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Dysfunctional vestibular system causes a blood pressure drop in astronauts returning from space.
Hallgren E, Migeotte PF, Kornilova L, Delière Q, Fransen E, Glukhikh D, Moore ST, Clément G, Diedrich A, MacDougall H, Wuyts FL
(2015) Sci Rep 5: 17627
MeSH Terms: Adult, Astronauts, Blood Pressure, Cardiovascular System, Humans, Male, Middle Aged, Posture, Space Flight, Vestibule, Labyrinth, Vision, Ocular
Show Abstract · Added October 14, 2016
It is a challenge for the human body to maintain stable blood pressure while standing. The body's failure to do so can lead to dizziness or even fainting. For decades it has been postulated that the vestibular organ can prevent a drop in pressure during a position change--supposedly mediated by reflexes to the cardiovascular system. We show--for the first time--a significant correlation between decreased functionality of the vestibular otolith system and a decrease in the mean arterial pressure when a person stands up. Until now, no experiments on Earth could selectively suppress both otolith systems; astronauts returning from space are a unique group of subjects in this regard. Their otolith systems are being temporarily disturbed and at the same time they often suffer from blood pressure instability. In our study, we observed the functioning of both the otolith and the cardiovascular system of the astronauts before and after spaceflight. Our finding indicates that an intact otolith system plays an important role in preventing blood pressure instability during orthostatic challenges. Our finding not only has important implications for human space exploration; they may also improve the treatment of unstable blood pressure here on Earth.
0 Communities
1 Members
0 Resources
11 MeSH Terms
Insm1 promotes neurogenic proliferation in delaminated otic progenitors.
Lorenzen SM, Duggan A, Osipovich AB, Magnuson MA, García-Añoveros J
(2015) Mech Dev 138 Pt 3: 233-45
MeSH Terms: Animals, Cell Differentiation, Cell Proliferation, DNA-Binding Proteins, Ear, Inner, Female, Gene Expression Regulation, Developmental, Hair Cells, Auditory, Inner, Hair Cells, Auditory, Outer, Male, Mice, Mice, Knockout, Mice, Transgenic, Neural Stem Cells, Neurogenesis, Pregnancy, RNA, Messenger, Repressor Proteins, Spiral Ganglion, Transcription Factors, Vestibule, Labyrinth, Zinc Fingers
Show Abstract · Added November 14, 2015
INSM1 is a zinc-finger protein expressed throughout the developing nervous system in late neuronal progenitors and nascent neurons. In the embryonic cortex and olfactory epithelium, Insm1 may promote the transition of progenitors from apical, proliferative, and uncommitted to basal, terminally-dividing and neuron producing. In the otocyst, delaminating and delaminated progenitors express Insm1, whereas apically-dividing progenitors do not. This expression pattern is analogous to that in embryonic olfactory epithelium and cortex (basal/subventricular progenitors). Lineage analysis confirms that auditory and vestibular neurons originate from Insm1-expressing cells. In the absence of Insm1, otic ganglia are smaller, with 40% fewer neurons. Accounting for the decrease in neurons, delaminated progenitors undergo fewer mitoses, but there is no change in apoptosis. We conclude that in the embryonic inner ear, Insm1 promotes proliferation of delaminated neuronal progenitors and hence the production of neurons, a similar function to that in other embryonic neural epithelia. Unexpectedly, we also found that differentiating, but not mature, outer hair cells express Insm1, whereas inner hair cells do not. Insm1 is the earliest known gene expressed in outer versus inner hair cells, demonstrating that nascent outer hair cells initiate a unique differentiation program in the embryo, much earlier than previously believed.
Copyright © 2015 Elsevier B.V. All rights reserved.
3 Communities
2 Members
0 Resources
22 MeSH Terms
Inner Ear Vestibular Signals Regulate Bone Remodeling via the Sympathetic Nervous System.
Vignaux G, Ndong JD, Perrien DS, Elefteriou F
(2015) J Bone Miner Res 30: 1103-11
MeSH Terms: Animals, Bone Remodeling, Female, Mice, Mice, Knockout, Osteoblasts, Osteoporosis, Propranolol, Sympathetic Nervous System, Vestibular Diseases, Vestibule, Labyrinth
Show Abstract · Added January 20, 2015
The inner ear vestibular system has numerous projections on central brain centers that regulate sympathetic outflow, and skeletal sympathetic projections affect bone remodeling by inhibiting bone formation by osteoblasts and promoting bone resorption by osteoclasts. In this study, we show that bilateral vestibular lesions in mice cause a low bone mass phenotype associated with decreased bone formation and increased bone resorption. This reduction in bone mass is most pronounced in lower limbs, is not associated with reduced locomotor activity or chronic inflammation, and could be prevented by the administration of the β-blocker propranolol and by genetic deletion of the β2-adrenergic receptor, globally or specifically in osteoblasts. These results provide novel experimental evidence supporting a functional autonomic link between central proprioceptive vestibular structures and the skeleton. Because vestibular dysfunction often affects the elderly, these results also suggest that age-related bone loss might have a vestibular component and that patients with inner ear pathologies might be at risk for fracture. Lastly, these data might have relevance to the bone loss observed in microgravity, as vestibular function is altered in this condition as well. © 2015 American Society for Bone and Mineral Research.
© 2015 American Society for Bone and Mineral Research.
0 Communities
3 Members
0 Resources
11 MeSH Terms
Bone remodeling is regulated by inner ear vestibular signals.
Vignaux G, Besnard S, Ndong J, Philoxène B, Denise P, Elefteriou F
(2013) J Bone Miner Res 28: 2136-44
MeSH Terms: Adrenergic beta-Antagonists, Animals, Bone Remodeling, Densitometry, Female, Homeostasis, Motor Activity, Organ Size, Phenotype, Propranolol, Rats, Rats, Sprague-Dawley, Receptors, Adrenergic, beta, Signal Transduction, Vestibule, Labyrinth, Video Recording
Show Abstract · Added November 14, 2013
Bone remodeling allows the conservation of normal bone mass despite constant changes in internal and external environments. The adaptation of the skeleton to these various stimuli leads credence to the notion that bone remodeling is a true homeostatic function, and as such is under the control of specific centers in the central nervous system (CNS). Hypothalamic and brainstem centers, as well as the sympathetic nervous system (SNS), have been identified as regulators of bone remodeling. However, the nature of the afferent CNS stimuli that may modulate CNS centers involved in the control of bone remodeling, with the exception of leptin, remains unclear. Based on the partial efficacy of exercise and mechanical stimulation regimens to prevent microgravity-induced bone loss and the known alterations in vestibular functions associated with space flights, we hypothesized that inner ear vestibular signals may contribute to the regulation of bone remodeling. Using an established model of bilateral vestibular lesions and microtomographic and histomorphometric bone analyses, we show here that induction of bilateral vestibular lesion in rats generates significant bone loss, which is restricted to weight-bearing bones and associated with a significant reduction in bone formation, as observed in rats under microgravity conditions. Importantly, this bone loss was not associated with reduced locomotor activity or metabolic abnormalities, was accompanied with molecular signs of increased sympathetic outflow, and could be prevented by the β-blocker propranolol. Collectively, these data suggest that the homeostatic process of bone remodeling has a vestibulosympathetic regulatory component and that vestibular system pathologies might be accompanied by bone fragility.
© 2013 American Society for Bone and Mineral Research.
1 Communities
1 Members
0 Resources
16 MeSH Terms
Bmp4 is essential for the formation of the vestibular apparatus that detects angular head movements.
Chang W, Lin Z, Kulessa H, Hebert J, Hogan BL, Wu DK
(2008) PLoS Genet 4: e1000050
MeSH Terms: Animals, Animals, Genetically Modified, Bone Morphogenetic Protein 4, Bone Morphogenetic Proteins, Carrier Proteins, Chick Embryo, Down-Regulation, Female, Forkhead Transcription Factors, Gene Expression Regulation, Developmental, Head Movements, Male, Mice, Mice, Knockout, Mice, Mutant Strains, Mice, Transgenic, Nerve Tissue Proteins, Phenotype, Postural Balance, Pregnancy, Semicircular Canals, Semicircular Ducts, Signal Transduction, Smad6 Protein, Vestibule, Labyrinth, Zebrafish Proteins
Show Abstract · Added February 28, 2014
Angular head movements in vertebrates are detected by the three semicircular canals of the inner ear and their associated sensory tissues, the cristae. Bone morphogenetic protein 4 (Bmp4), a member of the Transforming growth factor family (TGF-beta), is conservatively expressed in the developing cristae in several species, including zebrafish, frog, chicken, and mouse. Using mouse models in which Bmp4 is conditionally deleted within the inner ear, as well as chicken models in which Bmp signaling is knocked down specifically in the cristae, we show that Bmp4 is essential for the formation of all three cristae and their associated canals. Our results indicate that Bmp4 does not mediate the formation of sensory hair and supporting cells within the cristae by directly regulating genes required for prosensory development in the inner ear such as Serrate1 (Jagged1 in mouse), Fgf10, and Sox2. Instead, Bmp4 most likely mediates crista formation by regulating Lmo4 and Msx1 in the sensory region and Gata3, p75Ngfr, and Lmo4 in the non-sensory region of the crista, the septum cruciatum. In the canals, Bmp2 and Dlx5 are regulated by Bmp4, either directly or indirectly. Mechanisms involved in the formation of sensory organs of the vertebrate inner ear are thought to be analogous to those regulating sensory bristle formation in Drosophila. Our results suggest that, in comparison to sensory bristles, crista formation within the inner ear requires an additional step of sensory and non-sensory fate specification.
1 Communities
0 Members
0 Resources
26 MeSH Terms
Vestibular influences on autonomic cardiovascular control in humans.
Biaggioni I, Costa F, Kaufmann H
(1998) J Vestib Res 8: 35-41
MeSH Terms: Animals, Autonomic Nervous System, Cardiovascular Physiological Phenomena, Cardiovascular System, Humans, Neural Pathways, Posture, Stress, Physiological, Vestibule, Labyrinth
Show Abstract · Added December 10, 2013
There is substantial evidence that anatomical connections exist between vestibular and autonomic nuclei. Animal studies have shown functional interactions between the vestibular and autonomic systems. The nature of these interactions, however, is complex and has not been fully defined. Vestibular stimulation has been consistently found to reduce blood pressure in animals. Given the potential interaction between vestibular and autonomic pathways this finding could be explained by a reduction in sympathetic activity. However, rather than sympathetic inhibition, vestibular stimulation has consistently been shown to increase sympathetic outflow in cardiac and splanchnic vascular beds in most experimental models. Several clinical observations suggest that a link between vestibular and autonomic systems may also exist in humans. However, direct evidence for vestibular/autonomic interactions in humans is sparse. Motion sickness has been found to induce forearm vasodilation and reduce baroreflex gain, and head down neck flexion induces transient forearm and calf vasoconstriction. On the other hand, studies using optokinetic stimulation have found either very small, variable, or inconsistent changes in heart rate and blood pressure, despite substantial symptoms of motion sickness. Furthermore, caloric stimulation severe enough to produce nystagmus, dizziness, and nausea had no effect on sympathetic nerve activity measured directly with microneurography. No effect was observed on heart rate, blood pressure, or plasma norepinephrine. Several factors may explain the apparent discordance of these results, but more research is needed before we can define the potential importance of vestibular input to cardiovascular regulation and orthostatic tolerance in humans.
0 Communities
2 Members
0 Resources
9 MeSH Terms
Effect of neurovestibular stimulation on autonomic regulation.
Costa F, Lavin P, Robertson D, Biaggioni I
(1995) Clin Auton Res 5: 289-93
MeSH Terms: Adult, Autonomic Nervous System, Blood Pressure, Cold Temperature, Electric Stimulation, Electronystagmography, Epinephrine, Female, Heart Rate, Humans, Male, Muscle, Skeletal, Nystagmus, Physiologic, Physical Stimulation, Sympathetic Nervous System, Tympanic Membrane, Vestibule, Labyrinth
Show Abstract · Added December 10, 2013
Conditions associated with nausea and vomiting, such as motion sickness or side effects of medications, are commonly associated with a clinical picture consistent with parasympathetic activation and sympathetic withdrawal. It can be postulated, therefore, that vestibular stimulation contributes to sympathetic withdrawal. To test this hypothesis five normal volunteers, 24-33 years old, were studied during caloric vestibular stimulation while monitoring muscle sympathetic nerve activity directly through a needle electrode placed in a peroneal nerve. The ear was irrigated with water at a flow rate of 450 ml/min and 37 degrees C. The water temperature was sequentially lowered by 7 degree C intervals until intolerable side effects developed or a temperature of 16 degrees C was reached. Nystagmus was induced in all subjects, but heart rate, blood pressure, muscle sympathetic nerve activity and plasma norepinephrine levels did not change significantly during or after caloric stimulation, even when the subjects felt dizzy and nauseated. No evidence of sympathetic withdrawal was observed in any subject either by muscle sympathetic nerve activity or plasma norepinephrine measurements. In conclusion, we have found that selective vestibular stimulation is not accompanied by significant changes in the sympathetic nervous system function. In particular, no sympathetic withdrawal was observed. It could be argued that lack of sympathetic stimulation is an inadequate response to the symptoms associated with caloric stimulation.
0 Communities
2 Members
0 Resources
17 MeSH Terms