Abstract
The functional relevance of reactive gliosis for recovery from acute unilateral vestibulopathy is unknown. In the present study, glial activation was visualized in vivo by [18F]GE180-PET in a rat model of unilateral labyrinthectomy (UL) and compared to behavioral vestibular compensation (VC) overtime. 14 Sprague-Dawley rats underwent a UL by transtympanic injection of bupivacaine/arsenilate, 14 rats a SHAM UL (injection of normal saline). Glial activation was depicted with [18F]GE180-PET and ex vivo autoradiography at baseline and 7, 15, 30 days after UL/SHAM UL. Postural asymmetry and nystagmus were registered at 1, 2, 3, 7, 15, 30 days after UL/SHAM UL. Signs of vestibular imbalance were found only after UL, which significantly decreased until days 15 and 30. In parallel, [18F]GE180-PET and ex vivo autoradiography depicted glial activation in the ipsilesional vestibular nerve and nucleus on days 7 and 15 after UL. Correlation analysis revealed a strong negative association of [18F]GE180 uptake in the ipsilesional vestibular nucleus on day 7 with the rate of postural recovery (R = −0.90, p < 0.001), suggesting that glial activation accelerates VC. In conclusion, glial activation takes place in the ipsilesional vestibular nerve and nucleus within the first 30 days after UL in the rat and can be visualized in vivo by [18F]GE180-PET.
Highlights
Acute unilateral vestibulopathy (AUV) induces spontaneous nystagmus, head roll tilt, and falling to the lesion side [1, 2]
Comparative analysis of behavioral and [18F]GE180 kinetics in our study suggest that microglial activation in the VN initially parallels the occurrence of vestibular imbalance measured in postural asymmetry scores (Figures 2 and 3)
The data of the current study suggest that conceptually it seems important to think about AUV as a disease with various etiologies, which results in a common pathophysiological neuroinflammatory response of the first- and second-order vestibular neurons
Summary
Acute unilateral vestibulopathy (AUV) induces spontaneous nystagmus, head roll tilt, and falling to the lesion side [1, 2]. Signs and symptoms recover over days to weeks due to central vestibular compensation (VC) [3]. VC is an interesting model for studying post-lesional plasticity in the adult intact brain [4]. Several hypotheses have been proposed to explain VC. It is commonly accepted that VC is not a single process but involves multiple, synchronous, and synergistic adaptations in neuronal networks of various brain areas [5,6,7,8,9]. Microglial cells play an important role in brain plasticity following neuronal damage by modulating synaptic function, neurotransmission, and immune
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