Initial, rapid phase of recovery from unilateral vestibular lesion in rat not dependent on survival of central portion of vestibular nerve

Sirkin, David W.; Precht, W.; Courjon, J

doi:10.1016/0006-8993(84)90237-3

Cited by 218 publications

(28 citation statements)

References 30 publications

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“…The authors propose that this unilateral vestibular damage (UVD) should eliminate the ability of the sensory periphery to encode head movement while not completely abolishing the spontaneous firing of vestibular afferents. On the other hand, the more standard labyrinthectomy approach that we used here produced a complete and permanent silencing of vestibular afferents (Jensen 1983;Sirkin et al 1984), thereby resulting in a functional deafferentation of central vestibular neurons. Because static deficits are largely due to the imbalance in the spontaneous firing rate of vestibular nuclei neurons located on each side of the brain stem (for review, see Dieringer 1995; Smith and Curthoys 1989), the persistence of these symptoms in the Lc/ϩ suggests that the cerebellum plays a role in rebalancing the spontaneous discharge through the vestibular complex (see cellular mechanisms in the following text).…”

Section: Compensation In Wt Versus Cerebellar-deficient Mice: Acute Smentioning

confidence: 99%

“…Such lesions trigger static deficits, which affect posture and eye position at rest (i.e., a spontaneous nystagmus with slow phase and headtilt directed toward the lesioned side) as well as changes in the ability of the vestibuloocular (VOR) and vestibulocollic (VCR) reflexes to stabilize gaze and posture (reviewed in Curthoys 2000;Dieringer 1995;Vibert et al 1997). While static deficits disappear over the course of few days in most species (Darlington et al 2002;de Waele et al 1989;Sirkin et al 1984;Smith and Curthoys 1989), the response dynamics of vestibularly driven reflexes never fully recover. For example, despite an initial improvement in response to head movement with relatively low velocities/accelerations that are in the low-and middle-frequency range (ϳ0.1-10 Hz), the performance of the VOR in response to higher frequency and velocity/acceleration stimulation remains impaired on the long term (e.g., cat: Broussard et al 1999;guinea pig: Gilchrist et al 1998;macaque: Fetter and Zee 1988;Sadeghi et al 2006;squirrel monkey: Lasker et al 2000;Paige 1983; human: Crane and Demer 1998; Halmagyi et al 1990).…”

Section: Introductionmentioning

confidence: 99%

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Asymmetric Recovery in Cerebellar-Deficient Mice Following Unilateral Labyrinthectomy

Beraneck¹,

McKee²,

Aleisa³

et al. 2008

Journal of Neurophysiology

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Beraneck M, McKee JL, Aleisa M, Cullen KE. Asymmetric recovery in cerebellar-deficient mice following unilateral labyrinthectomy. J Neurophysiol 100: 945-958, 2008. First published May 28, 2008 doi:10.1152/jn.90319.2008. The term "vestibular compensation" refers to the resolution of motor deficits resulting from a peripheral vestibular lesion. We investigated the role of the cerebellum in the compensation process by characterizing the vestibuloocular reflex (VOR) evoked by head rotations at frequencies and velocities similar to those in natural behaviors in wild-type (WT) versus cerebellardeficient Lurcher (Lc/ϩ) mice. We found that during exploratory activity, normal mice produce head rotations largely consisting of frequencies Յ4 Hz and velocities and accelerations as large as 400°/s and 5,000°/s 2 , respectively. Accordingly, the VOR was characterized using sinusoidal rotations (0.2-4 Hz) as well as transient impulses (ϳ400°/s; ϳ2,000°/s 2 ). Before lesions, WT and Lc/ϩ mice produced similar VOR responses to sinusoidal rotation. Lc/ϩ mice, however, had significantly reduced gains for transient stimuli. After unilateral labyrinthectomy, VOR recovery followed a similar course for WT and Lc/ϩ groups during the first week: gain was reduced by 80% for ipsilesionally directed head rotations on day 1 and improved for both strains to values of ϳ0.4 by day 5. Moreover, responses evoked by contralesionally directed rotations returned to prelesion in both strains within this period. However, unlike WT, which showed improving responses to ipsilesionally directed rotations, recovery plateaued after first week for Lc/ϩ mice. Our results show that despite nearly normal recovery in the acute phase, long-term compensation is compromised in Lc/ϩ. We conclude that cerebellar pathways are critical for longterm restoration of VOR during head rotation toward the lesioned side, while noncerebellar pathways are sufficient to restore proper gaze stabilization during contralesionally directed movements.

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Section: Compensation In Wt Versus Cerebellar-deficient Mice: Acute Smentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Asymmetric Recovery in Cerebellar-Deficient Mice Following Unilateral Labyrinthectomy

Beraneck¹,

McKee²,

Aleisa³

et al. 2008

Journal of Neurophysiology

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“…The static deficits, which include postural distortions and a spontaneous ocular nystagmus, disappear over 3-4 days in the guinea pig and rat as in most mammalian species (Darlington et al 2002;de Waele et al 1989;Sirkin et al 1984;Smith and Curthoys 1989). The dynamic deficits include a reduced gain and abnormal timing of the vestibuloocular and vestibulospinal synergies.…”

Section: Introductionmentioning

confidence: 99%

“…During the first week after UL, the recovery of a normal resting discharge by the ipsilesional medial VNn (MVNn) plays a key role in the disappearance of the static syndrome by restoring the balance between the activity of neurons in both vestibular nuclei (Ris et al 1995(Ris et al , 1997. Because the ipsilesional labyrinth afferents stay silent (Jensen 1979;Sirkin et al 1984), this recovery is a model of plasticity in the CNS.…”

Section: Introductionmentioning

confidence: 99%

Long-Term Plasticity of Ipsilesional Medial Vestibular Nucleus Neurons After Unilateral Labyrinthectomy

Beraneck

Hachemaoui²,

Idoux³

et al. 2003

Journal of Neurophysiology

109

142

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. Long-term plasticity of ipsilesional medial vestibular nucleus neurons after unilateral labyrinthectomy. J Neurophysiol 90: 184 -203, 2003. First published March 20, 2003 10.1152/jn.01140.2002. Unilateral labyrinthectomy results in oculomotor and postural disturbances that regress in a few days during vestibular compensation. The long-term (after 1 mo) consequences of unilateral labyrinthectomy were investigated by characterizing the static and dynamic membrane properties of the ipsilesional vestibular neurons recorded intracellularly in guinea pig brain stem slices. We compared the responses of type A and type B medial vestibular nucleus neurons identified in vitro to current steps and ramps and to sinusoidal currents of various frequencies. All ipsilesional vestibular neurons were depolarized by 6 -10 mV at rest compared with the cells recorded from control slices. Both their average membrane potential and firing threshold were more depolarized, which suggests that changes in active conductances compensated for the loss of excitatory afferents. The afterhyperpolarization and discharge regularity of type B but not type A neurons were increased. All ipsilesional vestibular cells became more sensitive to current injections over a large range of frequencies (0.2-30 Hz), but this increase in sensitivity was greater for type B than for type A neurons. This was associated with an increase of the peak frequency of linear response restricted to type B neurons, from 4 -6 to 12-14 Hz. Altogether, we show that long-term vestibular compensation involves major changes in the membrane properties of vestibular neurons on the deafferented side. Many of the static and dynamic membrane properties of type B neurons became more similar to those of type A neurons than in control slices, leading to an increase in the overall homogeneity of medial vestibular nucleus neurons.

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“…Moreover, since regeneration after a complete destruction of the vestibular labyrinth or the vestibular nerve is lacking [3], recovery must be attributed to central neuronal plasticity.…”

Section: Basic Principles Of the Vestibular Systemmentioning

confidence: 99%

Neurobiological Mechanisms of Acute Vertigo

Tarnutzer

Palla

2013

Future Neurol.

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The vestibular system provides us with reflexive responses of eye movements and balance control, as well as with perceptual estimates of self-motion and gravity direction. Crucial to its proper functioning is a bilaterally balanced vestibular signal originating from the vestibular end organs in the inner ears and projecting via vestibular nerve afferents to the brainstem vestibular nuclei. Disturbances of the bilateral vestibular interplay become evident in cases of acute unilateral peripheral vestibular deafferentation. The resultant sudden imbalance of vestibular afferent tone at the level of the vestibular nuclei leads to pronounced ocular-motor and postural impairment, as well as to intensive vertigo and/or dizziness, accompanied by autonomic symptoms, such as nausea and vomiting. Subsequent compensatory mechanisms efficiently diminish these static symptoms (such as spontaneous nystagmus) within days and allow functional recovery of dynamic symptoms (such as blurred vision during fast head turns) to such a degree that most patients return to their normal daily activities within weeks. This article aims to provide an understanding about the pathophysiological changes after unilateral vestibular deafferentation and the current knowledge on the compensatory mechanisms. SummaryThe vestibular system provides us with reflexive responses of eye movement and

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Initial, rapid phase of recovery from unilateral vestibular lesion in rat not dependent on survival of central portion of vestibular nerve

Cited by 218 publications

References 30 publications

Asymmetric Recovery in Cerebellar-Deficient Mice Following Unilateral Labyrinthectomy

Asymmetric Recovery in Cerebellar-Deficient Mice Following Unilateral Labyrinthectomy

Long-Term Plasticity of Ipsilesional Medial Vestibular Nucleus Neurons After Unilateral Labyrinthectomy

Neurobiological Mechanisms of Acute Vertigo

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