In vitro effects of ultrasound with different energies on the conduction properties of neural tissue

Tsui, Po-Hsiang; Wang, Shyh-Hau; Huang, Chih-Chung

doi:10.1016/j.ultras.2004.12.003

Cited by 125 publications

(96 citation statements)

References 11 publications

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“…In vitro [41][42][43] and in vivo studies have shown that US interacts with 44 and could be used to activate 31,45 neurons. The cholinergic anti-inflammatory pathway provides a physiologic means by which US, possibly through interacting with the splenic nerve, may interfere with the pathogenesis of IRI.…”

Section: Discussionmentioning

confidence: 99%

Ultrasound Prevents Renal Ischemia-Reperfusion Injury by Stimulating the Splenic Cholinergic Anti-Inflammatory Pathway

Gigliotti

Huang

et al. 2013

Journal of the American Society of Nephrology

164

200

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AKI affects both quality of life and health care costs and is an independent risk factor for mortality. At present, there are few effective treatment options for AKI. Here, we describe a nonpharmacologic, noninvasive, ultrasound-based method to prevent renal ischemia-reperfusion injury in mice, which is a model for human AKI. We exposed anesthetized mice to an ultrasound protocol 24 hours before renal ischemia. After 24 hours of reperfusion, ultrasound-treated mice exhibited preserved kidney morphology and function compared with sham-treated mice. Ultrasound exposure before renal ischemia reduced the accumulation of CD11b + Ly6G high neutrophils and CD11b + F4/80 high myeloid cells in kidney tissue. Furthermore, splenectomy and adoptive transfer studies revealed that the spleen and CD4 + T cells mediated the protective effects of ultrasound. Last, blockade or genetic deficiency of the a7 nicotinic acetylcholine receptor abrogated the protective effect of ultrasound, suggesting the involvement of the cholinergic anti-inflammatory pathway. Taken together, these results suggest that an ultrasound-based treatment could have therapeutic potential for the prevention of AKI, possibly by stimulating a splenic anti-inflammatory pathway.

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Section: Discussionmentioning

confidence: 99%

Ultrasound Prevents Renal Ischemia-Reperfusion Injury by Stimulating the Splenic Cholinergic Anti-Inflammatory Pathway

Gigliotti

Huang

et al. 2013

Journal of the American Society of Nephrology

164

200

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“…We believe that the splenic nerve is the proximal target of ultrasound treatment, a hypothesis supported by observations that ultrasound alters frog peripheral nerve activity. 36 Transcranial ultrasound-induced neuromodulation in rodents induces limb movement, 37 thereby further suggesting a biomechanical effect of ultrasound. Although we have not shown a direct effect of ultrasound on splenic nerve activity, which would be technically difficult in the mouse, we used 6-OHDA, which selectively destroys catecholaminergic nerve terminals peripherally 15 or when injected directly in brain regions, 38,39 to denervate the spleen and interrupt the cholinergic antiinflammatory signaling pathway.…”

Section: Neural Control Of Inflammationmentioning

confidence: 99%

Ultrasound Modulates the Splenic Neuroimmune Axis in Attenuating AKI

Gigliotti

Huang

Bajwa

et al. 2015

Journal of the American Society of Nephrology

122

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We showed previously that prior exposure to a modified ultrasound regimen prevents kidney ischemiareperfusion injury (IRI) likely via the splenic cholinergic anti-inflammatory pathway (CAP) and a7 nicotinic acetylcholine receptors (a7nAChR). However, it is unclear how ultrasound stimulates the splenic CAP. Further investigating the role of the spleen in ischemic injury, we found that prior splenectomy (-7d) or chemical sympathectomy of the spleen with 6-hydroxydopamine (6OHDA; -14d) exacerbated injury after subthreshold (24-minute ischemia) IRI. 6-OHDA-induced splenic denervation also prevented ultrasoundinduced protection of kidneys from moderate (26-minute ischemia) IRI. Ultrasound-induced protection required hematopoietic but not parenchymal a7nAChRs, as shown by experiments in bone marrow chimeras generated with wild-type and a7nAChR -/-mice. Ultrasound protection was associated with reduced expression of circulating and kidney-derived cytokines. However, splenocytes isolated from mice 24 hours after ultrasound treatment released more IL-6 ex vivo in response to LPS than splenocytes from sham mice. Adoptive transfer of splenocytes from ultrasound-treated (but not sham) mice to naïve mice was sufficient to protect kidneys of recipient mice from IRI. Ultrasound treatment 24 hours before cecal ligation puncture-induced sepsis was effective in reducing plasma creatinine in this model of AKI. Thus, splenocytes of ultrasound-treated mice are capable of modulating IRI in vivo, supporting our ongoing hypothesis that a modified ultrasound regimen has therapeutic potential for AKI and other inflammatory conditions.

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“…The hypothesized mechanisms for this effect include ultrasoundinduced microstreaming caused by local pressure gradients within the bone microstructure, or the generation of an electric field caused by mechanical movement of ionic fluids within the bone. Another author observed similar effects using low-amplitude, unfocused shock waves (van der Jagt et al 2013), and the hypothesized mechanism was acoustic cavitation. However, the majority of evidence suggests that neither treatment of the intact bone by shock waves nor treatment of the bone by LIPUS is efficient in mitigating bone loss (Carvalho and Cliquet Junior 2004;Warden et al 2001a;Yang et al 2005).…”

Section: Introductionmentioning

confidence: 80%

“…Ultrasound has also been used in animal models in an attempt to mitigate bone loss induced by spinal cord injury, ovariectomy and neurectomy, yet the results remain controversial (Carvalho and Cliquet Junior 2004;Cook et al 2001;Ferreri et al 2011;Gollwitzer et al 2013;van der Jagt et al 2013;Warden et al 2001a;Yang et al 2005). In particular, Ferreri et al (2011) applied LIPUS to the L4 and L5 vertebrae in ovariectomized rats for 20 min daily, 5 d a wk, for 4 wk, and observed partial mitigation of trabecular bone loss compared with the control group.…”

Section: Introductionmentioning

confidence: 99%

Pulsed focused ultrasound treatment of muscle mitigates paralysis-induced bone loss in the adjacent bone: A study in a mouse model

Poliachik

Khokhlova

Wang

et al. 2013

The Journal of the Acoustical Society of America

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Bone loss can result from bed rest, space flight, spinal cord injury or age-related hormonal changes. Current bone loss mitigation techniques include pharmaceutical interventions, exercise, pulsed ultrasound targeted to bone and whole body vibration. In this study, we attempted to mitigate paralysis-induced bone loss by applying focused ultrasound to the midbelly of a paralyzed muscle. We employed a mouse model of disuse that uses onabotulinumtoxinA-induced paralysis, which causes rapid bone loss in 5 d. A focused 2 MHz transducer applied pulsed exposures with pulse repetition frequency mimicking that of motor neuron firing during walking (80 Hz), standing (20 Hz), or the standard pulsed ultrasound frequency used in fracture healing (1 kHz). Exposures were applied daily to calf muscle for 4 consecutive d. Trabecular bone changes were characterized using micro-computed tomography. Our results indicated that application of certain focused pulsed ultrasound parameters was able to mitigate some of the paralysis-induced bone loss.

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In vitro effects of ultrasound with different energies on the conduction properties of neural tissue

Cited by 125 publications

References 11 publications

Ultrasound Prevents Renal Ischemia-Reperfusion Injury by Stimulating the Splenic Cholinergic Anti-Inflammatory Pathway

Ultrasound Prevents Renal Ischemia-Reperfusion Injury by Stimulating the Splenic Cholinergic Anti-Inflammatory Pathway

Ultrasound Modulates the Splenic Neuroimmune Axis in Attenuating AKI

Pulsed focused ultrasound treatment of muscle mitigates paralysis-induced bone loss in the adjacent bone: A study in a mouse model

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