scholarly journals Neural Hyperactivity of the Central Auditory System in Response to Peripheral Damage

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Yi Zhao ◽  
Qiang Song ◽  
Xinyi Li ◽  
Chunyan Li

It is increasingly appreciated that cochlear pathology is accompanied by adaptive responses in the central auditory system. The cause of cochlear pathology varies widely, and it seems that few commonalities can be drawn. In fact, despite intricate internal neuroplasticity and diverse external symptoms, several classical injury models provide a feasible path to locate responses to different peripheral cochlear lesions. In these cases, hair cell damage may lead to considerable hyperactivity in the central auditory pathways, mediated by a reduction in inhibition, which may underlie some clinical symptoms associated with hearing loss, such as tinnitus. Homeostatic plasticity, the most discussed and acknowledged mechanism in recent years, is most likely responsible for excited central activity following cochlear damage.

2002 ◽  
Vol 111 (5_suppl) ◽  
pp. 38-41 ◽  
Author(s):  
Anu Sharma ◽  
Anthony Spahr ◽  
Michael Dorman ◽  
N. Wendell Todd

The goal of this study was to determine whether there is a sensitive period during early development when a cochlear implantation can occur into a minimally degenerate and/or highly plastic central auditory system. Our measure of central auditory deprivation was latency of the P1 auditory evoked potential, whose generators include auditory thalamocortical areas. Auditory evoked potentials were recorded in 18 congenitally deaf children who were fitted with cochlear implants by 3.5 years of age. The P1 latencies of the children with implants were compared with the P1 latencies of their age-matched peers with normal hearing. There was no significant difference between the P1 latencies of the children with implants and the children with normal hearing. The present results suggest that early implantation occurs in a central auditory system that is minimally degenerate and/or highly plastic. Studies are ongoing to assess the consequences to the developing central auditory system of initiating electrical stimulation at later ages.


2018 ◽  
Author(s):  
Wei-Wei Cai ◽  
Jian-Gang Liang ◽  
Zhi-Hui Li ◽  
Yu-lin Huang ◽  
Li Wang ◽  
...  

AbstractThis resting-state functional magnetic resonance imaging (rs-fMRI) study in tinnitus patients was conducted to observe the spontaneous neural activity of the central auditory system using a derived index, mean amplitude of low-frequency fluctuation (mALFF). Tinnitus subjects with right-ear hearing impairment (THL) and without hearing loss (TNH) and two age-, sex-, and education-matched control groups (NC1 and NC2) were recruited for rs-fMRI. mALFF maps of the tinnitus and matched NC groups were plotted in the central auditory system, including the primary auditory cortex (PAC), higher auditory cortex (HAC), and hubs of the central auditory pathway. mALFF values of the activity clusters in the central auditory system of THL and TNH patients were extracted and correlated with each clinical characteristic. Significantly increased mALFF clusters were found in bilateral PAC and HAC of THL-NC1 maps and in the left inferior colliculus and right HAC of TNH-NC2 maps. Thus, subgroups of tinnitus with and without hearing impairment might exhibit different homeostatic plasticity in the central auditory system. mALFF values of aberrant active clusters in the central auditory system are partly associated with specific clinical tinnitus characteristics.


Biomedicines ◽  
2021 ◽  
Vol 9 (1) ◽  
pp. 77
Author(s):  
Kristin M. Barry ◽  
Donald Robertson ◽  
Wilhelmina H. A. M. Mulders

In the adult auditory system, loss of input resulting from peripheral deafferentation is well known to lead to plasticity in the central nervous system, manifested as reorganization of cortical maps and altered activity throughout the central auditory pathways. The auditory system also has strong afferent and efferent connections with cortico-limbic circuitry including the prefrontal cortex and the question arises whether this circuitry is also affected by loss of peripheral input. Recent studies in our laboratory showed that PFC activation can modulate activity of the auditory thalamus or medial geniculate nucleus (MGN) in normal hearing rats. In addition, we have shown in rats that cochlear trauma resulted in altered spontaneous burst firing in MGN. However, whether the PFC influence on MGN is changed after cochlear trauma is unknown. We investigated the effects of electrical stimulation of PFC on single neuron activity in the MGN in anaesthetized Wistar rats 2 weeks after acoustic trauma or sham surgery. Electrical stimulation of PFC showed a variety of effects in MGN neurons both in sham and acoustic trauma groups but inhibitory responses were significantly larger in the acoustic trauma animals. These results suggest an alteration in functional connectivity between PFC and MGN after cochlear trauma. This change may be a compensatory mechanism increasing sensory gating after the development of altered spontaneous activity in MGN, to prevent altered activity reaching the cortex and conscious perception.


2021 ◽  
pp. 108165
Author(s):  
Carlos R. Benítez-Barrera ◽  
Alexandra P. Key ◽  
Todd Andrew Ricketts ◽  
Anne Marie Tharpe

Neuroscience ◽  
2010 ◽  
Vol 170 (4) ◽  
pp. 1270-1281 ◽  
Author(s):  
K. Charitidi ◽  
R.D. Frisina ◽  
O.N. Vasilyeva ◽  
X. Zhu ◽  
B. Canlon

Science ◽  
1983 ◽  
Vol 219 (4588) ◽  
pp. 1087-1089 ◽  
Author(s):  
G Rose ◽  
R. Capranica

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