panic disorder and 14 healthy subjects. Of these two groups, 7 patients and 10 healthy subjects were scanned twice, once at baseline and once after injection of doxapram, a drug that induces panic attacks.ResultsNK(1) receptor binding in patients (n = 14) compared with that in healthy subjects (n = 14) was significantly decreased by 12% to 21% in all brain regions. Doxapram effectively produced panic attacks in 6 of 7 patients with panic disorder but only 2 of 10 healthy subjects. Doxapram caused no significant change of [(18)F]SPA-RQ binding in either patients or healthy subjects.ConclusionsAlthough induction of a panic attack has no significant effect on [(18)F]SPA-RQ binding to NK(1) receptors, patients with panic disorder have widespread reduction of NK(1) receptor binding in brain.

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