Significance: The ability of vagus nerve stimulation to generate anti-inflammatory and tissue-protective effects has been known for some time. We have made use of cutting-edge tools to precisely map the neural circuits that contribute to beneficial effects of vagus nerve stimulation. Stimulation was specifically restricted to either the afferent or efferent neurons in the vagus nerve by genetically programming the appropriate cells to express a light-sensitive cation channel. We show that, while both afferent and efferent signals provide protection from kidney injury, afferent stimulation generates a sympathetic response that protects mice in the absence of efferent vagus signals. This provides an insight into the pathways of neuroimmune protection and potential therapeutics.

The vestibular system, which is essential for maintaining balance, contributes to the sympathetic response. Although this response is involved in hypergravity load-induced hypothermia in mice, the underlying mechanism remains unknown. This study showed that hypergravity (2g) decreased plasma catecholamines, which resulted in hypoactivity of the interscapular brown adipose tissue (iBAT). Hypothermia induced by 2g load was significantly suppressed by administration of beta-adrenergic receptor agonists, suggesting the involvement of decrease in iBAT activity through sympathoinhibition. Bilateral chemogenetic activation of vesicular glutamate transporter 2 (VGLUT2)-expressing neurons in the vestibular nuclear complex (VNC) induced hypothermia. The VGLUT2-expressing neurons contributed to 2g load-induced hypothermia, since their deletion suppressed hypothermia. Although activation of vesicular gamma-aminobutyric acid transporter-expressing neurons in the VNC induced slight hypothermia instead of hyperthermia, their deletion did not affect 2g load-induced hypothermia. Thus, we concluded that 2g load-induced hypothermia resulted from sympathoinhibition via the activation of VGLUT2-expressing neurons in the VNC.

Background: The vestibular lesion (VL) is required to examine the physiological function of the vestibular system in animals. Toxic chemicals or electrical apparatus have been used for the VL, however, they are not ideal as they have low specificity, and can result in unintended damage, and systemic toxic effect. New method: Localized vibration-induced VL, using an ultrasonicator, is expected to overcome the problems associated with chemical and electrical lesions. Thus, we examined the effect of the ultrasonication on the VL from the aspects of both the physiological function and histology in the present study. Results: and Comparison with Existing Method(s) Complete VL, which was evaluated by deterioration of swimming skills, righting reflex, and body stability, was induced using an ultrasonicator or electrical apparatus. Histological evaluation shows that hair cell layers in the saccule and utricle were completely destroyed in both methods Furthermore, significant drop in body mass was observed in VL. However, abscess at the cranial base was observed in VL induced by the electrical apparatus in ICR mice. Complete chemically-induced VL was observed in C57BL/6J but not ICR mice, and systemic leakage of the toxic chemicals (arsenic) was not detectable even 1 day after surgery. Conclusions: Compared to the electrical apparatus, the ultrasonicator is useful for inducing VL in ICR and C57BL/6J mice, as it results in less non-specific damage. Toxic chemicals can be used for inducing VL in C57BL/6J mice; however, this method does not ensure complete disruption of the hair cells in the saccule and utricle. (C) 2017 The Author(s). Published by Elsevier B.V.

It is unclear whether the degree of change in vestibular-related physiological function depends on gravitational loading. Present study showed that exposure to hypergravity-induced degrees of change in metabolism and vestibular function depended on the gravitational loading. The response of body mass depended on the gravitational loading size. Especially in 2 G environment, water intake, body temperature, and vestibular function were influenced. These changes could involve plastic alteration of vestibular-related autonomic and motor functions.