Journal articles: 'Central auditory pathway'

1

Bizley, Jennifer K., and Yihan Dai. "Non-auditory processing in the central auditory pathway." Current Opinion in Physiology 18 (December 2020): 100–105. http://dx.doi.org/10.1016/j.cophys.2020.09.003.

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Izumi, Shuji. "Imaging of the Central Auditory Pathway." Japan Journal of Logopedics and Phoniatrics 53, no. 3 (2012): 183–86. http://dx.doi.org/10.5112/jjlp.53.183.

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Bamiou, Doris-Eva, David Werring, Karen Cox, John Stevens, Frank E. Musiek, Martin M. Brown, and Linda M. Luxon. "Patient-Reported Auditory Functions After Stroke of the Central Auditory Pathway." Stroke 43, no. 5 (May 2012): 1285–89. http://dx.doi.org/10.1161/strokeaha.111.644039.

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King, A. J. "The auditory midbrain: Structure and function in the central auditory pathway." Neuroscience 21, no. 3 (June 1987): 1025–26. http://dx.doi.org/10.1016/0306-4522(87)90061-3.

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Bruyn, G. W. "The auditory midbrain. Structure and function in the central auditory pathway." Journal of the Neurological Sciences 79, no. 1-2 (June 1987): 239–40. http://dx.doi.org/10.1016/0022-510x(87)90278-4.

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Matsubara, J. A. "The auditory midbrain, structure and function in the central auditory pathway." Neurochemistry International 10, no. 4 (January 1987): 596–97. http://dx.doi.org/10.1016/0197-0186(87)90094-5.

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Chang, Chia-Hao, Chia-Der Lin, and Ching-Liang Hsieh. "Electroacupuncture Promotes Neuroplasticity of Central Auditory Pathway: An Auditory Evoked Potentials Study." Evidence-Based Complementary and Alternative Medicine 2022 (November 21, 2022): 1–9. http://dx.doi.org/10.1155/2022/6855775.

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Our previous studies found that electroacupuncture at the right Zhongzhu acupoint (TE3) can enhance auditory recovery in rats with noise-induced hearing loss. Here, we investigated the changes in auditory brainstem response (ABR) and long late latency (LLR) evoked potential to explain the mechanisms of electroacupuncture at TE3. The auditory evoked potentials were recorded, including ABR and LLR, at baseline and on day 3 (D3), D5, and D8 after baseline. The 2-Hz electroacupuncture at the right TE3 was applied on D3, D4, and D5 in the electroacupuncture group but not in the control group. In ABR, compared with the control group, the latency shift of waves I (0.298 ± 0.033 vs −0.045 ± 0.057 ms), III (0.718 ± 0.038 vs −0.163 ± 0.130 ms), and V (1.160 ± 0.082 vs −0.207 ± 0.138 ms) on D3 (all p < 0.01 ) and of wave V (0.616 ± 0.433 vs −0.352 ± 0.209 ms, p < 0.05 ) on D5 was greater in the electroacupuncture group than that in the control group. Moreover, the interpeak latency shift of I–III (0.420 ± 0.041 vs −0.118 ± 0.177 ms) and I–V (0.863 ± 0.088 vs −0.162 ± 0.156 ms) on D3 (both p < 0.05 ) and of III–V (0.342 ± 0.193 vs −0.190 ± 0.110 ms) and I–V (0.540 ± 0.352 vs −0.343 ± 0.184 ms) on D5 (both p < 0.05 ) was greater in the electroacupuncture group than that in the control group. In LLR, the latency shift of P0 was greater in the electroacupuncture group than in the control group on D3 (3.956 ± 2.975 vs −1.178 ± 1.358 ms, p < 0.01 ) and D5 (2.200 ± 1.889 vs −0.311 ± 1.078 ms, p < 0.05 ). These findings indicate that electroacupuncture at the right TE3 can modulate the neuroplasticity of the central auditory pathway, including the brain stem and the primary and secondary auditory cortex.

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Pantelemon, Cristina, Violeta Necula, Livia Livint Popa, Steluta Palade, Stefan Strilciuc, and Dafin Fior Muresanu. "The Potential Use of P1 CAEP as a Biomarker for Assessing Central Auditory Pathway Maturation in Hearing loss and Associated Disabilities: a case report." Journal of Medicine and Life 12, no. 4 (October 2019): 457–60. http://dx.doi.org/10.25122/jml-2019-0096.

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We report a case in which we quantified the maturation of the central auditory pathway in children with hearing loss and associated disabilities; the audiological intervention was performed using the BAHA softband. The hearing aid was applied according to the international clinical protocols. The presented case reveals the importance of using the P1 CAEP biomarker in clinical practice along with a neuropsychological evaluation to assess the maturation of the central auditory pathways and to objectively quantify the results of auditory rehabilitation in children with hearing loss and associated disabilities.

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Juichi Ito, Miyahiko Murata, Saburo. "Regeneration of the Central Auditory Pathway in Adult Rats." Acta Oto-Laryngologica 119, no. 2 (January 1999): 132–34. http://dx.doi.org/10.1080/00016489950181512.

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Middleton, Michele L., Keith M. Wilson, and Robert W. Keith. "Central Auditory Evaluation of Patients with Spasmodic Dysphonia." Ear, Nose & Throat Journal 76, no. 10 (October 1997): 710–15. http://dx.doi.org/10.1177/014556139707601007.

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Spasmodic dysphonia is a focal laryngeal dystonia characterized by inappropriate contractions of the intrinsic laryngeal musculature. The prevalence of associated neurological findings has led to detailed investigation of the central nervous system. Previous research revealed latency abnormalities in patients’ auditory brainstem responses. The present study further investigated central auditory findings in patients with spasmodic dysphonia, including brainstem and cortical function. Fourteen normal-hearing patients with spasmodic dysphonia were tested using the auditory brainstem response (ABR) and SCAN-A test of central auditory processing. The ABR estimated brainstem transmission time and evaluated auditory pathway integrity at a high stimulus rate. SCAN-A assessed the auditory cerebral cortex. Implications of these findings are discussed. We found no ABR abnormalities in subjects with spasmodic dysphonia. Positive SCAN-A findings were negligible. The ABR findings contradict previous reports.

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Bulkin, David A., and Jennifer M. Groh. "Distribution of eye position information in the monkey inferior colliculus." Journal of Neurophysiology 107, no. 3 (February 2012): 785–95. http://dx.doi.org/10.1152/jn.00662.2011.

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The inferior colliculus (IC) is thought to have two main subdivisions, a central region that forms an important stop on the ascending auditory pathway and a surrounding shell region that may play a more modulatory role. In this study, we investigated whether eye position affects activity in both the central and shell regions. Accordingly, we mapped the location of eye position-sensitive neurons in six monkeys making spontaneous eye movements by sampling multiunit activity at regularly spaced intervals throughout the IC. We used a functional map based on auditory response patterns to estimate the anatomical location of recordings, in conjunction with structural MRI and histology. We found eye position-sensitive sites throughout the IC, including at 27% of sites in tonotopically organized recording penetrations (putatively the central nucleus). Recordings from surrounding tissue showed a larger proportion of sites indicating an influence of eye position (33–43%). When present, the magnitude of the change in activity due to eye position was often comparable to that seen for sound frequency. Our results indicate that the primary ascending auditory pathway is influenced by the position of the eyes. Because eye position is essential for visual-auditory integration, our findings suggest that computations underlying visual-auditory integration begin early in the ascending auditory pathway.

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Coordes, Annekatrin, Moritz Gröschel, Arne Ernst, and Dietmar Basta. "Apoptotic Cascades in the Central Auditory Pathway after Noise Exposure." Journal of Neurotrauma 29, no. 6 (April 10, 2012): 1249–54. http://dx.doi.org/10.1089/neu.2011.1769.

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Matas, Carla Gentile, Sandro Luiz de Andrade Matas, Caroline Rondina Salzano de Oliveira, and Isabela Crivellaro Gonçalves. "Auditory evoked potentials and multiple sclerosis." Arquivos de Neuro-Psiquiatria 68, no. 4 (August 2010): 528–34. http://dx.doi.org/10.1590/s0004-282x2010000400010.

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Multiple sclerosis (MS) is an inflammatory, demyelinating disease that can affect several areas of the central nervous system. Damage along the auditory pathway can alter its integrity significantly. Therefore, it is important to investigate the auditory pathway, from the brainstem to the cortex, in individuals with MS. OBJECTIVE: The aim of this study was to characterize auditory evoked potentials in adults with MS of the remittent-recurrent type. METHOD: The study comprised 25 individuals with MS, between 25 and 55 years, and 25 age- and gender-matched healthy controls (research and control groups). Subjects underwent audiological and electrophysiological evaluations. RESULTS: Statistically significant differences were observed between the groups regarding the results of the auditory brainstem response and the latency of the Na and P300 waves. CONCLUSION: Individuals with MS present abnormalities in auditory evoked potentials indicating dysfunction of different regions of the central auditory nervous system.

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Musiek, Frank, and Stephanie Nagle. "The Middle Latency Response: A Review of Findings in Various Central Nervous System Lesions." Journal of the American Academy of Audiology 29, no. 09 (October 2018): 855–67. http://dx.doi.org/10.3766/jaaa.16141.

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AbstractThe middle latency response (MLR) first came to light as an auditory evoked potential in 1958. Since then, it has aroused substantial interest and investigation by clinicians and researchers alike. In recent history, its use and popularity have dwindled in tandem with various other auditory evoked potentials in audiology. One area for which MLR research and application has been overlooked is its potential value in measuring the neural integrity of the auditory thalamocortical pathway. In a broader sense, the MLR, when combined with the auditory brain stem response, can provide information concerning the status of much of the central auditory system pathways. This review is intended to provide information concerning the MLR as a measure of central auditory function for the reader to consider.To review and synthesize the scientific literature regarding the potential value of the MLR in assessing the integrity of the central auditory system and to provide the reader an informed perspective on the value of the MLR in this regard. Information is also provided on the MLR generator sites and fundamental characteristics of this evoked potential essential to its clinical and or research application.A systematic review and synthesis of the literature focusing on the MLR and lesions of the central auditory system.Studies and individual cases were reviewed and analyzed that evidenced documented lesions of the central auditory nervous system.The authors searched and reviewed the literature (journal articles, book chapters, and books) pertaining to central auditory system lesion effects on the MLR.Although findings varied from study to study, overall, the MLR was reasonably sensitive and specific to neurological compromise of the central auditory system. This finding is consistent with the generator sites of this evoked potential.The MLR is a valuable tool for assessing the integrity of the central auditory system. It should be of interest to the clinician or researcher who focuses their attention on the function and dysfunction of the higher auditory system.

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Yao, Justin D., Peter Bremen, and John C. Middlebrooks. "Transformation of spatial sensitivity along the ascending auditory pathway." Journal of Neurophysiology 113, no. 9 (May 2015): 3098–111. http://dx.doi.org/10.1152/jn.01029.2014.

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Locations of sounds are computed in the central auditory pathway based primarily on differences in sound level and timing at the two ears. In rats, the results of that computation appear in the primary auditory cortex (A1) as exclusively contralateral hemifield spatial sensitivity, with strong responses to sounds contralateral to the recording site, sharp cutoffs across the midline, and weak, sound-level-tolerant responses to ipsilateral sounds. We surveyed the auditory pathway in anesthetized rats to identify the brain level(s) at which level-tolerant spatial sensitivity arises. Noise-burst stimuli were varied in horizontal sound location and in sound level. Neurons in the central nucleus of the inferior colliculus (ICc) displayed contralateral tuning at low sound levels, but tuning was degraded at successively higher sound levels. In contrast, neurons in the nucleus of the brachium of the inferior colliculus (BIN) showed sharp, level-tolerant spatial sensitivity. The ventral division of the medial geniculate body (MGBv) contained two discrete neural populations, one showing broad sensitivity like the ICc and one showing sharp sensitivity like A1. Dorsal, medial, and shell regions of the MGB showed fairly sharp spatial sensitivity, likely reflecting inputs from A1 and/or the BIN. The results demonstrate two parallel brainstem pathways for spatial hearing. The tectal pathway, in which sharp, level-tolerant spatial sensitivity arises between ICc and BIN, projects to the superior colliculus and could support reflexive orientation to sounds. The lemniscal pathway, in which such sensitivity arises between ICc and the MGBv, projects to the forebrain to support perception of sound location.

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Vonderschen, Katrin, and Hermann Wagner. "Tuning to Interaural Time Difference and Frequency Differs Between the Auditory Arcopallium and the External Nucleus of the Inferior Colliculus." Journal of Neurophysiology 101, no. 5 (May 2009): 2348–61. http://dx.doi.org/10.1152/jn.91196.2008.

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Barn owls process sound-localization information in two parallel pathways, the midbrain and the forebrain pathway. Exctracellular recordings of neural responses to auditory stimuli from far advanced stations of these pathways, the auditory arcopallium in the forebrain and the external nucleus of the inferior colliculus in the midbrain, demonstrated that the representations of interaural time difference and frequency in the forebrain pathway differ from those in the midbrain pathway. Specifically, low-frequency representation was conserved in the forebrain pathway, while it was lost in the midbrain pathway. Variation of interaural time difference yielded symmetrical tuning curves in the midbrain pathway. By contrast, the typical forebrain-tuning curve was asymmetric with a steep slope crossing zero time difference and a less-steep slope toward larger contralateral time disparities. Low sound frequencies contributed sensitivity to contralateral leading sounds underlying these asymmetries, whereas high frequencies enhanced the steepness of slopes at small interaural time differences. Furthermore, the peaks of time-disparity tuning curves were wider in the forebrain than in the midbrain. The distribution of the steepest slopes of best interaural time differences in the auditory arcopallium, but not in the external nucleus of the inferior colliculus, was centered at zero time difference. The distribution observed in the auditory arocpallium is reminiscent of the situation observed in small mammals. We speculate that the forebrain representation may serve as a population code supporting fine discrimination of central interaural time differences and coarse indication of laterality of a stimulus for large interaural time differences.

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Weber, H., K. Pfadenhauer, M. Stöhr, and A. Rösler. "Central hyperacusis with phonophobia in multiple sclerosis." Multiple Sclerosis Journal 8, no. 6 (December 2002): 505–9. http://dx.doi.org/10.1191/1352458502ms814oa.

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Hearing disorders are a well-described symptom in patients with multiple sclerosis (MS). Unilateral or bilateral hyperacusis or deafness in patients with normal sound audiometry is often attributed to demyelinating lesions in the central auditory pathway. Less known in MS is a central phonophobia, whereby acoustic stimuli provoke unpleasant and painful paresthesia and lead to the corresponding avoidance behaviour. In our comparison collective, patient 1 described acute shooting pain attacks in his right cheek, each time set off by the ringing of the telephone. Patient 2 complained of intensified, unbearable noise sensations when hearing nonlanguage acoustic stimuli. Patient 3 noticed hearing unpleasant echoes and disorders of the directional hearing. All patients had a clinical brainstem syndrome. ENT inspection, sound audiometry and stapedius reflex were normal. All three patients had pathologically changed auditory evoked potentials (AEPs) with indications of a brainstem lesion, and in magnetic resonance imaging (MRI) demyelinating lesions in the ipsilateral pons and in the central auditory pathway. The origin we presume in case 1 is an abnormal impulse conduction from the leminiscus lateralis to the central trigeminus pathway and, in the other cases, a disturbance in the central sensory modulation. All patients developed in the further course a clinically definite MS. Having excluded peripheral causes for a hyperacusis, such as, e.g., an idiopathic facial nerve palsy or myasthenia gravis, one should always consider the possibility of MS in a case of central phonophobia. Therapeutic possibilities include the giving of serotonin reuptake inhibitors or acoustic lenses for clearly definable disturbing frequencies.

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Leong, Alex T. L., Yong Gu, Ying-Shing Chan, Hairong Zheng, Celia M. Dong, Russell W. Chan, Xunda Wang, Yilong Liu, Li Hai Tan, and Ed X. Wu. "Optogenetic fMRI interrogation of brain-wide central vestibular pathways." Proceedings of the National Academy of Sciences 116, no. 20 (April 26, 2019): 10122–29. http://dx.doi.org/10.1073/pnas.1812453116.

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Blood oxygen level-dependent functional MRI (fMRI) constitutes a powerful neuroimaging technology to map brain-wide functions in response to specific sensory or cognitive tasks. However, fMRI mapping of the vestibular system, which is pivotal for our sense of balance, poses significant challenges. Physical constraints limit a subject’s ability to perform motion- and balance-related tasks inside the scanner, and current stimulation techniques within the scanner are nonspecific to delineate complex vestibular nucleus (VN) pathways. Using fMRI, we examined brain-wide neural activity patterns elicited by optogenetically stimulating excitatory neurons of a major vestibular nucleus, the ipsilateral medial VN (MVN). We demonstrated robust optogenetically evoked fMRI activations bilaterally at sensorimotor cortices and their associated thalamic nuclei (auditory, visual, somatosensory, and motor), high-order cortices (cingulate, retrosplenial, temporal association, and parietal), and hippocampal formations (dentate gyrus, entorhinal cortex, and subiculum). We then examined the modulatory effects of the vestibular system on sensory processing using auditory and visual stimulation in combination with optogenetic excitation of the MVN. We found enhanced responses to sound in the auditory cortex, thalamus, and inferior colliculus ipsilateral to the stimulated MVN. In the visual pathway, we observed enhanced responses to visual stimuli in the ipsilateral visual cortex, thalamus, and contralateral superior colliculus. Taken together, our imaging findings reveal multiple brain-wide central vestibular pathways. We demonstrate large-scale modulatory effects of the vestibular system on sensory processing.

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Gómez, Joaquín Guerra, and Jesús Devesa. "Growth Hormone and the Auditory Pathway: Neuromodulation and Neuroregeneration." International Journal of Molecular Sciences 22, no. 6 (March 11, 2021): 2829. http://dx.doi.org/10.3390/ijms22062829.

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Growth hormone (GH) plays an important role in auditory development during the embryonic stage. Exogenous agents such as sound, noise, drugs or trauma, can induce the release of this hormone to perform a protective function and stimulate other mediators that protect the auditory pathway. In addition, GH deficiency conditions hearing loss or central auditory processing disorders. There are promising animal studies that reflect a possible regenerative role when exogenous GH is used in hearing impairments, demonstrated in in vivo and in vitro studies, and also, even a few studies show beneficial effects in humans presented and substantiated in the main text, although they should not exaggerate the main conclusions.

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Yang, Frank F., Bradley McPherson, Huang Shu, Na Xie, and Kui Xiang. "Structural Abnormalities of the Central Auditory Pathway in Infants with Nonsyndromic Cleft Lip and/or Palate." Cleft Palate-Craniofacial Journal 49, no. 2 (March 2012): 137–45. http://dx.doi.org/10.1597/11-014.

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Objective To investigate possible structural abnormalities of the central auditory pathway in infants with nonsyndromic cleft lip and/or palate (NSCL/P). Participants Twenty-seven Chinese infants with NSCL/P, aged from 6 to 24 months. Intervention Morphological magnetic resonance imaging (MRI) measurements of the central auditory nervous system (CANS) in infants with NSCL/P were analyzed and compared with those of age- and sex-matched normal controls. Results No significant group differences were found in general brain measurements, including volumes of the brain stem and right hemisphere. However, infants with NSCL/P had statistically significantly smaller volumes of the left thalamus and left auditory cortex and notably decreased thickness of the left auditory cortex. Conclusion Cortical abnormalities were more marked compared with other MRI measurements. Structural CANS abnormalities in infants with NSCL/P may be located mainly in the left cerebral hemisphere. The development and maturation of the auditory cortex in infants with NSCL/P may be abnormal when compared with those of normal children.

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Ota, Y., D. L. Oliver, and D. F. Dolan. "Frequency-Specific Effects on Cochlear Responses During Activation of the Inferior Colliculus in the Guinea Pig." Journal of Neurophysiology 91, no. 5 (May 2004): 2185–93. http://dx.doi.org/10.1152/jn.01155.2003.

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The inferior colliculus (IC) is a major processing center in the ascending auditory pathway. The role of the IC in the descending efferent auditory system is less clear. Although the IC central nucleus (ICC) is the major relay station for the ascending auditory pathways, the IC's cortex receives its main input from the neocortex and nonauditory sources. The goal of this study was to determine if the IC subdivisions had different functions in the descending efferent auditory system. IC subdivisions were identified by their tuning curves evoked by tone stimulation, and the effects of localized electrical stimulation on the cochlear whole-nerve action potential (CAP). Sharp tuning curves were obtained from ICC in contrast to broad tuning curves from the lateral, external cortex. Electrical stimulation within the central nucleus had a sharply tuned effect on the CAP. The frequency region affected within the cochlea closely matched the best frequency of local cells within the central nucleus. The effect of electrical stimulation within the lateral, external cortex on the CAP was smaller in comparison to central nucleus stimulation. Similar to the broad tuning of cells within the lateral cortex, electrical stimulation had a broad frequency effect on CAP thresholds.

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Sinnathuray, A. R., D. R. Watson, B. Fruhstorfer, J. R. Olarte, and J. G. Toner. "Cochlear Implantation in Brown–Vialetto–Van-Laere syndrome." Journal of Laryngology & Otology 125, no. 3 (October 19, 2010): 314–17. http://dx.doi.org/10.1017/s0022215110001982.

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AbstractObjective:To report outcomes for the first known cochlear implantation procedures in two patients with Brown–Vialetto–Van-Laere syndrome.Patients:Two adult patients (a brother and sister) with post-lingual sensorineural deafness associated with Brown–Vialetto–Van-Laere syndrome. The female patient presented with a milder form of the syndrome.Intervention:Cochlear implantation.Main outcome measure:Post-implantation speech discrimination scores.Results:Auditory evoked potential testing suggested pathological changes in both patients' cochleae, auditory nerves, brainstem and (probably) central auditory pathways. In the male patient, despite implantation of the better ear, the Bamford–Kowal–Bench sentence score was zero at 21 months post-implantation. In the female patient, Bamford–Kowal–Bench sentence scores at six months post-implantation were 25 per cent in quiet and 3 per cent in noise.Conclusion:These poor clinical outcomes appear to be related to retrocochlear and probable central auditory pathway degeneration.

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Laszig, Roland, Nicolas Marangos, Wolf-Peter Sollmann, and Richard T. Ramsden. "Central Electrical Stimulation of the Auditory Pathway in Neurofibromatosis Type 2." Ear, Nose & Throat Journal 78, no. 2 (February 1999): 110–17. http://dx.doi.org/10.1177/014556139907800210.

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Thompson, Mary Ellen, and Sharon M. Abel. "Frequency and duration discrimination by patients with central auditory pathway lesions." Journal of the Acoustical Society of America 85, S1 (May 1989): S34. http://dx.doi.org/10.1121/1.2026921.

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Park, Sohyeon, Seung Hee Han, Byeong-Gon Kim, Myung-Whan Suh, Jun Ho Lee, Seung Ha Oh, and Moo Kyun Park. "Changes in microRNA Expression in the Cochlear Nucleus and Inferior Colliculus after Acute Noise-Induced Hearing Loss." International Journal of Molecular Sciences 21, no. 22 (November 20, 2020): 8792. http://dx.doi.org/10.3390/ijms21228792.

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Noise-induced hearing loss (NIHL) can lead to secondary changes that induce neural plasticity in the central auditory pathway. These changes include decreases in the number of synapses, the degeneration of auditory nerve fibers, and reorganization of the cochlear nucleus (CN) and inferior colliculus (IC) in the brain. This study investigated the role of microRNAs (miRNAs) in the neural plasticity of the central auditory pathway after acute NIHL. Male Sprague–Dawley rats were exposed to white band noise at 115 dB for 2 h, and the auditory brainstem response (ABR) and morphology of the organ of Corti were evaluated on days 1 and 3. Following noise exposure, the ABR threshold shift was significantly smaller in the day 3 group, while wave II amplitudes were significantly larger in the day 3 group compared to the day 1 group. The organ of Corti on the basal turn showed evidence of damage and the number of surviving outer hair cells was significantly lower in the basal and middle turn areas of the hearing loss groups relative to controls. Five and three candidate miRNAs for each CN and IC were selected based on microarray analysis and quantitative reverse transcription PCR (RT-qPCR). The data confirmed that even short-term acoustic stimulation can lead to changes in neuroplasticity. Further studies are needed to validate the role of these candidate miRNAs. Such miRNAs may be used in the early diagnosis and treatment of neural plasticity of the central auditory pathway after acute NIHL.

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van Zwieten, Gusta, Ali Jahanshahi, Marlieke L. van Erp, Yasin Temel, Robert J. Stokroos, Marcus L. F. Janssen, and Jasper V. Smit. "Alleviation of Tinnitus With High-Frequency Stimulation of the Dorsal Cochlear Nucleus: A Rodent Study." Trends in Hearing 23 (January 2019): 233121651983508. http://dx.doi.org/10.1177/2331216519835080.

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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.

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Profant, O., A. Škoch, Z. Balogová, J. Tintěra, J. Hlinka, and J. Syka. "Diffusion tensor imaging and MR morphometry of the central auditory pathway and auditory cortex in aging." Neuroscience 260 (February 2014): 87–97. http://dx.doi.org/10.1016/j.neuroscience.2013.12.010.

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Rahman, Monzilur, Ben D. B. Willmore, Andrew J. King, and Nicol S. Harper. "Simple transformations capture auditory input to cortex." Proceedings of the National Academy of Sciences 117, no. 45 (October 23, 2020): 28442–51. http://dx.doi.org/10.1073/pnas.1922033117.

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Sounds are processed by the ear and central auditory pathway. These processing steps are biologically complex, and many aspects of the transformation from sound waveforms to cortical response remain unclear. To understand this transformation, we combined models of the auditory periphery with various encoding models to predict auditory cortical responses to natural sounds. The cochlear models ranged from detailed biophysical simulations of the cochlea and auditory nerve to simple spectrogram-like approximations of the information processing in these structures. For three different stimulus sets, we tested the capacity of these models to predict the time course of single-unit neural responses recorded in ferret primary auditory cortex. We found that simple models based on a log-spaced spectrogram with approximately logarithmic compression perform similarly to the best-performing biophysically detailed models of the auditory periphery, and more consistently well over diverse natural and synthetic sounds. Furthermore, we demonstrated that including approximations of the three categories of auditory nerve fiber in these simple models can substantially improve prediction, particularly when combined with a network encoding model. Our findings imply that the properties of the auditory periphery and central pathway may together result in a simpler than expected functional transformation from ear to cortex. Thus, much of the detailed biological complexity seen in the auditory periphery does not appear to be important for understanding the cortical representation of sound.

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Moore, Jean K., John K. Niparko, Michele R. Miller, Lucy M. Perazzo, and Fred H. Linthicum. "Effect of Adult-Onset Deafness on the Human Central Auditory System." Annals of Otology, Rhinology & Laryngology 106, no. 5 (May 1997): 385–90. http://dx.doi.org/10.1177/000348949710600505.

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Degenerative change in the central auditory system was assessed in seven subjects with profound bilateral adult-onset deafness. The degree of transneuronal atrophy was determined by measuring cell size at three levels of the brain stem auditory pathway (anteroventral cochlear nucleus, medial superior olivary nucleus, and inferior colliculus). Within subjects, the relative degree of cell shrinkage was similar across all levels of the central pathway. Across subjects, the best neuronal preservation was seen in a case of viral labyrinthitis with 1 year of bilateral deafness and a near-normal population of cochlear ganglion cells. Reduction in cell size was greatest in cases of bacterial labyrinthitis or Scheibe degeneration with reduced populations of ganglion cells and longer periods of deafness. At the level of the cochlear nucleus, there was no consistent difference in cell size between the side stimulated by a functioning prosthetic device and the nonstimulated side.

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Huang, Qiuhong, Yongkang Ou, Hao Xiong, Haidi Yang, Zhigang Zhang, Suijun Chen, Yongyi Ye, and Yiqing Zheng. "The miR-34a/Bcl-2 Pathway Contributes to Auditory Cortex Neuron Apoptosis in Age-Related Hearing Loss." Audiology and Neurotology 22, no. 2 (2017): 96–103. http://dx.doi.org/10.1159/000454874.

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Hypothesis: The miR-34a/Bcl-2 signaling pathway may play a role in the mechanisms related to age-related hearing loss (AHL) in the auditory cortex. Background: The auditory cortex plays a key role in the recognition and processing of complex sound. It is difficult to explain why patients with AHL have poor speech recognition, so increasing numbers of studies have focused on its central change. Although micro (mi)RNAs in the central nervous system have recently been increasingly reported to be associated with age-related diseases, the molecular mechanisms of AHL in the auditory cortex are not fully understood. Methods: The auditory brainstem response was used to assess the hearing ability of C57BL/6 mice, and q-PCR, immunohistochemistry, and Western blotting were used to detect the expression levels of miR-34a and Bcl-2 in the mouse auditory cortex. TUNEL and DNA fragmentation were adopted to detect the apoptosis of neurons in the auditory cortex. To verify the relationship of miR-34a and Bcl-2, we transfected an miR-34a mimic or miR-34a inhibitor into primary auditory cortex neurons. Results: In this study, miR-34a/Bcl-2 signaling was examined in auditory cortex neurons during aging. miR-34a and apoptosis increased in the auditory cortex neurons of C57BL/6 mice with aging, whereas an age-related decrease in Bcl-2 was determined. In the primary neurons of the auditory cortex, miR-34a overexpression inhibited Bcl-2, leading to an increase in apoptosis. Moreover, miR-34a knockdown increased Bcl-2 expression and diminished apoptosis. Conclusion: Our results support a link between age-related apoptosis in auditory cortex neurons and miR-34a/Bcl-2 signaling, which may serve as a potential mechanism of the expression of AHL in the auditory cortex.

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Cohen, Yale E., Greg L. Miller, and Eric I. Knudsen. "Forebrain Pathway for Auditory Space Processing in the Barn Owl." Journal of Neurophysiology 79, no. 2 (February 1, 1998): 891–902. http://dx.doi.org/10.1152/jn.1998.79.2.891.

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Cohen, Yale E., Greg L. Miller, and Eric I. Knudsen. Forebrain pathway for auditory space processing in the barn owl. J. Neurophysiol. 79: 891–902, 1998. The forebrain plays an important role in many aspects of sound localization behavior. Yet, the forebrain pathway that processes auditory spatial information is not known for any species. Using standard anatomic labeling techniques, we used a “top-down” approach to trace the flow of auditory spatial information from an output area of the forebrain sound localization pathway (the auditory archistriatum, AAr), back through the forebrain, and into the auditory midbrain. Previous work has demonstrated that AAr units are specialized for auditory space processing. The results presented here show that the AAr receives afferent input from Field L both directly and indirectly via the caudolateral neostriatum. Afferent input to Field L originates mainly in the auditory thalamus, nucleus ovoidalis, which, in turn, receives input from the central nucleus of the inferior colliculus. In addition, we confirmed previously reported projections of the AAr to the basal ganglia, the external nucleus of the inferior colliculus (ICX), the deep layers of the optic tectum, and various brain stem nuclei. A series of inactivation experiments demonstrated that the sharp tuning of AAr sites for binaural spatial cues depends on Field L input but not on input from the auditory space map in the midbrain ICX: pharmacological inactivation of Field L eliminated completelyauditory responses in the AAr, whereas bilateral ablation of the midbrain ICX had no appreciable effect on AAr responses. We conclude, therefore, that the forebrain sound localization pathway can process auditory spatial information independently of the midbrain localization pathway.

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Bina, Alireza. "The link between Brain and Hearing system." Journal of Otolaryngology-ENT Research 12, no. 4 (2020): 114–17. http://dx.doi.org/10.15406/joentr.2020.12.00467.

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There are some studies which confirmed that dysfunction in Central Nervous System(CNS) may cause a malfunction in the Peripheral Auditory system (Cochlea_ Auditory Nerve, Auditory Neuropathy), but the question is could Brain Disorder without any lesion in the Cochlea and/or Auditory nerve cause Sensorineural Hearing Loss? It means that the Audiogram shows that the patient suffers from sensorineural hearing loss but the site of the lesion is neither Sensory nor Neural while Brain may be involved in charge of this. And if the answer is yes then could we hear with our Brain and without Cochlea and /or Auditory nerve? We deal with this subject in this paper by: Otosclerosis and Meniere’s disease and The Brain Involvement. Hearing Loss following dysfunction in the Central Auditory and/or central non auditory system. Auditory Brainstem Implant in Patients who suffer from Neurofibromatosis Type two compare to Non Tumor cases, Mondini Syndrome, Michel aplasia. Possible role of Utricle and Saccule in Auditory (Hearing) System We propose a new Hypothesis that the External Ear Canal is not the only input of Auditory Signals, Sounds could transfer by our eyes and skin to the Cerebral Cortex and approach to the Cochlea (Backward Auditory input pathway of Sounds).

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Dougherty, Kelsey, Alexandra Hustedt-Mai, Anna Hagedorn, and Hari Bharadwaj. "Central gain in aging, tinnitus, and temporary hearing loss." Journal of the Acoustical Society of America 150, no. 4 (October 2021): A341. http://dx.doi.org/10.1121/10.0008520.

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The nervous system adapts in many ways to changes in the statistics of the inputs it receives. An example of such plasticity observed in animal models is that central auditory neurons tend to retain their driven firing rate outputs despite reductions in cochlear input due to hearing loss or deafferentation. The perceptual consequences of such “central gain” are unknown; pathological versions of such gain are often hypothesized to underlie tinnitus and hyperacusis. To investigate central gain in humans, we designed an electroencephalogram (EEG)-based paradigm that concurrently elicits robust separable responses from different levels of the auditory pathway. Using this measure, we find that cortical responses are relatively invariant despite a large monotonic decrease in auditory nerve responses with age, and that this central gain is also associated with perceptual deficits in co-modulation processing. We then applied the same measures to a cohort of individuals with persistent tinnitus and to a third cohort where a week-long monaural conductive hearing loss was induced using silicone earplugs. Overall, our results suggest that central gain is ubiquitous in response to reduced peripheral input and may affect auditory scene analysis, but does not in itself account for tinnitus perception.

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ITO, TOSHIKAZU. "Studies on the regeneration of central auditory pathway of the adult rat." AUDIOLOGY JAPAN 40, no. 5 (1997): 645–46. http://dx.doi.org/10.4295/audiology.40.645.

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Carney, Laurel H., and Miriam Furst. "Extending signal detection theory approaches up the central pathway: Auditory midbrain models." Journal of the Acoustical Society of America 145, no. 3 (March 2019): 1685. http://dx.doi.org/10.1121/1.5101176.

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Garcia-Lazaro, Jose A., Bashir Ahmed, and Jan W. H. Schnupp. "Emergence of Tuning to Natural Stimulus Statistics along the Central Auditory Pathway." PLoS ONE 6, no. 8 (August 5, 2011): e22584. http://dx.doi.org/10.1371/journal.pone.0022584.

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Gröschel, Moritz, Nikolai Hubert, Susanne Müller, Arne Ernst, and Dietmar Basta. "Age-dependent changes of calcium related activity in the central auditory pathway." Experimental Gerontology 58 (October 2014): 235–43. http://dx.doi.org/10.1016/j.exger.2014.08.014.

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Reser, David H., and Thomas R. Van De Water. "Implications of Neurotrophin Supported Auditory Neuron Survival for Maintenance of the Tonotopic Organization of the Central Auditory Pathway." Acta Oto-Laryngologica 117, no. 2 (January 1997): 239–43. http://dx.doi.org/10.3109/00016489709117779.

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Koya, Goyo, and Fumiaki Mori. "Auditory Brainstem Response and Fos Immunoreactivity in Central Auditory Pathway in an Acquired Audiogenic Seizure Model in Rats." Journal of the Japan Epilepsy Society 12, no. 3 (1994): 255–63. http://dx.doi.org/10.3805/jjes.12.255.

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Draper, T. H. J., and D.-E. Bamiou. "Auditory neuropathy in a patient exposed to xylene: case report." Journal of Laryngology & Otology 123, no. 4 (April 28, 2008): 462–65. http://dx.doi.org/10.1017/s0022215108002399.

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AbstractObjective:To report the case of an adult patient who developed auditory complaints following xylene exposure, and to review the literature on the effects of solvent exposure on hearing.Case report:The patient presented with a gradual deterioration in his ability to hear in difficult acoustic environments and also to hear complex sounds such as music, over a 40-year period. His symptoms began following exposure to the solvent xylene, and in the absence of any other risk factor. Our audiological investigations revealed normal otoacoustic emissions with absent auditory brainstem responses and absent acoustic reflexes in both ears, consistent with a diagnosis of bilateral auditory neuropathy. Central test results were also abnormal, indicating possible involvement of the central auditory pathway.Conclusions:To our knowledge, this is the first report of retrocochlear hearing loss following xylene exposure. The test results may provide some insight into the effect of xylene as an isolated agent on the human auditory pathway.

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Nölle, Corinna, Ingo Todt, Rainer O. Seidl, and Arne Ernst. "Pathophysiological Changes of the Central Auditory Pathway after Blunt Trauma of the Head." Journal of Neurotrauma 21, no. 3 (March 2004): 251–58. http://dx.doi.org/10.1089/089771504322972040.

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Ranasinghe, K. G., W. A. Vrana, C. J. Matney, and M. P. Kilgard. "Increasing diversity of neural responses to speech sounds across the central auditory pathway." Neuroscience 252 (November 2013): 80–97. http://dx.doi.org/10.1016/j.neuroscience.2013.08.005.

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Poulet, J. F. A., and B. Hedwig. "A Corollary Discharge Mechanism Modulates Central Auditory Processing in Singing Crickets." Journal of Neurophysiology 89, no. 3 (March 1, 2003): 1528–40. http://dx.doi.org/10.1152/jn.0846.2002.

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Crickets communicate using loud (100 dB SPL) sound signals that could adversely affect their own auditory system. To examine how they cope with this self-generated acoustic stimulation, intracellular recordings were made from auditory afferent neurons and an identified auditory interneuron—the Omega 1 neuron (ON1)—during pharmacologically elicited singing (stridulation). During sonorous stridulation, the auditory afferents and ON1 responded with bursts of spikes to the crickets' own song. When the crickets were stridulating silently, after one wing had been removed, only a few spikes were recorded in the afferents and ON1. Primary afferent depolarizations (PADs) occurred in the terminals of the auditory afferents, and inhibitory postsynaptic potentials (IPSPs) were apparent in ON1. The PADs and IPSPs were composed of many summed, small-amplitude potentials that occurred at a rate of about 230 Hz. The PADs and the IPSPs started during the closing wing movement and peaked in amplitude during the subsequent opening wing movement. As a consequence, during silent stridulation, ON1's response to acoustic stimuli was maximally inhibited during wing opening. Inhibition coincides with the time when ON1 would otherwise be most strongly excited by self-generated sounds in a sonorously stridulating cricket. The PADs and the IPSPs persisted in fictively stridulating crickets whose ventral nerve cord had been isolated from muscles and sense organs. This strongly suggests that the inhibition of the auditory pathway is the result of a corollary discharge from the stridulation motor network. The central inhibition was mimicked by hyperpolarizing current injection into ON1 while it was responding to a 100 dB SPL sound pulse. This suppressed its spiking response to the acoustic stimulus and maintained its response to subsequent, quieter stimuli. The corollary discharge therefore prevents auditory desensitization in stridulating crickets and allows the animals to respond to external acoustic signals during the production of calling song.

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Tahaei, Ali Akbar, Hassan Ashayeri, Akram Pourbakht, and Mohammad Kamali. "Speech Evoked Auditory Brainstem Response in Stuttering." Scientifica 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/328646.

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Auditory processing deficits have been hypothesized as an underlying mechanism for stuttering. Previous studies have demonstrated abnormal responses in subjects with persistent developmental stuttering (PDS) at the higher level of the central auditory system using speech stimuli. Recently, the potential usefulness of speech evoked auditory brainstem responses in central auditory processing disorders has been emphasized. The current study used the speech evoked ABR to investigate the hypothesis that subjects with PDS have specific auditory perceptual dysfunction.Objectives. To determine whether brainstem responses to speech stimuli differ between PDS subjects and normal fluent speakers.Methods. Twenty-five subjects with PDS participated in this study. The speech-ABRs were elicited by the 5-formant synthesized syllable/da/, with duration of 40 ms.Results. There were significant group differences for the onset and offset transient peaks. Subjects with PDS had longer latencies for the onset and offset peaks relative to the control group.Conclusions. Subjects with PDS showed a deficient neural timing in the early stages of the auditory pathway consistent with temporal processing deficits and their abnormal timing may underlie to their disfluency.

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Berding, Georg, and Thomas Lenarz. "Imaging in hearing using radiotracers." Current Directions in Biomedical Engineering 3, no. 2 (September 7, 2017): 187–90. http://dx.doi.org/10.1515/cdbme-2017-0039.

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AbstractRadiotracers offer unique options for brain imaging of functional and molecular processes related to hearing. Such imaging can be applied in a broad spectrum of situations from preclinical research to clinical patient care. Functional imaging to assess activation in brain regions and networks involved in auditory processing uses markers of blood flow or energy-metabolism in well-defined conditions with and without auditory stimulation. Molecular markers can be used in hearing research for example to study changes in inhibitory neurotransmission systems related to hearing loss. For imaging either positron emission tomography (PET) or single-photon emission computed tomography (SPECT) are employed. Data analysis can encompasses voxel-wise statistical analysis of activation and calculation of quantitative parameters like receptor binding-potentials based on bio-kinetic modeling. Functional imaging has been frequently used in the context of auditory implantation. Before implantation it aims to assess intactness of the central auditory pathway and prognosis. After implantation it is used to improve understanding of the outcome with respect to auditory function and finally speech understanding, e.g. by measuring correlates of central auditory processing and neuroplasticity.

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Samelli, Alessandra Giannella, Carla Gentile Matas, Camila Maia Rabelo, Fernanda Cristina Leite Magliaro, Natália Paião Luiz, and Lidiane Dias Silva. "Peripheral and central auditory assessment in among the elderly." Revista Brasileira de Geriatria e Gerontologia 19, no. 5 (October 2016): 839–49. http://dx.doi.org/10.1590/1809-98232016019.150226.

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Abstract Introduction: Presbycusis can affect different portions of the auditory system, causing impacts of varying degrees of seriousness on the daily routine of elderly persons. It is essential that the extent of the deficit as well as the degree of handicap is evaluated, so that the hearing of the elderly can be effectively rehabilitated, improving their quality of life. Purpose: To characterize the peripheral and central hearing of elderly individuals and assess their auditory handicaps. Methods: A cross sectional observational study was performed. We evaluated 83 elderly persons (60-85 years; 33 men, 50 women) with normal hearing or sensorineural hearing loss. Individuals were divided into 3 groups according to the 3 to 6kHz hearing thresholds: G1 - mean of 0 to 39 dBHL (80 ears); G2 - mean of 40 to 59 dBHL (48 ears); G3 - mean of 60 to 120dBHL (38 ears). All individuals responded to the Hearing Handicap Inventory for the Elderly (HHIE), and underwent Pure Tone Audiometry, Auditory Brainstem Response (ABR) and Long Latency Response (P300) evaluation. Results: Men had higher auditory thresholds at frequencies from 500 to 12,000Hz (with a statistical difference between 2-8 kHz) and also significantly greater latencies for ABR components. There was no difference between genders for the P300 evaluation. Comparison between groups showed: a statistically significant difference for age; greater ABR wave latencies and interwave intervals; that questionnaire scores worsened as hearing threshold declined; and similar P300 latencies. Conclusions: Elderly people have impairment throughout the auditory pathway (peripheral and central). The P300 was less accurate at identifying the losses that come with age. The HHIE demonstrated negative effects on the social life of elderly people, agreeing with the hearing thresholds found.

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Shi, Lin, Katie Palmer, Haolin Wang, Matthew A. Xu-Friedman, and Wei Sun. "Low Intensity Noise Exposure Enhanced Auditory Loudness and Temporal Processing by Increasing Excitability of DCN." Neural Plasticity 2022 (November 21, 2022): 1–11. http://dx.doi.org/10.1155/2022/6463355.

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Sound stimulation is generally used for tinnitus and hyperacusis treatment. Recent studies found that long-term noise exposure can change synaptic and firing properties in the central auditory system, which will be detected by the acoustic startle reflex. However, the perceptual consequences of long-term low-intensity sound exposure are indistinct. This study will detect the effects of moderate-level noise exposure (83 dB SPL) on auditory loudness, and temporal processing was evaluated using CBA/CaJ mice. C-Fos staining was used to detect neural activity changes in the central auditory pathway. With two weeks of 83 dB SPL noise exposure (8 hours per day), no persistent threshold shift of the auditory brainstem response (ABR) was identified. On the other hand, noise exposure enhanced the acoustic startle response (ASR) and gap-induced prepulse inhibition significantly (gap-PPI). Low-level noise exposure, according to the findings, can alter temporal acuity. Noise exposure increased the number of c-Fos labeled neurons in the dorsal cochlear nucleus (DCN) and caudal pontine reticular nucleus (PnC) but not at a higher level in the central auditory nuclei. Our results suggested that noise stimulation can change acoustical temporal processing presumably by increasing the excitability of auditory brainstem neurons.

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Silva, Gracinda, Rita Gonçalves, Isabel Taveira, Maria Mouzinho, Rui Osório, and Hipólito Nzwalo. "Stroke-Associated Cortical Deafness: A Systematic Review of Clinical and Radiological Characteristics." Brain Sciences 11, no. 11 (October 22, 2021): 1383. http://dx.doi.org/10.3390/brainsci11111383.

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Background: Stroke is the leading cause of cortical deafness (CD), the most severe form of central hearing impairment. CD remains poorly characterized and perhaps underdiagnosed. We perform a systematic review to describe the clinical and radiological features of stroke-associated CD. Methods: PubMed and the Web of Science databases were used to identify relevant publications up to 30 June 2021 using the MeSH terms: “deafness” and “stroke”, or “hearing loss” and “stroke” or “auditory agnosia” and “stroke”. Results: We found 46 cases, caused by bilateral lesions within the central auditory pathway, mostly located within or surrounding the superior temporal lobe gyri and/or the Heschl’s gyri (30/81%). In five (13.51%) patients, CD was caused by the subcortical hemispheric and in two (0.05%) in brainstem lesions. Sensorineural hearing loss was universal. Occasionally, a misdiagnosis by peripheral or psychiatric disorders occurred. A few (20%) had clinical improvement, with a regained oral conversation or evolution to pure word deafness (36.6%). A persistent inability of oral communication occurred in 43.3%. A full recovery of conversation was restricted to patients with subcortical lesions. Conclusions: Stroke-associated CD is rare, severe and results from combinations of cortical and subcortical lesions within the central auditory pathway. The recovery of functional hearing occurs, essentially, when caused by subcortical lesions.

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Ogg, Mattson, Thomas A. Carlson, and L. Robert Slevc. "The Rapid Emergence of Auditory Object Representations in Cortex Reflect Central Acoustic Attributes." Journal of Cognitive Neuroscience 32, no. 1 (January 2020): 111–23. http://dx.doi.org/10.1162/jocn_a_01472.

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Human listeners are bombarded by acoustic information that the brain rapidly organizes into coherent percepts of objects and events in the environment, which aids speech and music perception. The efficiency of auditory object recognition belies the critical constraint that acoustic stimuli necessarily require time to unfold. Using magnetoencephalography, we studied the time course of the neural processes that transform dynamic acoustic information into auditory object representations. Participants listened to a diverse set of 36 tokens comprising everyday sounds from a typical human environment. Multivariate pattern analysis was used to decode the sound tokens from the magnetoencephalographic recordings. We show that sound tokens can be decoded from brain activity beginning 90 msec after stimulus onset with peak decoding performance occurring at 155 msec poststimulus onset. Decoding performance was primarily driven by differences between category representations (e.g., environmental vs. instrument sounds), although within-category decoding was better than chance. Representational similarity analysis revealed that these emerging neural representations were related to harmonic and spectrotemporal differences among the stimuli, which correspond to canonical acoustic features processed by the auditory pathway. Our findings begin to link the processing of physical sound properties with the perception of auditory objects and events in cortex.

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Straka, Małgorzata M., Samuel Schmitz, and Hubert H. Lim. "Response features across the auditory midbrain reveal an organization consistent with a dual lemniscal pathway." Journal of Neurophysiology 112, no. 4 (August 15, 2014): 981–98. http://dx.doi.org/10.1152/jn.00008.2014.

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The central auditory system has traditionally been divided into lemniscal and nonlemniscal pathways leading from the midbrain through the thalamus to the cortex. This view has served as an organizing principle for studying, modeling, and understanding the encoding of sound within the brain. However, there is evidence that the lemniscal pathway could be further divided into at least two subpathways, each potentially coding for sound in different ways. We investigated whether such an interpretation is supported by the spatial distribution of response features in the central nucleus of the inferior colliculus (ICC), the part of the auditory midbrain assigned to the lemniscal pathway. We recorded responses to pure tone stimuli in the ICC of ketamine-xylazine-anesthetized guinea pigs and used three-dimensional brain reconstruction techniques to map the location of the recording sites. Compared with neurons in caudal-and-medial regions within an isofrequency lamina of the ICC, neurons in rostral-and-lateral regions responded with shorter first-spike latencies with less spiking jitter, shorter durations of spiking responses, a higher proportion of spikes occurring near the onset of the stimulus, lower thresholds, and larger local field potentials with shorter latencies. Further analysis revealed two distinct clusters of response features located in either the caudal-and-medial or the rostral-and-lateral parts of the isofrequency laminae of the ICC. Thus we report substantial differences in coding properties in two regions of the ICC that are consistent with the hypothesis that the lemniscal pathway is made up of at least two distinct subpathways from the midbrain up to the cortex.

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Journal articles on the topic 'Central auditory pathway'

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