Abstract #0437
No reversal of ketamine-induced functional connectivity changes in the rat brain after acute dosing of antipsychotics
Dany D'Souza 1 , Andreas Bruns 2 , Basil Knnecke 2 , Daniel Alberati 3 , Edilio Borroni 4 , Markus von Kienlin 2 , Annemie Van der Linden 5 , and Thomas Mueggler 2
1
Pharma Research & Early Development
Informatics, Disease & Translational Informatics, F.
Hoffmann-La Roche Ltd., Basel, Basel Stadt, Switzerland,
2
Pharma
Research & Early Development, DTA Neuroscience,
Behaviour Pharmacology & Preclinical Imaging, F.
Hoffmann-La Roche Ltd., Basel Stadt, Switzerland,
3
Pharma
Research & Early Development, DTA Neuroscience,
Functional Neuroscience, F. Hoffmann-La Roche Ltd.,
Basel Stadt, Switzerland,
4
Pharma Research &
Early Development, DTA Neuroscience, Biomarkers and
Clinical Imaging, F. Hoffmann-La Roche Ltd., Basel Stadt,
Switzerland,
5
Bio-Imaging
Lab, University of Antwerp, Antwerp, Belgium
In the present resting-state fMRI study we investigated
whether an acute dose of a first or second generation
antipsychotic (haloperidol, clozapine, & risperidone) or
an mGlu2/3 agonist (LY354740) can reverse the hyper
functional connectivity specifically across cortical
areas in the rat brain elicited by acute treatment with
ketamine. While acute antipsychotic dosing failed to
block the effect of the NMDA antagonist (ketamine) we
identified a set of brain regions, i.e. substantia nigra
and motor cortex, commonly modulated by haloperidol,
clozapine, or LY354740 likely reflecting the direct or
indirect modulation of dopamine transmission originating
in the nigrostriatal pathway, respectively.
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