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Vortrag

Acute ketamine administration modulates glutamatergic neurotransmission and functional brain activation in prefrontal cortex implications for major depression

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http://pubman.mpdl.mpg.de/cone/persons/resource/persons84402

Henning,  A
Department High-Field Magnetic Resonance, Max Planck Institute for Biological Cybernetics, Max Planck Society;

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Zitation

Scheidegger, M., Henning, A., Walter M, Fuchs A, Krähenmann R, Böker H, Bösiger P, Seifritz, E., & Grimm, S. (2011). Acute ketamine administration modulates glutamatergic neurotransmission and functional brain activation in prefrontal cortex implications for major depression. Talk presented at 27. Symposium der Arbeitsgemeinschaft für Neuropsychopharmakologie und Pharmakopsychiatrie (AGNP). München, Germany.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-0013-B8E6-4
Zusammenfassung
Background: Ketamine is a potent NMDA receptor antagonist with rapid antidepressant properties at subanaesthetic doses. This multimodal imaging study reveals the effects of a subanaesthetic ketamine infusion on fMRI-BOLD responses during an emotional processing task and their relationship to glutamatergic metabolite concentrations in the pregenual anterior cingulate cortex (PACC) assessed by proton magnetic resonance spectroscopy (1H-MRS). Methods: 23 healthy subjects were asked to judge photographs from the International Affective Picture System (IAPS) by button press according to their valence in two separate fMRI sessions (baseline/ketamine) on a Philips 3T MR unit. S-ketamine was administered as an i.v. bolus of 0.12 mg/kg, followed by an infusion of 0.25 mg/kg/h over 60 min. 1H-MRS spectra from the bilateral PACC could be obtained in 16 subjects immediately after the task using a JPRESS sequence. Results and Conclusion: In the PACC, changes in NBRs correlated with glutamine to glutamate ratios as a putative marker of glutamatergic neurotransmission after ketamine administration compared to baseline. These changes are most likely interpreted in terms of an increased glutamate-glutamine-cycling rate after ketamine administration. Thus, the antidepressant effect of ketamine might be linked to a beneficial short-term influence on glutamatergic neurotransmission.