Detecting Noise-Induced Cochlear Synaptopathy by Auditory Brainstem Response in Tinnitus Patients With Normal Hearing Thresholds: A Meta-Analysis

Noise-induced cochlear synaptopathy (CS) is defined as a permanent loss of synapses in the auditory nerve pathway following noise exposure. Several studies using auditory brainstem response (ABR) have indicated the presence of CS and increased central gain in tinnitus patients with normal hearing thresholds (TNHT), but the results were inconsistent. This meta-analysis aimed to review the evidence of CS and its pathological changes in the central auditory system in TNHT. Published studies using ABR to study TNHT were reviewed. PubMed, EMBASE, and Scopus databases were selected to search for relevant literature. Studies (489) were retrieved, and 11 were included for meta-analysis. The results supported significantly reduced wave I amplitude in TNHT, whereas the alternations in wave V amplitude were inconsistent among the studies. Consistently increased V/I ratio indicated noise-induced central gain enhancement. The results indicated the evidence of noise-induced cochlear synaptopathy in tinnitus patients with normal hearing. However, inconsistent changes in wave V amplitude may be explained by that the failure of central gain that triggers the pathological neural changes in the central auditory system and/or that increased central gain may be necessary to generate tinnitus but not to maintain tinnitus.

Emergence and function of cortical offset responses in sound termination detection

Offset responses in auditory processing appear after a sound terminates. They arise in neuronal circuits within the peripheral auditory system, but their role in the central auditory system remains unknown. Here, we ask what the behavioral relevance of cortical offset responses is and what circuit mechanisms drive them. At the perceptual level, our results reveal that experimentally minimizing auditory cortical offset responses decreases the mouse performance to detect sound termination, assigning a behavioral role to offset responses. By combining in vivo electrophysiology in the auditory cortex and thalamus of awake mice, we also demonstrate that cortical offset responses are not only inherited from the periphery but also amplified and generated de novo. Finally, we show that offset responses code more than silence, including relevant changes in sound trajectories. Together, our results reveal the importance of cortical offset responses in encoding sound termination and detecting changes within temporally discontinuous sounds crucial for speech and vocalization.

Effect of tinnitus on the performance of central auditory system: a review

Background and Aim: Tinnitus is one of the most difficult challenges in audiology and oto­logy. Previous studies have been shown that tinn­itus may interfere with the function of central auditory system (CAS). Involvement of CAS abilities including speech perception and audi­tory processing has led to serious problems in people with tinnitus. Due to the lack of enough information about the impact of tinnitus on CAS and its function, and given that there is no standardized protocol for assessment and mana­gement of tinnitus, this study aimed to review the studies on the effect of tinnitus on the CAS function. Recent Findings: Sixteen eligible articles were reviewed. Temporal and spectral resolution, fre­quency differentiation and speech perception deficits were reported in patients with tinnitus, especially in background noise. This was repor­ted even in tinnitus patients with normal hearing. Conclusion: Assessment of central auditory pro­cessing and speech perception in noise seems to be useful for proper management of tinnitus in clinical practice. Keywords: Tinnitus; auditory system; central auditory processing; speech in noise performance

Bioinspired Auditory Model for Vowel Recognition

In this work, a bioinspired or neuromorphic model to replicate the vowel recognition process for an auditory system is presented. A bioinspired peripheral and central auditory system model is implemented and a neuromorphic higher auditory system model based on artificial neuronal nets for vowel recognition is proposed. For their verification, ten Hispanic Spanish language-speaking adults (five males and five females) were used. With the proposed bioinspired model based on artificial neuronal nets it is possible to recognize with high levels of accuracy and sensibility the vowels phonemes of speech signals and the assessment of cochlear implant stimulation strategies in terms of vowel recognition.

A RELAÇÃO ENTRE O PROCESSAMENTO AUDITIVO CENTRAL E A APRENDIZAGEM DE CRIANÇAS COM DISLEXIA

The proper functioning of the PAC allows the development of language in children in the acquisition phase, especially with regard to the construction and internalization of language levels.3 Learning difficulties in the school phase can be related to several causes, one of them is dyslexia .4.5In the literature, we can find important evidence that indicates a relationship between learning disorders, such as dyslexia, and poor performance in tests that assess the central auditory system. It is known that individuals with dyslexia also have difficulties in the perception of sounds and in terms of sensitivity to the melody of words. Such a deficit becomes a hindrance in the interpretation of sounds, causing learning difficulties.8

Central Auditory Plasticity from Molecules to Behavior

Understanding how, when, and for how long the adult central auditory system adapts to hearing loss and aging is an important topic that is currently studied across the globe [...]

α3β4* Nicotinic acetylcholine receptors strongly modulate the excitability of VIP neurons in the mouse inferior colliculus

The inferior colliculus (IC), the midbrain hub of the central auditory system, receives extensive cholinergic input from the pontomesencephalic tegmentum. Activation of nicotinic acetylcholine receptors (nAChRs) in the IC can alter acoustic processing and enhance auditory task performance. However, how nAChRs affect the excitability of specific classes of IC neurons remains unknown. Recently, we identified vasoactive intestinal peptide (VIP) neurons as a distinct class of glutamatergic principal neurons in the IC. Here, in experiments using male and female mice, we show that cholinergic terminals are routinely located adjacent to the somas and dendrites of VIP neurons. Using whole-cell electrophysiology in brain slices, we found that acetylcholine drives surprisingly strong and long-lasting excitation and inward currents in VIP neurons. This excitation was unaffected by the muscarinic receptor antagonist atropine. Application of nAChR antagonists revealed that acetylcholine excites VIP neurons mainly via activation of α3β4* nAChRs, a nAChR subtype that is rare in the brain. Furthermore, we show that cholinergic excitation is intrinsic to VIP neurons and does not require activation of presynaptic inputs. Lastly, we found that low frequency trains of acetylcholine puffs elicited temporal summation in VIP neurons, suggesting that in vivo-like patterns of cholinergic input can reshape activity for prolonged periods. These results reveal the first cellular mechanisms of nAChR regulation in the IC, identify a functional role for α3β4* nAChRs in the auditory system, and suggest that cholinergic input can potently influence auditory processing by increasing excitability in VIP neurons and their postsynaptic targets.Key points summaryThe inferior colliculus (IC), the midbrain hub of the central auditory system, receives extensive cholinergic input and expresses a variety of nicotinic acetylcholine receptor (nAChR) subunits.In vivo activation of nAChRs alters the input-output functions of IC neurons and influences performance in auditory tasks. However, how nAChR activation affects the excitability of specific IC neuron classes remains unknown.Here we show in mice that cholinergic terminals are located adjacent to the somas and dendrites of VIP neurons, a class of IC principal neurons.We find that acetylcholine elicits surprisingly strong, long-lasting excitation of VIP neurons and this is mediated mainly through activation of α3β4* nAChRs, a subtype that is rare in the brain.Our data identify a role for α3β4* nAChRs in the central auditory pathway and reveal a mechanism by which cholinergic input can influence auditory processing in the IC and the postsynaptic targets of VIP neurons.

Emergence and function of cortical offset responses in sound termination detection

Offset responses in auditory processing appear after a sound terminates. They arise in neuronal circuits within the peripheral auditory system, but their role in the central auditory system remains unknown. Here we ask what the behavioural relevance of cortical offset responses is and what circuit mechanisms drive them. At the perceptual level, our results reveal that experimentally minimizing auditory cortical offset responses decreases the mouse performance to detect sound termination, assigning a behavioural role to offset responses. By combining in vivo electrophysiology in the auditory cortex and thalamus of awake mice, we also demonstrate that cortical offset responses are not only inherited from the periphery but also amplified and generated de novo. Finally, we show that offset responses code more than silence, including relevant changes in sound trajectories. Together, our results reveal the importance of cortical offset responses in encoding sound termination and detecting changes within temporally discontinuous sounds crucial for speech and vocalization.