Anatomic organization of the auditory cortex

Hackett, Troy A.

doi:10.1016/b978-0-444-62630-1.00002-0

Cited by 90 publications

(72 citation statements)

References 312 publications

(263 reference statements)

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“…Multiple other organizational schemes divide HG into three regions along its long axis based on cytoarchitectonic criteria (von Economo and Koskinas, 1925; Beck, 1928; von Economo & Horn, 1930; Morosan et al, 2001; reviewed in Hackett, 2007, 2015). These parcellation schemes are consistent with the distribution of FFR changes along HG reported in the present study (see Fig.…”

Section: Discussionmentioning

confidence: 99%

“…Delineation of auditory cortex on Heschl’s gyrus (HG) remains controversial despite decades of research, (Hackett, 2007, 2015). Studies in non-human primates suggest a framework in which the auditory cortex is hierarchically organized into several core, belt and parabelt regions (Rauschecker et al, 1995; Hackett et al, 1998; Brugge and Howard, 2002; Kaas and Hackett, 2005).…”

Section: Introductionmentioning

confidence: 99%

“…Most anatomical and functional neuroimaging studies in humans conclude that the posteromedial portion (approximately two thirds) of HG is comprised of core auditory cortex (e.g., Rivier and Clarke, 1997; Talavage et al, 2000; Hackett et al, 2001; Wallace et al, 2002; Sweet et al, 2005; Woods et al, 2009). However, even at the fundamental level of cytoarchitectonics, there have been a variety of interpretations of the data (reviewed in Hackett, 2007, 2015). For instance, the most posteromedial aspect of HG has been variously labeled as core (Rivier and Clarke et al, 1997; Morosan et al, 2001; Wallace et al, 2002; Sweet at el., 2005) or belt areas (Galaburda and Sanides, 1980; Fullerton and Pandya, 2007).…”

Section: Introductionmentioning

confidence: 99%

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Electrocorticographic delineation of human auditory cortical fields based on effects of propofol anesthesia

et al. 2017

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The functional organization of human auditory cortex remains incompletely characterized. While the posteromedial two thirds of Heschl’s gyrus (HG) is generally considered to be part of core auditory cortex, additional subdivisions of HG remain speculative. To further delineate the hierarchical organization of human auditory cortex, we investigated regional heterogeneity in the modulation of auditory cortical responses under varying depths of anesthesia induced by propofol. Non-invasive studies have shown that propofol differentially affects auditory cortical activity, with a greater impact on non-core areas. Subjects were neurosurgical patients undergoing removal of intracranial electrodes placed to identify epileptic foci. Stimuli were 50 Hz click trains, presented continuously during an awake baseline period, and subsequently, while propofol infusion was incrementally titrated to induce general anesthesia. Electrocorticographic recordings were made with depth electrodes implanted in HG and subdural grid electrodes implanted over superior temporal gyrus (STG). Depth of anesthesia was monitored using spectral entropy. Averaged evoked potentials (AEPs), frequency-following responses (FFRs) and high gamma (70–150 Hz) event-related band power (ERBP) were used to characterize auditory cortical activity. Based on the changes in AEPs and FFRs during the induction of anesthesia, posteromedial HG could be divided into two subdivisions. In the most posteromedial aspect of the gyrus, the earliest AEP deflections were preserved and FFRs increased during induction. In contrast, the remainder of the posteromedial HG exhibited attenuation of both the AEP and the FFR. The anterolateral HG exhibited weaker activation characterized by broad, low-voltage AEPs and the absence of FFRs. Lateral STG exhibited limited activation by click trains, and FFRs there diminished during induction. Sustained high gamma activity was attenuated in the most posteromedial portion of HG, and was absent in all other regions. These differential patterns of auditory cortical activity during the induction of anesthesia may serve as useful physiological markers for field delineation. In this study, the posteromedial HG could be parcellated into at least two subdivisions. Preservation of the earliest AEP deflections and FFRs in the posteromedial HG likely reflects the persistence of feedforward synaptic activity generated by inputs from subcortical auditory pathways, including the medial geniculate nucleus.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Electrocorticographic delineation of human auditory cortical fields based on effects of propofol anesthesia

et al. 2017

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“…Both auditory and visual stimuli from peripheral organs are sent to the thalamus, and then to the primary auditory or visual area in the cerebral cortex (Tamietto and de Gelder, 2010;Hackett, 2015). Functions of the thalamus are impaired in ASD schoolchildren, adolescents, and adults (Hardan et al, 2008;Lai et al, 2010).…”

Section: Neuroinflammation In Social Cognitive Deficitsmentioning

confidence: 99%

Involvement of Neuroinflammation during Brain Development in Social Cognitive Deficits in Autism Spectrum Disorder and Schizophrenia

Nakagawa¹,

Chiba²

2016

Journal of Pharmacology and Experimental Therapeutics

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Development of social cognition, a unique and high-order function, depends on brain maturation from childhood to adulthood in humans. Autism spectrum disorder (ASD) and schizophrenia have similar social cognitive deficits, although age of onset in each disorder is different. Pathogenesis of these disorders is complex and contains several features, including genetic risk factors, environmental risk factors, and sites of abnormalities in the brain. Although several hypotheses have been postulated, they seem to be insufficient to explain how brain alterations associated with symptoms in these disorders develop at distinct developmental stages. Development of ASD appears to be related to cerebellar dysfunction and subsequent thalamic hyperactivation in early childhood. By contrast, schizophrenia seems to be triggered by thalamic hyperactivation in late adolescence, whereas hippocampal aberration has been possibly initiated in childhood. One of the possible culprits is metal homeostasis disturbances that can induce dysfunction of blood-cerebrospinal fluid barrier. Thalamic hyperactivation is thought to be induced by microglia-mediated neuroinflammation and abnormalities of intracerebral environment. Consequently, it is likely that the thalamic hyperactivation triggers dysregulation of the dorsolateral prefrontal cortex for lower brain regions related to social cognition. In this review, we summarize the brain aberration in ASD and schizophrenia and provide a possible mechanism underlying social cognitive deficits in these disorders based on their distinct ages of onset.

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“…S251). The auditory cortex was identified based on the rhinal sulcus, midline, and hippocampus, as previously described [30,31,32]. The primary cells were suspended in high-glucose Dulbecco's modified Eagle's medium (DMEM; Gibco, New York, NY, USA) containing 10% fetal bovine serum (Gibco) and 1% penicillin-streptomycin (Sigma-Aldrich, St. Louis, MO, USA), plated onto 96-well, 24-well, or 6-well plates (Sigma-Aldrich), and incubated at 37°C in a 95% air/5% CO 2 humidified incubator (Thermo 3111; Thermo Scientific, New York, NY, USA).…”

Section: Methodsmentioning

confidence: 99%

Role of the Ubiquitin C-Terminal Hydrolase L1-Modulated Ubiquitin Proteasome System in Auditory Cortex Senescence

Zhang

Huang²,

Zhao³

et al. 2017

ORL

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Background/Aims: According to recent studies, central auditory impairments are closely related to neurodegenerative diseases. However, the mechanism of central presbycusis remains unclear. Ubiquitin C-terminal hydrolase L1 (UCHL1) is important in maintaining proteasomal activity; however, the detailed mechanism has not yet been fully elucidated. This study aims to investigate the molecular alterations involved in UCHL1 regulation during auditory cortex aging. Methods:D-Galactose (D-gal) induces oxidative stress and senescence in the auditory cortex, as reported in our previous studies. Primary auditory cortex cells were treated with D-gal for 72 h or 5 days. The proteins related to the ubiquitin proteasome system (UPS) and proteasomal activities were evaluated. UCHL1 was overexpressed, and the effects of UCHL1 on the UPS and proteasomal activity were analyzed. Results: Proteasomal activity was elevated at 72 h and decreased at 5 days in D-gal-treated primary auditory cortex cells. We also found that overexpression of UCHL1 increased the UPS-related proteins UBE1, PSMA7, ubiquitinated proteins, and monoubiquitin, and proteasomal activity. Conclusion: The results suggest that UCHL1 may modify the aging process in the auditory cortex by regulating UPS- related proteins.

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Anatomic organization of the auditory cortex

Cited by 90 publications

References 312 publications

Electrocorticographic delineation of human auditory cortical fields based on effects of propofol anesthesia

Electrocorticographic delineation of human auditory cortical fields based on effects of propofol anesthesia

Involvement of Neuroinflammation during Brain Development in Social Cognitive Deficits in Autism Spectrum Disorder and Schizophrenia

Role of the Ubiquitin C-Terminal Hydrolase L1-Modulated Ubiquitin Proteasome System in Auditory Cortex Senescence

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