Abstract
BackgroundDue to their anti-inflammatory action, corticosteroids are the reference treatment for brain injuries and many inflammatory diseases. However, the benefits of acute corticotherapy are now being questioned, particularly in the case of acute peripheral vestibulopathies (APV), characterized by a vestibular syndrome composed of sustained spinning vertigo, spontaneous ocular nystagmus and oscillopsia, perceptual-cognitive, posturo-locomotor, and vegetative disorders. We assessed the effectiveness of acute corticotherapy, and the functional role of acute inflammation observed after sudden unilateral vestibular loss.MethodsWe used the rodent model of unilateral vestibular neurectomy, mimicking the syndrome observed in patients with APV. We treated the animals during the acute phase of the vestibular syndrome, either with placebo or methylprednisolone, an anti-inflammatory corticosteroid. At the cellular level, impacts of methylprednisolone on endogenous plasticity mechanisms were assessed through analysis of cell proliferation and survival, glial reactions, neuron’s membrane excitability, and stress marker. At the behavioral level, vestibular and posturo-locomotor functions’ recovery were assessed with appropriate qualitative and quantitative evaluations.ResultsWe observed that acute treatment with methylprednisolone significantly decreases glial reactions, cell proliferation and survival. In addition, stress and excitability markers were significantly impacted by the treatment. Besides, vestibular syndrome’s intensity was enhanced, and vestibular compensation delayed under acute methylprednisolone treatment.ConclusionsWe show here, for the first time, that acute anti-inflammatory treatment alters the expression of the adaptive plasticity mechanisms in the deafferented vestibular nuclei and generates enhanced and prolonged vestibular and postural deficits. These results strongly suggest a beneficial role for acute endogenous neuroinflammation in vestibular compensation. They open the way to a change in dogma for the treatment and therapeutic management of vestibular patients.
Highlights
Neuroinflammation is a cellular and molecular complex process, supporting the brain’s response to various aggressions such as injury, infection or stress
Among all unilateral vestibular deafferentation (UVD) models to study AVP, we focused on unilateral vestibular neurectomy (UVN), consisting in the section of one of the two vestibular nerves [50, 51, 70, 86]
We investigated the effects induced by pharmacological blockade of acute inflammation following UVN on the expression of the plasticity mechanisms observed in the deafferented Vestibular nuclei (VNs), as well as on the kinetics of vestibular compensation in the adult rodent
Summary
Neuroinflammation is a cellular and molecular complex process, supporting the brain’s response to various aggressions such as injury, infection or stress. Acute neuroinflammation is the brain’s immediate response. Chronic inflammation is a self-propagating and long-lasting reaction caused by a persistent stress [92] or dysregulations of the acute inflammatory resolution process [88]. Chronic inflammation has deleterious consequences leading to neurodegeneration and is associated with CNS disorders [58, 90]. Due to their anti-inflammatory action, corticosteroids are the reference treatment for brain injuries and many inflammatory diseases. We assessed the effectiveness of acute corticotherapy, and the functional role of acute inflammation observed after sudden unilateral vestibular loss
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