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Sci Rep. 2017 Nov 20;7(1):15865. doi: 10.1038/s41598-017-16129-3.

Optogenetic silencing of nociceptive primary afferents reduces evoked and ongoing bladder pain.

Author information

1
Washington University Pain Center and Department of Anesthesiology, St. Louis, MO, 63110, USA.
2
Washington University School of Medicine, 660 S. Euclid Ave, Box 8054, St. Louis, MO, 63110, USA.
3
Department of Materials Science and Engineering, University of Illinois at Urbana-Champaign, Urbana, Illinois, 61801, USA.
4
Washington University Department of Surgery - Division of Urologic Surgery, St. Louis, MO, 63110, USA.
5
Department of Civil and Environmental Engineering, Mechanical Engineering, Materials Science and Engineering, Northwestern University, Evanston, IL, 60208, USA.
6
Departments of Materials Science and Engineering, Biomedical Engineering, Chemistry, Mechanical Engineering, Electrical Engineering and Computer Science, and Neurological Surgery, Center for Bio-Integrated Electronics, Simpson Querrey Institute for Nano/biotechnology, Northwestern University, Evanston, IL, 60208, USA.
7
Washington University Pain Center and Department of Anesthesiology, St. Louis, MO, 63110, USA. gereaur@wustl.edu.
8
Washington University School of Medicine, 660 S. Euclid Ave, Box 8054, St. Louis, MO, 63110, USA. gereaur@wustl.edu.

Abstract

Patients with interstitial cystitis/bladder pain syndrome (IC/BPS) suffer from chronic pain that severely affects quality of life. Although the underlying pathophysiology is not well understood, inhibition of bladder sensory afferents temporarily relieves pain. Here, we explored the possibility that optogenetic inhibition of nociceptive sensory afferents could be used to modulate bladder pain. The light-activated inhibitory proton pump Archaerhodopsin (Arch) was expressed under control of the sensory neuron-specific sodium channel (sns) gene to selectively silence these neurons. Optically silencing nociceptive sensory afferents significantly blunted the evoked visceromotor response to bladder distension and led to small but significant changes in bladder function. To study of the role of nociceptive sensory afferents in freely behaving mice, we developed a fully implantable, flexible, wirelessly powered optoelectronic system for the long-term manipulation of bladder afferent expressed opsins. We found that optogenetic inhibition of nociceptive sensory afferents reduced both ongoing pain and evoked cutaneous hypersensitivity in the context of cystitis, but had no effect in uninjured, naïve mice. These results suggest that selective optogenetic silencing of nociceptive bladder afferents may represent a potential future therapeutic strategy for the treatment of bladder pain.

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