There is growing evidence suggests that noise-induced cochlear damage may lead to hyperexcitability in the central auditory system(CAS)which may give rise to tinnitus.However,the correlation between the onset of the n...There is growing evidence suggests that noise-induced cochlear damage may lead to hyperexcitability in the central auditory system(CAS)which may give rise to tinnitus.However,the correlation between the onset of the neurophysiological changes in the CAS and the onset of tinnitus has not been well studied.To investigate this relationship,chronic electrodes were implanted into the auditory cortex(AC) and sound evoked activities were measured from awake rats before and after noise exposure.The auditory brainstem response(ABR) was used to assess the degree of noise-induced hearing loss.Tinnitus was evaluated by measuring gap-induced prepulse inhibition(gap-PPI).Rats were exposed monaurally to a high-intensity narrowband noise centered at 12 kHz at a level of 120 dB SPL for 1 h.After the noise exposure,all the rats developed either permanent(>2 weeks) or temporary(<3 days) hearing loss in the exposed ear(s).The AC amplitudes increased significantly 4 h after the noise exposure.Most of the exposed rats also showed decreased gap-PPI.The post-exposure AC enhancement showed a positive correlation with the amount of hearing loss.The onset of tinnitus-like behavior was happened after the onset of AC enhancement.展开更多
Tinnitus is a subjective perception of phantom sound that currently cannot be objectively measured. However, there is growing evidence suggesting that the biological source of tinnitus may exist in one or more than on...Tinnitus is a subjective perception of phantom sound that currently cannot be objectively measured. However, there is growing evidence suggesting that the biological source of tinnitus may exist in one or more than one place in the auditory pathway. Recent studies have found that neurotransmitters or modulators, such as glutamate, γ-aminobutyric acid(GABA), serotonin, dynorphin, dopamine, neurosteroid, acetylcholine(ACh) and substance P, are involved in tinnitus generation. Animal and human studies have shown that some of these neurotransmitters and the agonists or antagonists of their receptors either affect tinnitus behaviors or demonstrate some degree of treatment effects on tinnitus. However, due to the unclear biological mechanisms of tinnitus and side effects of these drugs, the value of clinical usage of such drugs in treating tinnitus is yet to be established. Revealing the relationship between tinnitus and neurotransmitter receptor functions will help identify more effective drugs for tinnitus treatment. This article reviews the literature of neurophysiological studies on tinnitus in both animal and human subject studies at various levels of the auditory pathway.展开更多
文摘There is growing evidence suggests that noise-induced cochlear damage may lead to hyperexcitability in the central auditory system(CAS)which may give rise to tinnitus.However,the correlation between the onset of the neurophysiological changes in the CAS and the onset of tinnitus has not been well studied.To investigate this relationship,chronic electrodes were implanted into the auditory cortex(AC) and sound evoked activities were measured from awake rats before and after noise exposure.The auditory brainstem response(ABR) was used to assess the degree of noise-induced hearing loss.Tinnitus was evaluated by measuring gap-induced prepulse inhibition(gap-PPI).Rats were exposed monaurally to a high-intensity narrowband noise centered at 12 kHz at a level of 120 dB SPL for 1 h.After the noise exposure,all the rats developed either permanent(>2 weeks) or temporary(<3 days) hearing loss in the exposed ear(s).The AC amplitudes increased significantly 4 h after the noise exposure.Most of the exposed rats also showed decreased gap-PPI.The post-exposure AC enhancement showed a positive correlation with the amount of hearing loss.The onset of tinnitus-like behavior was happened after the onset of AC enhancement.
文摘Tinnitus is a subjective perception of phantom sound that currently cannot be objectively measured. However, there is growing evidence suggesting that the biological source of tinnitus may exist in one or more than one place in the auditory pathway. Recent studies have found that neurotransmitters or modulators, such as glutamate, γ-aminobutyric acid(GABA), serotonin, dynorphin, dopamine, neurosteroid, acetylcholine(ACh) and substance P, are involved in tinnitus generation. Animal and human studies have shown that some of these neurotransmitters and the agonists or antagonists of their receptors either affect tinnitus behaviors or demonstrate some degree of treatment effects on tinnitus. However, due to the unclear biological mechanisms of tinnitus and side effects of these drugs, the value of clinical usage of such drugs in treating tinnitus is yet to be established. Revealing the relationship between tinnitus and neurotransmitter receptor functions will help identify more effective drugs for tinnitus treatment. This article reviews the literature of neurophysiological studies on tinnitus in both animal and human subject studies at various levels of the auditory pathway.
