Cellular Mechanisms of Vestibular Compensation

Paterson, Janet M.; Menzies, John; Bergquist, Filip; Dutia, Mayank B.

doi:10.1159/000096796

Cited by 22 publications

(31 citation statements)

References 99 publications

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“…The effects of unilateral vestibular deafferentation (UVD) on oculomotor and postural control, and on the activity of neurons in the ipsi-lesional and contralesional vestibular nuclei, have been well-documented (reviews [12,[14][15][16][17]49,56]). In addition, both unilateral and bilateral vestibular deafferentation have profound effects on neurons in the hippocampus and re-lated cortical areas (review [55]), in line with the important dynamic contribution of vestibular signals to spatial cognition and navigation.…”

Section: Introductionmentioning

confidence: 99%

“…The vestibular nuclei are good candidates for key plasticity sites in VC, since they are the primary central target of semicircular canal and otolith afferents from the ipsilateral inner ear, and give rise to second-order projections that mediate the vestibulo-ocular and vestibulo-collic reflexes and also relay vestibular information to higher regions of the brain. Immediately after UVD, the normally high resting activity of MVN neurons is largely abolished on the lesioned side ('ipsi-lesional' side), while contralesional MVN neurons are either normal or hyperactive (reviews [49,56]). This large imbalance in the activity of the MVNs of the two sides is believed to be a root cause of the severe oculomotor and postural symptoms that immediately follow UVD [12,49].…”

Section: Introductionmentioning

confidence: 99%

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Rebalancing the commissural system: Mechanisms of vestibular compensation

Olabi

Bergquist

Dutia

2010

VES

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Vestibular compensation after unilateral vestibular loss is a complex, multi-factored process involving synaptic and neuronal plasticity in many areas of the brain, and it is a challenge to identify the key sites of plasticity that determine the rate and extent of behavioural recovery. Experimental evidence strongly implicates the vestibular commissural inhibitory system which links the brainstem vestibular nuclei of the two sides, both in causing the initial severe oculomotor and postural symptoms of vestibular deafferentation, and in the subsequent recovery that takes place in the early stages of compensation. Of particular interest are changes in GABAergic neurotransmission within the commissural system, and the possibility that histaminergic drugs as well as stress steroids and neurosteroids that can modulate compensation, may do so at least in part by their effects on commissural inhibition. A fuller understanding of the role of the commissural system in compensation and the effects of GABAergic neuromodulators is likely to reveal the mechanisms of action of histamine in the vestibular system and the interactions between stress, anxiety and vestibular dysfunction.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Rebalancing the commissural system: Mechanisms of vestibular compensation

Olabi

Bergquist

Dutia

2010

VES

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“…On the basis of experimental evidence, at least four candidate synergistic mechanisms have been proposed which may be important in the early stages of VC34.

Changes in the responsiveness of vestibular nucleus neurons to inhibitory neurotransmitters GABA and glycine.

…”

Section: Mechanisms Of Vestibular Compensationmentioning

confidence: 99%

“…The development of vestibular compensation after UL is significantly affected by stress, as well as conditions such as anxiety and depression, where the normal function of the hypothalamo-pituitary-adrenal (HPA) stress axis is altered34;36. Glucocorticoids (GCs) released by the adrenal cortex in response to stress have important modulatory effects on neuronal and synaptic function in the brain.…”

Section: Interactions Between Stress and Brain Plasticity During Vcmentioning

confidence: 99%

Advances in auditory and vestibular medicine

Hamid

Trune

Dutia

2009

Audiological Medicine

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“…Among the four main vestibular nuclei in vertebrates, the medial vestibular nucleus (MVN) is the one most extensively studied (for review, see Paterson et al, 2004). The MVN contains a wide diversity of neuron classes which project to the oculomotor nuclei, spinal cord, cerebellum, thalamus, contralateral vestibular nuclei, or function as interneurons (for review, see Straka et al, 2005; Highstein and Holstein, 2006).…”

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confidence: 99%

Electrophysiological properties of morphologically-identified medial vestibular nucleus neurons projecting to the abducens nucleus in the chick embryo

et al. 2011

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Neurons in the medial vestibular nucleus (MVN) show a wide range of axonal projection pathways, intrinsic firing properties, and responses to head movements. To determine whether MVN neurons participating in the vestibulocular reflexes (VOR) have distinctive electrophysiological properties related to their output pathways, a new preparation was devised using transverse brain slices containing the chicken MVN and abducens nucleus. Biocytin Alexa Fluor was injected extracellularly into the abducens nucleus so that MVN neurons whose axons projected to the ipsilateral (MVN/ABi) and contralateral (MVN/ABc) abducens nuclei were labeled selectively. Whole-cell, patch-clamp recordings were performed to study the active and passive membrane properties, sodium conductances, and spontaneous synaptic events in morphologically-identified MVN/AB neurons and compare them to MVN neurons whose axons could not be traced (MVN/n). Located primarily in the rostral half of the ventrolateral part of the MVN, MVN/AB neurons mainly have stellate cell bodies with diameters of 20-25 μm. Compared to MVNn neurons, MVN/ABi and MVN/ABc neurons had lower input resistances. Compared to all other MVN neuron groups studied, MVN/ABc neurons showed unique firing properties, including type A-like waveform, silence at resting membrane potential, and failure to fire repetitively on depolarization. It is interesting that the frequency of spontaneous excitatory and inhibitory synaptic events was similar for all the MVN neurons studied. However, the ratio for miniature to spontaneous inhibitory events was significantly lower for MVN/ABi neurons compared to MVN/n neurons, suggesting that MVN/ABi neurons retained a larger number and/or more active inhibitory presynaptic neurons within the brain slices. Also, MVN/ABi neurons had mEPSCs with slower decay time and half width compared to MVN/n neurons. Altogether, these findings underscore the diversity of electrophysiological properties of MVN neuron classes distinguished by axonal projection pathways. This represents the first study of MVN/AB neurons in brain slice preparations and supports the concept that the in vitro brain slice preparation provides an advantageous model to investigate the cellular and molecular events in vestibular signal processing.

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Cellular Mechanisms of Vestibular Compensation

Cited by 22 publications

References 99 publications

Rebalancing the commissural system: Mechanisms of vestibular compensation

Rebalancing the commissural system: Mechanisms of vestibular compensation

Advances in auditory and vestibular medicine

Electrophysiological properties of morphologically-identified medial vestibular nucleus neurons projecting to the abducens nucleus in the chick embryo

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