Abstract
Background and aim Reactive gliosis may be beneficial for central compensation after unilateral inner ear damage. The aim of the present study was to visualize whole brain glial activation in vivo and over time by serial [ 18 F]-GE180- μ PET in a rat model of chemical unilateral labyrinthectomy (UL). Methods Ten Sprague–Dawley rats underwent a left-sided UL by transtympanic injection of bupivacaine and arsenilate, ten rats received a left-sided middle-ear injection of saline as a control group. Behavioural testing for symptoms of vestibular tone imbalance including registration of nystagmus and postural asymmetry was performed 1 day before and at days 1, 3, 7, 15, 30 after UL/sham injection. For functional imaging of glial activation, whole-brain μ PET with [ 18 F]-GE180, a novel translocator protein (tspo) ligand, was performed before and on 7, 15, 30 days after UL/sham injection. In vivo autoradiography was done at the respective time points for crosscheck and combined with Nissl-staining of the corresponding slices for detailed anatomic mapping. Results All rats showed clinical signs of an acute vestibular syndrome following UL with a maximum at 2 and 3 days. Nystagmus disappeared until day 5, postural asymmetry decreased significantly until day 15. In the UL group, [ 18 F]-GE180- μ PET depicted a glial activation in the ipsilesional vestibular, cochlear and facial nucleus at day 7, which further increased until day 15 and was only slightly visible at day 30. In addition no other regions of the brain showed signs of glial activation. In the sham group, glial activation was found in the facial nucleus at day 7 and 15. The time course and anatomic localization of glial activations were confirmed by in vivo [ 18 F]-GE180 autoradiography and Nissl-staining. Conclusions Glial activation takes place in the ipsilesional vestibular and cochlear nucleus within the first 30 days after an inner ear lesion and thereby parallels the establishment of central vestibular compensation. μ PET is a feasible method to show upregulation of the tspo protein in vivo as a sign of reactive gliosis induced by unilateral labyrinthectomy. Our data suggest that synthetic tspo ligands may be a novel therapeutic principle to augment central vestibular compensation.
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