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Minor, Lloyd B.; Lasker, David M.
doi: 10.3233/ves-2009-0353pmid: 20495233
Processes of vestibular compensation mediate recovery of many aspects of vestibular dysfunction following unilateral vestibular injury. The VOR in response to high-frequency, high-acceleration head movements, however, retains an enduring asymmetry. Head movements that are inhibitory with respect to semicircular canals on the intact side lead to a diminished VOR whereas head movements that are excitatory for semicircular canals on the intact side lead to a VOR that returns close to normal. We review our work directed toward understanding the processes of VOR compensation to high-frequency, high-acceleration head movements and the related topic of adaptation to changes in the visual requirements for a compensatory VOR. Our work has shown that the processes of both compensation and adaptation to these stimuli can be described by a mathematical model with inputs from tonic and phasic components. We have further shown that the dynamics of regular afferents have close resemblance to the tonic pathway whereas the dynamics of irregular afferents match those of the phasic pathway.
Cullen, Kathleen E.; Minor, Lloyd B.; Beraneck, Mathieu; Sadeghi, Soroush G.
doi: 10.3233/ves-2009-0357pmid: 20495234
The vestibulo-ocular reflex (VOR), which functions to stabilize gaze and ensure clear vision during everyday activities, shows impressive adaptation in response to environmental requirements. In particular, the VOR exhibits remarkable recovery following the loss of unilateral labyrinthine input as a result of injury or disease. The relative simplicity of the pathways that mediate the VOR, make it an excellent model system for understanding the changes (learning) that occur in the brain following peripheral vestibular loss to yield adaptive changes. This mini review considers the findings of behavioral, single unit recording and lesion studies of VOR compensation. Recent experiments have provided evidence that the brain makes use of multiple plasticity mechanisms (i.e., changes in peripheral as well as central processing) during the course of vestibular compensation to accomplish the sensory-motor transformations required to accurately guide behavior.
Yates, Bill J.; Miller, Derek M.
doi: 10.3233/ves-2009-0337pmid: 20495235
Inputs from the skin and muscles of the limbs and trunk as well as the viscera are relayed to the medial, inferior, and lateral vestibular nuclei. Vestibular nucleus neurons very quickly regain spontaneous activity following a bilateral vestibular neurectomy, presumably due to the presence of such nonlabyrinthine inputs. The firing of a small fraction of vestibular nucleus neurons in animals lacking labyrinthine inputs can be modulated by whole-body tilts; these responses are eliminated by a spinal transection, showing that they are predominantly elicited by inputs from the trunk and limbs. The ability to adjust blood distribution in the body and maintain stable blood pressure during movement is diminished following a bilateral vestibular neurectomy, but compensation occurs within a week. However, bilateral lesions of the caudal portions of the vestibular nuclei produce severe and long-lasting cardiovascular disturbances during postural alterations, suggesting that the presence of nonlabyrinthine signals to the vestibular nuclei is essential for compensation of posturally-related autonomic responses to occur. Despite these observations, the functional significance of nonlabyrinthine inputs to the central vestibular system remains unclear, either in modulating the processing of vestibular inputs or compensating for their loss.
Shao, Mei; Popratiloff, Anastas; Hirsch, June C.; Peusner, Kenna D.
doi: 10.3233/ves-2009-0348pmid: 20495236
Vestibular compensation refers to the recovery of function occurring after unilateral vestibular deafferentation, but some patients remain uncompensated. Similarly, more than half of the operated chickens compensate three days after unilateral vestibular ganglionectomy (UVG), but the rest remain uncompensated. This review focuses on the studies performed on the principal cells of the chick tangential nucleus after UVG. The tangential nucleus is a major avian vestibular nucleus whose principal cells are all second-order, vestibular reflex projection neurons participating in the vestibuloocular and vestibulocollic reflexes controlling posture, balance, and eye movements. Using whole-cell patch-clamp approach in brain slice preparations, spontaneous spike firing, ionic conductances, and spontaneous excitatory postsynaptic currents (sEPSCs) are recorded in principal cells from controls and operated chickens three days after UVG. In compensated chickens, the proportion of spontaneous spike firing principal cells and their spike discharge rate are symmetric on the lesion and intact sides, with the rates increased over controls. However, in the uncompensated chickens, the spike discharge rate increases on the lesion side, but not on the intact side, where only silent principal cells are recorded. In all the experimental groups, including controls, silent principal cells are distinguished from spontaneous spiking cells by smaller persistent sodium conductances and higher activation thresholds for the fast sodium channel. In addition, silent principal cells on the intact side of uncompensated chickens have larger dendrotoxin-sensitive potassium conductances, with a higher ratio of immunolabeling for surface/cytoplasmic expression of a dendrotoxin-sensitive, potassium channel subunit, Kv1.1. Finally, in compensated chickens, sEPSC frequency is symmetric bilaterally, but in uncompensated chickens sEPSC frequency increased only on the lesion side, where the expression of Kv1.2 decreased in synaptotagmin-labeled terminal profiles on the principal cell bodies. Altogether, the specific sodium and potassium channels important for the development of spike firing pattern and/or presynaptic glutamate release on vestibular reflex projection neurons may be critically involved in changing postsynaptic neuron excitability after vestibular deafferentation.
Olabi, Bayanne; Bergquist, Filip; Dutia, Mayank B.
doi: 10.3233/ves-2009-0367pmid: 20495237
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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