scholarly journals Direct Visualization of the Murine Dorsal Cochlear Nucleus for Optogenetic Stimulation of the Auditory Pathway

Author(s):  
Elliott D. Kozin ◽  
Keith N. Darrow ◽  
Ariel E. Hight ◽  
Ashton E. Lehmann ◽  
Alyson B. Kaplan ◽  
...  
2019 ◽  
Vol 23 ◽  
pp. 233121651983508 ◽  
Author(s):  
Gusta van Zwieten ◽  
Ali Jahanshahi ◽  
Marlieke L. van Erp ◽  
Yasin Temel ◽  
Robert J. Stokroos ◽  
...  

Deep brain stimulation of the central auditory pathway is emerging as a promising treatment modality for tinnitus. Within this pathway, the dorsal cochlear nucleus (DCN) plays a key role in the pathophysiology of tinnitus and is believed to be a tinnitus generator. We hypothesized that high-frequency stimulation (HFS) of the DCN would influence tinnitus-related abnormal neuronal activity within the auditory pathway and hereby suppress tinnitus. To this end, we assessed the effect of HFS of the DCN in a noise-induced rat model of tinnitus. The presence of tinnitus was verified using the gap prepulse inhibition of the acoustic startle response paradigm. Hearing thresholds were determined before and after noise trauma by measuring the auditory brainstem responses. In addition, changes in neuronal activity induced by noise trauma and HFS were assessed using c-Fos immunohistochemistry in related structures. Results showed tinnitus development after noise trauma and hearing loss ipsilateral to the side exposed to noise trauma. During HFS of the DCN, tinnitus was suppressed. There was no change in c-Fos expression within the central auditory pathway after HFS. These findings suggest that DCN-HFS changes patterns of activity and results in information lesioning within the network and hereby blocking the relay of abnormal tinnitus-related neuronal activity.


2018 ◽  
Vol 37 (24) ◽  
Author(s):  
Daniel Keppeler ◽  
Ricardo Martins Merino ◽  
David Lopez de la Morena ◽  
Burak Bali ◽  
Antoine Tarquin Huet ◽  
...  

2018 ◽  
Vol 10 (449) ◽  
pp. eaao0540 ◽  
Author(s):  
Christian Wrobel ◽  
Alexander Dieter ◽  
Antoine Huet ◽  
Daniel Keppeler ◽  
Carlos J. Duque-Afonso ◽  
...  

2016 ◽  
Vol 127 (9) ◽  
pp. e197
Author(s):  
G. van Zwieten ◽  
J. Smit ◽  
A. Jahanshahi ◽  
R. Stokroos ◽  
Y. Temel

2015 ◽  
Vol 113 (3) ◽  
pp. 956-970 ◽  
Author(s):  
Roxana A. Stefanescu ◽  
Seth D. Koehler ◽  
Susan E. Shore

Tinnitus has been associated with enhanced central gain manifested by increased spontaneous activity and sound-evoked firing rates of principal neurons at various stations of the auditory pathway. Yet, the mechanisms leading to these modifications are not well understood. In a recent in vivo study, we demonstrated that stimulus-timing-dependent bimodal plasticity mediates modifications of spontaneous and tone-evoked responses of fusiform cells in the dorsal cochlear nucleus (DCN) of the guinea pig. Fusiform cells from sham animals showed primarily Hebbian learning rules while noise-exposed animals showed primarily anti-Hebbian rules, with broadened profiles for the animals with behaviorally verified tinnitus (Koehler SD, Shore SE. J Neurosci 33: 19647–19656, 2013a). In the present study we show that well-timed bimodal stimulation induces alterations in the rate-level functions (RLFs) of fusiform cells. The RLF gains and maximum amplitudes show Hebbian modifications in sham and no-tinnitus animals but anti-Hebbian modifications in noise-exposed animals with evidence for tinnitus. These findings suggest that stimulus-timing bimodal plasticity produced by the DCN circuitry is a contributing mechanism to enhanced central gain associated with tinnitus.


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