TY - JOUR
T1 - Alleviation of Tinnitus With High-Frequency Stimulation of the Dorsal Cochlear Nucleus
T2 - A Rodent Study
AU - van Zwieten, Gusta
AU - Jahanshahi, Ali
AU - van Erp, Marlieke L.
AU - Temel, Yasin
AU - Stokroos, Robert J.
AU - Janssen, Marcus L.F.
AU - Smit, Jasper V.
PY - 2019/3/15
Y1 - 2019/3/15
N2 - 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.
AB - 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.
KW - Animals
KW - Auditory Pathways/physiopathology
KW - Cochlear Nucleus/physiopathology
KW - Deep Brain Stimulation/methods
KW - Disease Models, Animal
KW - Evoked Potentials, Auditory, Brain Stem/physiology
KW - Male
KW - Noise
KW - Rats
KW - Rats, Sprague-Dawley
KW - Reflex, Startle
KW - Tinnitus/physiopathology
UR - http://www.scopus.com/inward/record.url?scp=85062882464&partnerID=8YFLogxK
U2 - 10.1177/2331216519835080
DO - 10.1177/2331216519835080
M3 - Article
C2 - 30868944
AN - SCOPUS:85062882464
VL - 23
SP - 1
EP - 10
JO - Trends in Hearing
JF - Trends in Hearing
ER -