Species-conserved reconfigurations of brain network topology induced by ketamine

Citation: Translational Psychiatry (2016) 6, e786; doi:10.1038/tp.2016.53Published online 19 April 2016R Becker1,9, U Braun2,9, A J Schwarz3,4,5, N Gass1, J I Schweiger2, W Weber-Fahr1, E Schenker6, M Spedding7, C Clemm von Hohenberg1,2, C Risterucci8, Z Zang2, O Grimm2, H Tost2, A Sartorius1,2,9 and A Meyer-Lindenberg2,9 Top of page Introduction Ketamine, a potent N-methyl-d-aspartate (NMDA)-receptor antagonist, has spurred considerable interest in the preclinical as well as clinical applications. Its effects range from anesthesia after acute application of high doses to psychomimetic symptoms, derealization and cognitive disruption,1, 2 as well as relatively rapid but long-lasting antidepressant action after acute administration of lower doses.3, 4, 5 Furthermore, ketamine is widely studied in both human and laboratory animals as a translational pharmacological model of glutamatergic (dys-)function in schizophrenia.1, 6, 7, 8 Several studies have probed the underlying neurobiological substrates of these actions in humans2, 9, 10, 11, 12 and animals6, 9,…

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