Structural and Functional Neuroplasticity Following Bilateral Vestibular Loss: A Longitudinal [18F]-UCB-H/[18F]-FDG Dual Tracer Rat Study

Neuronal lesions trigger mechanisms of structural and functional neuroplasticity, which can support recovery. However, the temporal and spatial appearance of structure-function changes and their interrelation remain unclear. The current study aimed to directly compare serial whole-brain in vivo measurements of functional plasticity (by [ 18 F]-FDG-PET) and structural synaptic plasticity (by [ 18 F]-UCB-H-PET) before and after bilateral labyrinthectomy in rats and investigate the effect of locomotor training. Complex structure-function changes were found after bilateral labyrinthectomy: in brainstem-cerebellar circuits, regional cerebral glucose metabolism (rCGM) decreased early, followed by reduced synaptic density. In the thalamus, increased [ 18 F]-UCB-H binding preceded a higher rCGM uptake. In frontal-basal ganglia loops, an increase in synaptic density was paralleled by a decrease in rCGM. In the group with locomotor training, thalamic rCGM and [ 18 F]-UCB-H binding increased following bilateral labyrinthectomy compared to the no training group. Rats with training had relatively fewer body rotations. In conclusion, combined [ 18 F]-FDG/[ 18 F]-UCB-H dual tracer imaging reveals that adaptive neuroplasticity after bilateral vestibular loss is not a uniform process but is composed of complex spatial and temporal patterns of structure-function coupling in networks for vestibular, multisensory, and motor control, which can be modulated by early physical training.