The effect of a pharmacological ketamine challenge on working memory and brain 
metabolism

Scheidegger, M; Boeker, H; Seifritz, E; Boesiger, P; Bajbouj, M; Walter, M; Henning, A; Grimm, S

doi:10.1016/j.biopsych.2011.03.031

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The effect of a pharmacological ketamine challenge on working memory and brain metabolism

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https://www.sciencedirect.com/science/article/pii/S000632231100309X
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引用

Scheidegger, M., Boeker, H., Seifritz, E., Boesiger, P., Bajbouj, M., Walter, M., Henning, A., & Grimm, S. (2011). The effect of a pharmacological ketamine challenge on working memory and brain metabolism. Poster presented at 66th Society of Biological Psychiatry Annual Meeting 2011, San Francisco, CA, USA.

引用: https://hdl.handle.net/11858/00-001M-0000-0013-BC0C-A

要旨

Background / Purpose:
Ketamine is a potent glutamatergic NMDA receptor antagonist with rapid antidepressant properties at subanaesthetic doses, thus providing a valuable research tool for the investigation of the neurobiology of mood disorders. Increasing evidence under-scores the role of glutamate dependent neuroplasticity and glutamatergic neurotransmission and metabolism in the patho-physiology of major depressive disorder.Hence, the effects of ketamine on functional brain activity during emotional and cognitive processing have to be further investigated in order to understand its rapid antidepressant properties.
This imaging study in 14 healthy subjects aims at probing the neuropharmacological effects of a single intravenous subanaesthetic ketamine infusion on fMRI-BOLD responses during a working memory task using affective stimuli compared to baseline conditions.
Main conclusion:
Ketamine administration had no effect on working memory performance, accordingly neural activity in the DLPFC did not differ between the baseline and the ketamine session. However, there was a significant ketamine effect on negative BOLD- responses in anterior (pregenual anterior cingulate), but not posterior (posterior cingulate) regions of the default- mode network and thus seems to induce a decoupling of neural activity in anterior and posterior regions of the network.