Juha-Pekka Niskanen1,2, Antti M. Airaksinen1,
Alejandra Sierra1, Joanna K. Huttunen1, Pasi A.
Karjalainen2, Jari Nissinen1, Asla Pitknen1,3,
Olli Grhn1
1Department of
Neurobiology, A. I. Virtanen Institute for Molecular Sciences, University of
Eastern Finland, Kuopio, Finland; 2Department of Physics &
Mathematics, University of Eastern Finland, Kuopio, Finland; 3Department
of Neurology, Kuopio University Hospital, Kuopio, Finland
Previously, we have detected deficit and recovery of the rat somatosensory BOLD response following TBI, although SI appeared normal in structural MRI. To further investigate this phenomenon, simultaneous LFP/fMRI and histology were performed 2 and 35 days after TBI in rats. The ipsilateral BOLD and LFP responses were lost at 2d, but only partially at 35d. Furthermore, histology revealed gliosis in the ipsilateral ventral posterolateral (VPL) thalamic nucleus. Our results show that hemodynamic uncoupling is not the cause for the detected functional deficit in the rat SI after TBI, but rather neurodegeneration in the thalamic VPL.
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