The differential response of astrocytes within the vestibular and cochlear nuclei following unilateral labyrinthectomy or vestibular afferent activity blockade by transtympanic tetrodotoxin injection in the rat

Campos-Torres, Antonio; Touret, Monique; Vidal, Pierre‐Paul; Barnum, Scott R.; Waele, Catherine de

doi:10.1016/j.neuroscience.2004.08.052

Cited by 45 publications

(44 citation statements)

References 59 publications

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“…In line, recent findings have demonstrated reactive neurogenesis in the adult cat [5,6] and a strong microglial and astroglial reaction [5,7-9] after unilateral deafferentation in the deafferented VN. Campos-Torres et al [9] suggested that the glial reaction may be due to modifications of the environment of VN neurons and most probably to the central inflammatory tissue reaction consecutive to UL. Despite this inflammatory reaction, the central vestibular neurons did not show any sign of apoptosis after the permanent loss of their peripheral inputs [8].…”

Section: Introductionsupporting

confidence: 80%

Section: Discussionmentioning

confidence: 44%

“…However, the complete recovery of these postural functions is much longer than that reported in this species after mechanical UL [9,33]. Indeed, head tilt and postural asymmetry disappeared 3-4 days after mechanical UL [9], while 6 weeks were required in the present study. These differences in the time constant of the recovery process were already reported by Kim et al [34], who showed head deviation peaking 2 h and 3 days after mechanical UL and chemical UL, respectively.…”

Section: Discussionmentioning

confidence: 44%

“…Glial reaction in the vestibular nuclei may be a beneficial mechanism. It could both protect the injured tissue from long-lasting inflammation and promote the survival of deafferented vestibular neurons [9] or of newly generated neurons [6]. Finally, the inflammatory reaction could help in the vestibular compensation process.…”

Section: Introductionmentioning

confidence: 99%

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Changes in TNFα, NFκB and MnSOD protein in the vestibular nuclei after unilateral vestibular deafferentation

Liberge

Manrique

Bernard-Demanze

et al. 2010

J Neuroinflammation

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BackgroundUnilateral vestibular deafferentation results in strong microglial and astroglial activation in the vestibular nuclei (VN) that could be due to an inflammatory response. This study was aimed at determining if markers of inflammation are upregulated in the VN after chemical unilateral labyrinthectomy (UL) in the rat, and if the inflammatory response, if any, induces the expression of neuroprotective factors that could promote the plasticity mechanisms involved in the vestibular compensation process. The expressions of inflammatory and neuroprotective factors after chemical or mechanical UL were also compared to verify that the inflammatory response was not due to the toxicity of sodium arsanilate.MethodsImmunohistological investigations combined the labeling of tumor necrosis factor α (TNFα), as a marker of the VN inflammatory response, and of nuclear transcription factor κB (NFκB) and manganese superoxide dismutase (MnSOD), as markers of neuroprotection that could be expressed in the VN because of inflammation. Immunoreactivity (Ir) of the VN cells was quantified in the VN complex of rats. Behavioral investigations were performed to assess the functional recovery process, including both static (support surface) and dynamic (air-righting and landing reflexes) postural tests.ResultsChemical UL (arsanilate transtympanic injection) induced a significant increase in the number of TNFα-Ir cells in the medial and inferior VN on both sides. These changes were detectable as early as 4 h after vestibular lesion, persisted at 1 day, and regained nearly normal values at 3 days. The early increase in TNFα expression was followed by a slightly delayed upregulation of NFκB 8 h after chemical UL, peaking at 1 day, and regaining control values 3 days later. By contrast, upregulation of MnSOD was more strongly delayed (1 day), with a peak at 3 days, and a return to control values at 15 days. Similar changes of TNFα, NFκB, and MnSOD expression were found in rats submitted to mechanical UL. Behavioral observations showed strong posturo-locomotor deficits early after chemical UL (1 day) and a complete functional recovery 6 weeks later.ConclusionsOur results suggest that the upregulation of inflammatory and neuroprotective factors after vestibular deafferentation in the VN may constitute a favorable neuronal environment for the vestibular compensation process.

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Section: Introductionsupporting

confidence: 80%

Section: Discussionmentioning

confidence: 44%

Section: Discussionmentioning

confidence: 44%

Section: Introductionmentioning

confidence: 99%

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Changes in TNFα, NFκB and MnSOD protein in the vestibular nuclei after unilateral vestibular deafferentation

Liberge

Manrique

Bernard-Demanze

et al. 2010

J Neuroinflammation

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“…An increase in astrocytes was found in chick brainstem after CR in n. magnocellularis , the avian homolog of the anteroventral cochlear nucleus (Rubel and MacDonald, 1992, Lurie and Rubel, 1994). Prior studies in mammals have also shown that both microglia and astrocytes are upregulated in the cochlear nucleus in response to unilateral inner ear lesions in adult rats (de Waele et al, 1996, Campos Torres et al, 1999, Campos-Torres et al, 2005, Fuentes-Santamaria et al, 2012). These studies showed changes in the cochlear nucleus, the primary target denervated by CR.…”

Section: Discussionmentioning

confidence: 87%

Distribution of glial cells in the auditory brainstem: Normal development and effects of unilateral lesion

et al. 2014

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Auditory brainstem networks facilitate sound source localization through binaural integration. A key component of this circuitry is the projection from the ventral cochlear nucleus (VCN) to the medial nucleus of the trapezoid body (MNTB), a relay nucleus that provides inhibition to the superior olivary complex. This strictly contralateral projection terminates in the large calyx of Held synapse. The formation of this pathway requires spatiotemporal coordination of cues that promote cell maturation, axon growth, and synaptogenesis. Here we have examined the emergence of distinct classes of glial cells, which are known to function in development and in response to injury. Immunofluorescence for several astrocyte markers revealed unique expression patterns. ALDH1L1 was expressed earliest in both nuclei, followed by S100β, during the first postnatal week. GFAP expression was seen in the second postnatal week. GFAP-positive cell bodies remained outside the boundaries of VCN and MNTB, with a limited number of labeled fibers penetrating into the margins of the nuclei. OLIG2 expression revealed the presence of oligodendrocytes in VCN and MNTB from birth until after hearing onset. In addition, IBA1-positive microglia were observed after the first postnatal week. Following hearing onset, all glial populations were found in MNTB. We then determined the distribution of glial cells following early (P2) unilateral cochlear removal, which results in formation of ectopic projections from the intact VCN to ipsilateral MNTB. We found that following perturbation, astrocytic markers showed expression near the ectopic ipsilateral calyx. Taken together, the developmental expression patterns are consistent with a role for glial cells in the maturation of the calyx of Held and suggest that these cells may have a similar role in maturation of lesion-induced connections.

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Upregulation of insulin‐like growth factor and interleukin 1β occurs in neurons but not in glial cells in the cochlear nucleus following cochlear ablation

Fuentes–Santamaría

Alvarado

Gabaldón-Ull

et al. 2013

J of Comparative Neurology

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One of the main mechanisms used by neurons and glial cells to promote repair following brain injury is to upregulate activity-dependent molecules such as insulin-like growth factor 1 (IGF-1) and interleukin-1β (IL-1β). In the auditory system, IGF-1 is crucial for restoring synaptic transmission following hearing loss; however, whether IL-1β is also involved in this process is unknown. In this study, we evaluated the expression of IGF-1 and IL-1β within neurons and glial cells of the ventral cochlear nucleus in adult rats at 1, 7, 15, and 30 days following bilateral cochlear ablation. After the lesion, significant increases in both the overall mean gray levels of IGF-1 immunostaining and the mean gray levels within cells of the cochlear nucleus were observed at 1, 7, and 15 days compared with control animals. The expression and distribution of IL-1β in the ventral cochlear nucleus of ablated animals was temporally and spatially correlated with IGF-1. We also observed a lack of colocalization between IGF-1 and IL-1β with either astrocytes or microglia at any of the time points following ablation. These results suggest that the upregulation of IGF-1 and IL-1β levels within neurons-but not within glial cells-may reflect a plastic mechanism involved in repairing synaptic homeostasis of the overall cellular environment of the cochlear nucleus following bilateral cochlear ablation.

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The differential response of astrocytes within the vestibular and cochlear nuclei following unilateral labyrinthectomy or vestibular afferent activity blockade by transtympanic tetrodotoxin injection in the rat

Cited by 45 publications

References 59 publications

Changes in TNFα, NFκB and MnSOD protein in the vestibular nuclei after unilateral vestibular deafferentation

Changes in TNFα, NFκB and MnSOD protein in the vestibular nuclei after unilateral vestibular deafferentation

Distribution of glial cells in the auditory brainstem: Normal development and effects of unilateral lesion

Upregulation of insulin‐like growth factor and interleukin 1β occurs in neurons but not in glial cells in the cochlear nucleus following cochlear ablation

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