Ultrasonic Neuromodulation via Astrocytic TRPA1

Oh, Soo‐Jin; Lee, Jung Moo; Kim, Hyun-Bum; Lee, Jungpyo; Han, Sheng; Bae, Jin Young; Hong, Gyu-Sang; Koh, Wuhyun; Kwon, Jea; Hwang, Eun-Sang; Woo, Dong Ho; Youn, Inchan; Cho, Il‐Joo; Bae, Yong Chul; Lee, Sungon; Shim, Jae Wan; Park, Ji-Ho; Lee, C. Justin

doi:10.1016/j.cub.2020.02.042

Cited by 48 publications

(66 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…LILFU can specifically activate TRPA1 in astrocytes, which results in glutamate release through BEST1 (Oh et al 2019). In addition, the similar subcellular localization of TRPA1 and BEST1 in the astrocytic microdomains (Woo et al 2012;Oh et al 2019) provides a structural basis for TRPA1's unique ability to cooperate with the Ca 2+ -activated BEST1. In the current study, we have additionally demonstrated that astrocytic membrane expansion, induced by a transient volume increase, can activate TRPA1 and subsequently BEST1.…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

“…We have recently shown that astrocytic TRPA1 is modulated by low-intensity, low-frequency ultrasound (LILFU) and mechanical stimulus (poking) to induce an astrocytic Ca 2+ increase (Oh et al 2019). LILFU can specifically activate TRPA1 in astrocytes, which results in glutamate release through BEST1 (Oh et al 2019). In addition, the similar subcellular localization of TRPA1 and BEST1 in the astrocytic microdomains (Woo et al 2012;Oh et al 2019) provides a structural basis for TRPA1's unique ability to cooperate with the Ca 2+ -activated BEST1.…”

Section: Discussionmentioning

confidence: 99%

“…It has been reported that a rise in astrocytic Ca 2+ can be mediated by either Ca 2+ release from internal stores through IP 3 R2 upon GPCR activation (Agulhon et al 2010) or Ca 2+ entry via TRPA1 (Shigetomi et al 2011(Shigetomi et al , 2013, which is known to be one of the members of stretch-activated TRP channels (Corey et al 2004;Soya et al 2014). We have recently shown that ultrasound induces a Ca 2+ increase via TRPA1 and subsequently releases glutamate via BEST1 (Oh et al 2019). Therefore, we tested whether the astrocytic Ca 2+ increase elicited by the AQP4-dependent volume transient is mediated by TRPA1.…”

Section: Trpa1-mediated Ca 2+ Increase Leads To Volume Decreasementioning

confidence: 99%

See 3 more Smart Citations

The molecular mechanism of synaptic activity‐induced astrocytic volume transient

Woo

Jang

Lee

et al. 2020

The Journal of Physiology

Self Cite

View full text Add to dashboard Cite

Neuronal activity causes astrocytic volume change via K + uptake through TREK-1 containing two-pore domain potassium channels. r The volume transient is terminated by Cl − efflux through the Ca 2+-activated anion channel BEST1. r The source of the Ca 2+ required to open BEST1 appears to be the stretch-activated TRPA1 channel. r Intense neuronal activity is synaptically coupled with a physical change in astrocytes via volume transients.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Trpa1-mediated Ca 2+ Increase Leads To Volume Decreasementioning

confidence: 99%

See 2 more Smart Citations

The molecular mechanism of synaptic activity‐induced astrocytic volume transient

Woo

Jang

Lee

et al. 2020

The Journal of Physiology

Self Cite

View full text Add to dashboard Cite

show abstract

“…The mechanically gated channel Piezo2 is expressed in a subset of CA1 pyramidal neurons (Wang and Hamill, 2020). Piezo1 (Qiu et al, 2019) and TRP channels (Oh et al, 2020;Yoo et al, 2020) have been experimentally linked to ultrasound neuromodulation effects. In addition, most ion channels and membrane proteins, while not functioning physiologically as mechanoreceptors, are sensitive to mechanical stimuli to some extent, either through the energetics of their interactions with hydrophobic core of the lipid bilayer or through mechanical interactions with the cytoskeleton or extracellular matrix.…”

Section: Discussionmentioning

confidence: 99%

Spike-frequency dependent inhibition and excitation of neural activity by high-frequency ultrasound

Prieto

Firouzi

Khuri‐Yakub

et al. 2020

Preprint

View full text Add to dashboard Cite

Prieto et al. describe how ultrasound can either inhibit or potentiate action potential firing in hippocampal pyramidal neurons and demonstrate that these effects can be explained by increased potassium conductance. ABSTRACTUltrasound can modulate action potential firing in vivo and in vitro, but the mechanistic basis of this phenomenon is not well understood. To address this problem, we used patch-clamp recording to quantify the effects of focused, high-frequency (43 MHz) ultrasound on evoked action potential firing in CA1 pyramidal neurons in acute rodent hippocampal brain slices. We find that ultrasound can either inhibit or potentiate firing in a spike-frequency-dependent manner: at low (nearthreshold) input currents and low firing frequencies, ultrasound inhibits firing, while at higher input currents and higher firing frequencies, ultrasound potentiates firing. The net result of these two competing effects is that ultrasound increases the threshold current for action potential firing, the slope of frequency-input curves, and the maximum firing frequency. In addition, ultrasound slightly hyperpolarizes the resting membrane potential, decreases action potential width, and increases the depth of the afterhyperpolarization. All of these results can be explained by the hypothesis that ultrasound activates a sustained potassium conductance. According to this hypothesis, increased outward potassium currents hyperpolarize the resting membrane potential and inhibit firing at near-threshold input currents, but potentiate firing in response to higher input currents by limiting inactivation of voltage-dependent sodium channels during the action potential. This latter effect is a consequence of faster action-potential repolarization, which limits inactivation of voltage-dependent sodium channels, and deeper (more negative) afterhyperpolarization, which increases the rate of recovery from inactivation. Based on these results we propose that ultrasound activates thermosensitive and mechanosensitive, voltage-insensitive two-poredomain potassium (K2P) channels, through heating or mechanical effects of acoustic radiation force. Finite-element modelling of the effects of ultrasound on brain tissue suggests that the effects of ultrasound on firing frequency are caused by a small (less than 2°C) increase in temperature, with possible additional contributions from mechanical effects. 93force produced by reflection of the acoustic wave at the interface between the solution and the air 94 above it (Duck, 1998)). The mound of fluid was then aligned in the x-y plane to the center of a 95 reticle in one eyepiece of the dissecting microscope, and, after adding additional ACSF and the 96 tissue sample to the chamber, the center of the reticle was aligned with the region of the tissue 97 targeted for patch-clamp recording. The ultrasound intensity (50 W/cm 2 ) is the spatial peak, pulse 98 average intensity for the free field. The interval between ultrasound applications was at least 12 99 seconds. 101Electrophysiology. Current clamp re...

show abstract

Bidirectional Neuronal Control of Epileptiform Activity by Repetitive Transcranial Focused Ultrasound Stimulations

Choi,

Koo,

Joo

et al. 2023

Advanced Science

View full text Add to dashboard Cite

Repetitive stimulation procedures are used in neuromodulation techniques to induce persistent excitatory or inhibitory brain activity. The directivity of modulation is empirically regulated by modifying the stimulation length, interval, and strength. However, bidirectional neuronal modulations using ultrasound stimulations are rarely reported. This study presents bidirectional control of epileptiform activities with repetitive transcranial‐focused ultrasound stimulations in a rat model of drug‐induced acute epilepsy. It is found that repeated transmission of elongated (40 s), ultra‐low pressure (0.25 MPa) ultrasound can fully suppress epileptic activities in electro‐encephalography and cerebral blood volume measurements, while the change in bursting intervals from 40 to 20 s worsens epileptic activities even with the same burst length. Furthermore, the suppression induced by 40 s long bursts is transformed to excitatory states by a subsequent transmission. Bidirectional modulation of epileptic seizures with repeated ultrasound stimulation is achieved by regulating the changes in glutamate and γ‐Aminobutyric acid levels, as confirmed by measurements of expressed c‐Fos and GAD65 and multitemporal analysis of neurotransmitters in the interstitial fluid obtained via microdialysis.

show abstract

Ultrasonic Neuromodulation via Astrocytic TRPA1

Cited by 48 publications

References 0 publications

The molecular mechanism of synaptic activity‐induced astrocytic volume transient

The molecular mechanism of synaptic activity‐induced astrocytic volume transient

Spike-frequency dependent inhibition and excitation of neural activity by high-frequency ultrasound

Bidirectional Neuronal Control of Epileptiform Activity by Repetitive Transcranial Focused Ultrasound Stimulations

Contact Info

Product

Resources

About