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Holstein, Gay R.

doi:10.3389/fneur.2012.00004

Cited by 40 publications

(49 citation statements)

References 103 publications

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“…Such connections were demonstrated using cFos protein to identify vestibular neurons activated by sGVS (26). The sGVS-activated cells were concentrated in the caudal inferior and medial vestibular nuclei, otolith-recipient regions, and sent axonal projections to the rostral and caudal ventrolateral medullary areas (48).…”

Section: Discussionmentioning

confidence: 99%

Vasovagal Oscillations and Vasovagal Responses Produced by the Vestibulo-Sympathetic Reflex in the Rat

et al. 2014

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Sinusoidal galvanic vestibular stimulation (sGVS) induces oscillations in blood pressure (BP) and heart rate (HR), i.e., vasovagal oscillations, as well as transient decreases in BP and HR, i.e., vasovagal responses, in isoflurane-anesthetized rats. We determined the characteristics of the vasovagal oscillations, assessed their role in the generation of vasovagal responses, and determined whether they could be induced by monaural as well as by binaural sGVS and by oscillation in pitch. Wavelet analyses were used to determine the power distributions of the waveforms. Monaural and binaural sGVS and pitch generated vasovagal oscillations at the frequency and at twice the frequency of stimulation. Vasovagal oscillations and vasovagal responses were maximally induced at low stimulus frequencies (0.025–0.05 Hz). The oscillations were attenuated and the responses were rarely induced at higher stimulus frequencies. Vasovagal oscillations could occur without induction of vasovagal responses, but vasovagal responses were always associated with a vasovagal oscillation. We posit that the vasovagal oscillations originate in a low frequency band that, when appropriately activated by strong sympathetic stimulation, can generate vasovagal oscillations as a precursor for vasovagal responses and syncope. We further suggest that the activity responsible for the vasovagal oscillations arises in low frequency, otolith neurons with orientation vectors close to the vertical axis of the head. These neurons are likely to provide critical input to the vestibulo-sympathetic reflex to increase BP and HR upon changes in head position relative to gravity, and to contribute to the production of vasovagal oscillations and vasovagal responses and syncope when the baroreflex is inactivated.

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Section: Discussionmentioning

confidence: 99%

Vasovagal Oscillations and Vasovagal Responses Produced by the Vestibulo-Sympathetic Reflex in the Rat

et al. 2014

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“…The immediate early gene protein c-Fos is useful for mapping functional activity of the brain [39,40]. Several studies have demonstrated that hypotension elicits c-Fos protein expression in several forebrain and brain stem nuclei that affect cardiovascular function [23,41].…”

Section: Discussionmentioning

confidence: 99%

“…Anatomical evidence shows the existence of a direct projection from vestibular nuclei to the RVLM region [40,48]. Functional convergence from the vestibular and baroreceptor afferents to the same nuclei in the RVLM further suggests that this is the central point of interaction between the vestibular system and the baroreflex [38].…”

Section: Discussionmentioning

confidence: 99%

Additive Role of the Vestibular End Organ and Baroreceptors on the Regulation of Blood Pressure in Rats

Yang

Jian

et al. 2013

Korean J Physiol Pharmacol

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Contribution of the vestibular end organ to regulation of arterial pressure was quantitatively compared with the role of baroreceptors in terms of baroreflex sensitivity and c-Fos protein expression in the rostral ventrolateral medulla (RVLM). Baroreflex sensitivity and c-Fos protein expression in the RVLM were measured in conscious rats that had undergone bilateral labyrinthectomy (BL) and/or baroreceptor unloading. BL attenuated baroreflex sensitivity during intravenous infusion of sodium nitroprusside (SNP), but did not significantly affect the sensitivity following infusion of phenylephrine (PE). Baroreflex sensitivity became positive following sinoaortic denervation (SAD) during infusion of PE and attenuated sensitivity during infusion of SNP. Baroreflex sensitivity also became positive following double ablation (BL+SAD) during infusion of PE, and attenuated sensitivity during infusion of SNP. c-Fos protein expression increased significantly in the RVLM in the sham group after SNP administration. However, the BL, SAD, and SAD+BL groups showed significant decreases in c-Fos protein expression compared with that in the sham group. The SAD group showed more reduced c-Fos protein expression than that in the BL group, and the SAD+BL group showed less expression than that in the SAD group. These results suggest that the vestibular system cooperates with baroreceptors to maintain arterial pressure during hypotension but that baroreceptors regulate arterial pressure during both hypotension and hypertension. Additionally, afferent signals for maintaining blood pressure from the vestibular end organs and the baroreceptors may be integrated in the RVLM.

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“…Experimental studies on animals indicate that the vestibular system projects to cardiovascular centres in the central nervous system through the vestibular sympathetic reflex and modulates blood pressure and heart rate in response to changes in the head and body position relative to gravity [9][10][11][12][13][14][15][16]. The anatomical connection of the vestibular sympathetic reflex pathway has been described in animals [17]. The activated cells in this pathway were concentrated in the caudal inferior and medial vestibular nuclei, otolithrecipient regions, and sent axonal projections to the rostral and caudal ventrolateral medullary areas [18].…”

Section: Introductionmentioning

confidence: 99%