During the development of the CNS, each neuron extends an axon by generating forces, and is subjected to heterogeneous mechanical environment. How the mechanical properties of developing CNS tissue influence axon growth in vivo are currently unknown, and the potential neuronal response to mechanical signals in vivo is poorly understood. To date, it is emergent to develop a mechanical based stimulation strategy for in vivo studies. Ultrasound is considered as a promising tool for brain stimulation. It is shown to be able to trigger neuron like cells to outgrowth, axon branching, and accelerate nerve regeneration. However, the detailed mechanisms are unclear. We hypotheses that neurons can sense ultrasound through piezo1 channel to promote axon growth during development. To test this hypothesis, N2A and retinal ganglion cell (RGC) which highly express Piezo1 were utilized as in vitro model. Piezo1 knockdown cells with siRNA and Piezo1 blocker GsMTx-4 pre-treated cells were severed as control to test the role of Piezo1 in sensing ultrasound. The axon lengths after 24 h, the extension velocity of axons for all the experimental groups are analyzed from live cell imaging data. Our results show that ultrasound stimulation on wild type N2A cell and primary cultured RGC can promote axon outgrowth. The axon length and the extension velocity for Piezo1 knockdown and GsMTx-4 blocked neurons is significant decreased. These results showed that ultrasound as a mechanical wave is able to stimulate neurons and modulate the axon growth through mechanosensitive ion channels. Given the ability of focused into small region in human brain non-invasively, it is capable for investigate the mechanisms of mechanical effects on neural development in vivo.

The rodent anterior cingulate cortex (ACC) is critical for visceral pain and pain-related aversive response in chronic visceral hypersensitive (VH) state. Long-term potentiation (LTP), induced by theta burst stimulation (TBS) in the medial thalamus (MT)-ACC pathway, is blocked in VH rats. However, the neuronal intrinsic firing characteristics and the MT-ACC connectivity have not been investigated in visceral pain. Using repetitive distension of the colon and rectum (rCRD) as a sensitization paradigm, we have identified that the spontaneous firing rates of ACC neurons and the CRD-stimulated neuronal firings were increased after repetitive visceral noxious stimulation. This correlates with increases in visceral pain responses (visceromotor responses, VMRs). Two multichannel arrays of electrodes were implanted in the MT and ACC. Recordings were performed in free-moving rats before and after repeated CRD treatment. Power spectral density analysis showed that the local field potential (LFP) recorded in the ACC displayed increases in theta band power (4-10 Hz) that were modulated by rCRD. Neural spike activity in the ACC becomes synchronized with ongoing theta oscillations of LFP. Furthermore, cross correlation analysis showed augmented synchronization of thalamo-ACC theta band LFPs, which was consistent with an increase of neuronal communication between the two regions. In conclusion, these results reveal theta oscillations and theta-frequency phase-locking as prominent features of neural activity in the ACC and a candidate neural mechanism underlying acute visceral pain. (C) 2015 The Authors. Published by Elsevier Ltd. on behalf of IBRO.

International Journal of Developmental NeuroscienceVolume 24, Issue 8 p. 594-595 Abstract [P231]: Role of Nogo on axon divergence in the mouse optic chiasm J. Wang, Corresponding Author J. Wang n/a@.dne The Chinese University of Hong Kong, ChinaSearch for more papers by this authorS.O. Chan, S.O. Chan The Chinese University of Hong Kong, ChinaSearch for more papers by this author J. Wang, Corresponding Author J. Wang n/a@.dne The Chinese University of Hong Kong, ChinaSearch for more papers by this authorS.O. Chan, S.O. Chan The Chinese University of Hong Kong, ChinaSearch for more papers by this author First published: 16 November 2006 https://doi.org/10.1016/j.ijdevneu.2006.09.291Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume24, Issue8ABSTRACTS TO THE 16TH BIENNIAL MEETING OF THE INTERNATIONAL SOCIETY FOR DEVELOPMENTAL NEUROSCIENCE, 24-28 AUGUST 2006, BANFF, CANADADecember 2006Pages 594-595 RelatedInformation