The vestibular system is composed of highly tuned sensors for head and body motion situated in the peripheral vestibular endorgans. These receptors transmit signals to groups of neurons distributed discretely in the brain, with axonal outputs to cranial or spinal motor neurons to control gaze or posture, or ascending axons to cortical areas for conscious awareness of motion, spatial orientation and navigation. In all vertebrates, the peripheral vestibular system operates as a bilateral network so that the brain processes vestibular signals by comparing inputs from the two ears. The vestibular system offers an attractive model to study motor control because it permits a precise quantification of sensory input and motor output in the vestibuloocular and vestibulospinal networks. Recent research has described how vestibular information is processed from the periphery to the first brain centers in the vestibular nuclei and on to diverse neuron groups to ultimately generate motor commands. The experiments apply multiple structural and functional approaches on intact animals, isolated vestibular networks in culture, or brain slice preparations because sensorimotor transformation depends on both the functional properties of the whole neuronal network as a unit, as well as the synaptic and intrinsic membrane conductances of constituent neurons.
Although the vestibular system is phylogenetically old and highly conserved during evolution, it shows a remarkable capacity to adapt to changing environmental demands, to developmental changes, and in response to pathologies affecting the peripheral vestibular receptors. This adaptability, termed neural plasticity, is defined as long-lived changes in neuron structure or function, which affect behavior. Thus, the vestibular system offers an important model to study functional and postlesional brain plasticity. Peripheral vestibular lesions can precipitate a complex and debilitating syndrome of oculomotor and postural deficits with diverse symptoms including vertigo, nystagmus, head and body tilt, ataxia, imbalance, nausea and vomiting. Labyrinthine dysfunctions may be partial or complete, fluctuating or constant, progressive or recovering. Many consequences of a lesion diminish or disappear rapidly due to an adaptive process called vestibular compensation. The symptoms can be detected by behavioral testing in humans and experimental animals, while at the cellular/molecular level changes may include synaptic reorganization, long-term potentiation or depression of synaptic transmission, changes in synaptic efficacy, or changes in the active and passive membrane properties of neurons.
The study of the vestibular system is important to society, since vestibular function is often impaired with age resulting in deterioration of postural control and falls, a leading cause of death and institutionalization in senior citizens. Therefore, understanding the function of the vestibular system not only paves the way for new medications and rehabilitation procedures, but contributes to the design of better tests to measure gaze and balance deficits. These topics are directed toward clinicians who want to bridge the gap between new basic science concepts of vestibular function and treating patients for vestibular disorders, vestibular neuroscientists using structural and functional approaches to understand the labyrinth and its central pathways involved in motor control and neuronal plasticity, and sensory system neuroscientists intrigued by similarities and differences among the sensory systems. The six sections composing the topic are: (1) plasticity of peripheral vestibular receptors, (2) plasticity in vestibular nuclei neurons studied in vitro, (3) plasticity in central vestibular networks studied in vivo, (4) plasticity in vestibular networks forming vestibuloautonomic connections, (5) plasticity and testing gaze stabilization, and (6) plasticity and testing stabil
The vestibular system is composed of highly tuned sensors for head and body motion situated in the peripheral vestibular endorgans. These receptors transmit signals to groups of neurons distributed discretely in the brain, with axonal outputs to cranial or spinal motor neurons to control gaze or posture, or ascending axons to cortical areas for conscious awareness of motion, spatial orientation and navigation. In all vertebrates, the peripheral vestibular system operates as a bilateral network so that the brain processes vestibular signals by comparing inputs from the two ears. The vestibular system offers an attractive model to study motor control because it permits a precise quantification of sensory input and motor output in the vestibuloocular and vestibulospinal networks. Recent research has described how vestibular information is processed from the periphery to the first brain centers in the vestibular nuclei and on to diverse neuron groups to ultimately generate motor commands. The experiments apply multiple structural and functional approaches on intact animals, isolated vestibular networks in culture, or brain slice preparations because sensorimotor transformation depends on both the functional properties of the whole neuronal network as a unit, as well as the synaptic and intrinsic membrane conductances of constituent neurons.
Although the vestibular system is phylogenetically old and highly conserved during evolution, it shows a remarkable capacity to adapt to changing environmental demands, to developmental changes, and in response to pathologies affecting the peripheral vestibular receptors. This adaptability, termed neural plasticity, is defined as long-lived changes in neuron structure or function, which affect behavior. Thus, the vestibular system offers an important model to study functional and postlesional brain plasticity. Peripheral vestibular lesions can precipitate a complex and debilitating syndrome of oculomotor and postural deficits with diverse symptoms including vertigo, nystagmus, head and body tilt, ataxia, imbalance, nausea and vomiting. Labyrinthine dysfunctions may be partial or complete, fluctuating or constant, progressive or recovering. Many consequences of a lesion diminish or disappear rapidly due to an adaptive process called vestibular compensation. The symptoms can be detected by behavioral testing in humans and experimental animals, while at the cellular/molecular level changes may include synaptic reorganization, long-term potentiation or depression of synaptic transmission, changes in synaptic efficacy, or changes in the active and passive membrane properties of neurons.
The study of the vestibular system is important to society, since vestibular function is often impaired with age resulting in deterioration of postural control and falls, a leading cause of death and institutionalization in senior citizens. Therefore, understanding the function of the vestibular system not only paves the way for new medications and rehabilitation procedures, but contributes to the design of better tests to measure gaze and balance deficits. These topics are directed toward clinicians who want to bridge the gap between new basic science concepts of vestibular function and treating patients for vestibular disorders, vestibular neuroscientists using structural and functional approaches to understand the labyrinth and its central pathways involved in motor control and neuronal plasticity, and sensory system neuroscientists intrigued by similarities and differences among the sensory systems. The six sections composing the topic are: (1) plasticity of peripheral vestibular receptors, (2) plasticity in vestibular nuclei neurons studied in vitro, (3) plasticity in central vestibular networks studied in vivo, (4) plasticity in vestibular networks forming vestibuloautonomic connections, (5) plasticity and testing gaze stabilization, and (6) plasticity and testing stabil
