While several hypotheses about the neural mechanisms underlying auditory verbal hallucinations (AVH) have been suggested, the exact role of the recently highlighted intrinsic resting state activity of the brain remains unclear. Based on recent findings, we therefore developed what we call the 'resting state hypotheses' of AVH. Our hypothesis suggest that AVH may be traced back to abnormally elevated resting state activity in auditory cortex itself, abnormal modulation of the auditory cortex by anterior cortical midline regions as part of the default-mode network, and neural confusion between auditory cortical resting state changes and stimulus-induced activity. We discuss evidence in favour of our 'resting state hypothesis' and show its correspondence with phenomenal, i.e., subjective-experiential features as explored in phenomenological accounts. Therefore I speak of a 'neurophenomenal resting state hypothesis' of auditory hallucinations in schizophrenia.
Auditory Cortex ; Brain ; Hallucinations* ; Schizophrenia

Auditory Cortex ; metabolism ; Humans ; Magnetic Resonance Spectroscopy

Auditory Cortex ; Depression/drug therapy* ; Thalamus

Tinnitus is the most common disease in Otology, and extremely difficult for treatment in clinic, abnormal events in the cochlea (the abnormal events can result in abnormal neuronal activity in central auditory pathways that can then be finally perceived as tinnitus). Neuroplasticity events at the auditory cortex (AC) have been reported to include hyperactive of cortical neurons and an increase in neuronal synchronization. Our recent studies showed the changes markedly, in the expression of the excitatory glutamate receptor subtype NR2B in mRNA and protein levels, and also some changes in synaptic ultrastructure of neurons in auditory cortex of tinnitus animal. We propose that the mechanisms of tinnitus centralization may arise from abnormal events in the cochlea, and result in abnormal neuronal activity at multiple levels which promote abnormal propagation of neural activity in the central auditory pathway. The plastic change may be positive and adaptive as with learning or memory, or in the compensation after abnormal events in the cochlea that results in new neuronal networks that restore normal function. Alternatively, the neuroplasticity changes might be maladaptive leading perhaps to an imbalance in excitatory and inhibitory events in the brain. Indeed, tinnitus may be the consequence of such maladaptive neuroplasticity brain alterations (synaptic structure) has even gone a step further and described tinnitus as the perceptual manifestation of plastic brain changes that result in abnormal neuronal activity. The neuroplasticity changes may also make tinnitus persists, eventually leading to the existence of tinnitus cochlear-originated in the central pathway. They may also extend to non-sensory areas of the brain giving rise to the attentional and emotional aspects that often accompany the disorder. New pathophysiological insights maybe prompt the development of management approaches to directly target the neuroplasticity processes correlates of tinnitus.
Auditory Cortex ; Humans ; Neuronal Plasticity ; Tinnitus ; diagnosis ; etiology ; therapy

This study was aimed to clarify the change of neuropeptide Y -immunoreactive (NPY -IR) and NADPH -diaphorase (NADPH -d)-positive neurons associated with aging of ICR and C57Bl/6 mice. To verify the effect of aging on NPY and NADPH -d neurons in the cerebral cortex, the tissues were stained by the immunohistochemical and histochemical method. The coexistence of NADPH -d and NPY was found in the cerebral cortex of the ICR and C57Bl/6 mice. The 30 -week -old ICR mice showed a significant increase in the number of NPY - IR neurons in comparison with the 5 -week -old mice in primary motor, secondary somatosensory, ectorhinal, auditory and visual cortex. In the 30 -week -old C57Bl/6 mice, the number of NPY -IR neurons was significantly increased in primary and secondary somatosensory cortex, decreased in retrosplenial and visual cortex compared to the 5 -week -old group. However, the number of NPY -IR/NADPH -d positive neurons of ICR mice was no significant changes in most cerebral cortical areas except insular and perirhinal cortex in the 30 week -old group in comparison with 5 -week -old group of both mice group. The number of coexisted neurons of 30 -week -old C57Bl/6 mice was significantly decreased in primary motor and auditory cortex compared to the 5 -week - old group. These results provides the morphological evidence for the change of NPY -IR neurons that do not contain NADPH -d may be more susceptible to age -related change than NADPH -d -containing neurons in the cerebral cortex of mice.
Aging ; Animals ; Auditory Cortex ; Cerebral Cortex* ; Mice* ; Mice, Inbred ICR ; NADP ; Neurons* ; Neuropeptide Y ; Neuropeptides* ; Somatosensory Cortex ; Visual Cortex

PURPOSE: Several morphometric studies have been performed to investigate brain abnormalities in congenitally deaf people. But no report exists concerning structural brain abnormalities in congenitally deaf adolescents. We evaluated the regional volume changes in gray matter (GM) using voxel-based morphometry (VBM) in congenitally deaf adolescents. MATERIALS AND METHODS: A VBM8 methodology was applied to the T1-weighted magnetic resonance imaging (MRI) scans of eight congenitally deaf adolescents (mean age, 15.6 years) and nine adolescents with normal hearing. All MRI scans were normalized to a template and then segmented, modulated, and smoothed. Smoothed GM data were tested statistically using analysis of covariance (controlled for age, gender, and intracranial cavity volume). RESULTS: The mean values of age, gender, total volumes of GM, and total intracranial volume did not differ between the two groups. In the auditory centers, the left anterior Heschl's gyrus and both inferior colliculi showed decreased regional GM volume in the congenitally deaf adolescents. The GM volumes of the lingual gyri, nuclei accumbens, and left posterior thalamic reticular nucleus in the midbrain were also decreased. CONCLUSIONS: The results of the present study suggest that early deprivation of auditory stimulation in congenitally deaf adolescents might have caused significant underdevelopment of the auditory cortex (left Heschl's gyrus), subcortical auditory structures (inferior colliculi), auditory gain controllers (nucleus accumbens and thalamic reticular nucleus), and multisensory integration areas (inferior colliculi and lingual gyri). These defects might be related to the absence of general auditory perception, the auditory gating system of thalamocortical transmission, and failure in the maturation of the auditory-to-limbic connection and the auditorysomatosensory-visual interconnection.
Acoustic Stimulation ; Adolescent* ; Auditory Cortex ; Auditory Perception ; Brain ; Hearing ; Humans ; Inferior Colliculi ; Magnetic Resonance Imaging ; Mesencephalon

BACKGROUND AND OBJECTIVES: There is a need for fast and reliable objective measures of cochlear implant (CI) performance, especially in young children. The aim of the study was to investigate the detection and characterization of cortical auditory evoked potentials (CAEP) of different types of sound stimulation in CI listeners using a commercially available system, HEARLab™. SUBJECTS AND METHOD: Sound field CAEPs were obtained from 10 CI listeners, using three natural speech sounds (/m/, /g/, and /t/) presented at 55, 65, and 75 dB SPL. Detection rates, the latencies and amplitudes of CAEP waves were analyzed and compared with those of the normal hearing (NH) group. RESULTS: It was possible to detect CAEP responses in all CI listeners. Of the three stimuli (/m/, /g/, /t/), /g/ was the most robust waveform, although this was not statistically significant. Latencies for the /m/ stimulus were relatively longer than those for /t/ and especially for /g/, suggesting that CI listeners hear high-frequency sounds better than low-frequency sounds. When compared to the NH group, CAEP of CI listeners tended to show smaller amplitudes of various waves and longer latencies especially at P1 wave. CONCLUSION: CAEP responses could be obtained in all CI listeners and normal adults successfully, indicating that CAEP can be applied clinically as an objective assessment tool of hearing. Further studies are needed for CI listeners especially in infants and toddlers using this protocol to assess its clinical usefulness.
Adult ; Auditory Cortex ; Child ; Cochlear Implants* ; Evoked Potentials, Auditory* ; Hearing ; Humans ; Infant ; Methods ; Phonetics

Auditory Cortex ; Auditory Perceptual Disorders ; diagnosis ; Hearing Tests ; Humans ; Infant, Newborn ; Neonatal Screening

OBJECTIVE: To explore whether the characteristic responses to sound stimulations of the auditory neurons in the striatum is regulated in different behavioral states. METHODS: The auditory neurons in the striatum of awake C57BL/6J mice were selected for this study. We recorded the auditory response of the striatum to noises over a long period of time by building a synchronous in vivo electrophysiological and locomotion recording system and using glass microelectrode attachment recording. By analyzing the running speed of the mice, the behavioral states of the mice were divided into the quiet state and the active state, and the spontaneous activity and evoked responses of the auditory neurons in the striatum were analyzed in these two states. RESULTS: Compared with those recorded in the quiet state, the spontaneous activity of the auditory neurons in the striatum of the mice increased significantly (37.06±12.02 vs 18.51±10.91, P < 0.001) while the auditory response of the neurons decreased significantly (noise intensity=60 dB, 3.45±2.99 vs 3.04±2.76, P < 0.001) in the active state. CONCLUSION Locomotion has a significant inhibitory effect on the auditory response of the striatum, which may importantly contribute to the decline of sound information recognition ability in the active state.
Acoustic Stimulation ; Animals ; Auditory Cortex/physiology* ; Evoked Potentials, Auditory ; Locomotion/physiology* ; Mice ; Mice, Inbred C57BL ; Neurons

The anterior auditory field (AAF) is a core region of the auditory cortex and plays a vital role in discrimination tasks. However, the role of the AAF corticostriatal neurons in frequency discrimination remains unclear. Here, we used c-Fos staining, fiber photometry recording, and pharmacogenetic manipulation to investigate the function of the AAF corticostriatal neurons in a frequency discrimination task. c-Fos staining and fiber photometry recording revealed that the activity of AAF pyramidal neurons was significantly elevated during the frequency discrimination task. Pharmacogenetic inhibition of AAF pyramidal neurons significantly impaired frequency discrimination. In addition, histological results revealed that AAF pyramidal neurons send strong projections to the striatum. Moreover, pharmacogenetic suppression of the striatal projections from pyramidal neurons in the AAF significantly disrupted the frequency discrimination. Collectively, our findings show that AAF pyramidal neurons, particularly the AAF-striatum projections, play a crucial role in frequency discrimination behavior.
Acoustic Stimulation/methods* ; Neurons/physiology* ; Auditory Cortex/physiology* ; Auditory Perception ; Pyramidal Cells