Selectivity of Auditory Neurons for Vowels and Consonants in the Forebrain of the Mynah Bird

1981 ◽  
pp. 317-321
Author(s):  
G. Langner ◽  
D. Bonke ◽  
H. Scheich
Keyword(s):  
Auditory Neurons

Glial Cells in the Auditory Brainstem

2018 ◽  
pp. 680-706
Author(s):  
Giedre Milinkeviciute ◽  
Karina S. Cramer
Keyword(s):  
Nervous System ◽  
Glial Cells ◽  
Sound Localization ◽  
Auditory Brainstem ◽  
Synaptic Function ◽  
System Function ◽  
Auditory Neurons ◽  
System P ◽  
The Central Nervous System ◽  
Nervous System Function

The auditory brainstem carries out sound localization functions that require an extraordinary degree of precision. While many of the specializations needed for these functions reside in auditory neurons, additional adaptations are made possible by the functions of glial cells. Astrocytes, once thought to have mainly a supporting role in nervous system function, are now known to participate in synaptic function. In the auditory brainstem, they contribute to development of specialized synapses and to mature synaptic function. Oligodendrocytes play critical roles in regulating timing in sound localization circuitry. Microglia enter the central nervous system early in development, and also have important functions in the auditory system’s response to injury. This chapter highlights the unique functions of these non-neuronal cells in the auditory system.

The Auditory Brainstem Implant

2019 ◽  
pp. 758-770
Author(s):  
Robert V. Shannon
Keyword(s):  
Surgical Technique ◽  
Cochlear Nucleus ◽  
Meta Analysis ◽  
Auditory Brainstem ◽  
Auditory Information ◽  
Speech Understanding ◽  
Auditory Neurons ◽  
Auditory Brainstem Implant ◽  
The Brain ◽  
Implanted Device

The auditory brainstem implant (ABI) is a surgically implanted device to electrically stimulate auditory neurons in the cochlear nucleus complex of the brainstem in humans to restore hearing sensations. The ABI is similar in function to a cochlear implant, but overall outcomes are poorer. However, recent applications of the ABI to new patient populations and improvements in surgical technique have led to significant improvements in outcomes. While the ABI provides hearing benefits to patients, the outcomes challenge our understanding of how the brain processes neural patterns of auditory information. The neural pattern of activation produced by an ABI is highly unnatural, yet some patients achieve high levels of speech understanding. Based on a meta-analysis of ABI surgeries and outcomes, a theory is proposed of a specialized sub-system of the cochlear nucleus that is critical for speech understanding.

Extraction of Auditory Information by Modulation of Neuronal Ion Channels

2018 ◽  
pp. 272-300
Author(s):  
Leonard K. Kaczmarek
Keyword(s):  
Ion Channels ◽  
Neuronal Firing ◽  
Auditory Information ◽  
Auditory Neurons ◽  
Complex Sound ◽  
Medial Nucleus ◽  
Rapid Changes ◽  
Genes Encoding ◽  
Kinetics Of ◽  
Trapezoid Body

All neurons express a subset of over seventy genes encoding potassium channel subunits. These channels have been studied in auditory neurons, particularly in the medial nucleus of the trapezoid body. The amplitude and kinetics of various channels in these neurons can be modified by the auditory environment. It has been suggested that such modulation is an adaptation of neuronal firing patterns to specific patterns of auditory inputs. Alternatively, such modulation may allow a group of neurons, all expressing the same set of channels, to represent a variety of responses to the same pattern of incoming stimuli. Such diversity would ensure that a small number of genetically identical neurons could capture and encode many aspects of complex sound, including rapid changes in timing and amplitude. This review covers the modulation of ion channels in the medial nucleus of the trapezoid body and how it may maximize the extraction of auditory information.All neurons express a subset of over seventy genes encoding potassium channel subunits. These channels have been studied in auditory neurons, particularly in the medial nucleus of the trapezoid body. The amplitude and kinetics of various channels in these neurons can be modified by the auditory environment. It has been suggested that such modulation is an adaptation of neuronal firing patterns to specific patterns of auditory inputs. Alternatively, such modulation may allow a group of neurons, all expressing the same set of channels, to represent a variety of responses to the same pattern of incoming stimuli. Such diversity would ensure that a small number of genetically identical neurons could capture and encode many aspects of complex sound, including rapid changes in timing and amplitude. This review covers the modulation of ion channels in the medial nucleus of the trapezoid body and how it may maximize the extraction of auditory information.

scholarly journals Human Fetal Auditory Stem Cells Can Be Expanded In Vitro and Differentiate Into Functional Auditory Neurons and Hair Cell-Like Cells

Stem Cells ◽  
2009 ◽  
Vol 27 (5) ◽  
pp. 1196-1204 ◽  
Author(s):  
Wei Chen ◽  
Stuart L. Johnson ◽  
Walter Marcotti ◽  
Peter W. Andrews ◽  
Harry D. Moore ◽  
...  
Keyword(s):  
Stem Cells ◽  
Hair Cell ◽  
Auditory Neurons

Histochemical and Fluorescent Analyses of Mitochondrial Integrity in Chick Auditory Neurons following Deafferentation

2010 ◽  
Vol 21 (03) ◽  
pp. 204-218 ◽  
Author(s):  
Hope Elizabeth Karnes ◽  
Peter Nicholas Scaletty ◽  
Dianne Durham
Keyword(s):  
Cell Death ◽  
Mitochondrial Function ◽  
Apoptotic Cell ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Enzyme Reaction ◽  
Oxidative Enzymes ◽  
Mitochondrial Enzymes ◽  
Auditory Neurons ◽  
Mitotracker Red

Background: Neurons rely exclusively on mitochondrial oxidative phosphorylation to meet cellular energy demands, and disruption of mitochondrial function often precipitates neuronal cell death. Auditory neurons in the chick brain stem (n. magnocellularis [NM]) receive glutamatergic innervation exclusively from ipsilateral eighth nerve afferents. Cochlea removal permanently disrupts afferent support and ultimately triggers apoptotic cell death in 30–50% of ipsilateral, deafferented neurons. Here, we evaluated whether disruption of mitochondrial function occurs during deafferentation-induced neuronal cell death. Purpose: To determine whether mitochondrial dysfunction occurs preferentially within dying NM neurons. Research Design: An experimental study. All birds underwent unilateral cochlea removal. Normally innervated neurons contralateral to surgery served as within-animal controls. Study Sample: Hatchling broiler chickens between 8 and 12 days of age served as subjects. A total of 62 birds were included in the study. Intervention: Cochlea removal was performed to deafferent ipsilateral NM neurons and trigger neuronal cell death. Data Collection and Analysis: Following unilateral cochlea removal, birds were sacrificed 12, 24, 48, or 168 hours later, and brain tissue was harvested. Brainstems were sectioned through NM and evaluated histochemically for oxidative enzyme reaction product accumulation or reacted for Mitotracker Red, an indicator of mitochondrial membrane potential (m) and cytoplasmic TdT-mediated dUTP Nick-End Labeling (TUNEL), an indicator of cell death. Histochemical staining intensities for three mitochondrial enzymes, succinate dehydrogenase (SDH), cytochrome c oxidase (CO), and ATP synthase (ATPase) were measured in individual neurons and compared in ipsilateral and contralateral NM. Comparisons were made using unpaired t-tests (CO) or Kruskal Wallis one way ANOVA followed by Dunn's post hoc pairwise comparisons (ATPase, SDH). Mitotracker Red tissue was examined qualitatively for the presence of and extent of colocalization between Mitotracker Red and TUNEL label in NM. Results: Results showed global upregulation of all three oxidative enzymes within deafferented NM neurons compared to contralateral, unperturbed NM neurons. In addition, differential SDH and ATPase staining intensities were detected across neurons within the ipsilateral nucleus, suggesting functional differences in mitochondrial metabolism across deafferented NM. Quantitative analyses revealed that deafferented neurons with preferentially elevated SDH and ATPase activities represent the subpopulation destined to die following cochlea removal. In addition, Mitotracker Red accumulated intensely within the subset of deafferented NM neurons that also exhibited cytoplasmic TdT-mediated dUTP Nick-End Labeling (TUNEL) and subsequently died. Conclusions: Taken together, our results demonstrate that a subset of deafferented NM neurons, presumably those that die, preferentially upregulates SDH, perhaps via the tricarboxylic acid (TCA) cycle. These same neurons undergo ATPase uncoupling and an eventual loss of Δψm.

Intracellular recording from rat cortical auditory neurons responding to tone burst stimuli

1987 ◽  
Vol 5 ◽  
pp. S17
Author(s):  
Yutaka Hosokawa ◽  
Susumu Ito ◽  
Junsei Horikawa ◽  
Sadao Minami ◽  
Keiichi Murata
Keyword(s):  
Intracellular Recording ◽  
Tone Burst ◽  
Auditory Neurons

Peripheral and central target-derived trophic factor(s) effects on auditory neurons

1992 ◽  
Vol 58 (2) ◽  
pp. 185-192 ◽  
Author(s):  
Philippe P. Lefebvre ◽  
Thierry Weber ◽  
Jean-Michel Rigo ◽  
Hinrich Staecker ◽  
Gustave Moonen ◽  
...  
Keyword(s):  
Trophic Factor ◽  
Auditory Neurons ◽  
Central Target

scholarly journals Spectral-Temporal Receptive Fields of Nonlinear Auditory Neurons Obtained Using Natural Sounds

2000 ◽  
Vol 20 (6) ◽  
pp. 2315-2331 ◽  
Author(s):  
Frédéric E. Theunissen ◽  
Kamal Sen ◽  
Allison J. Doupe
Keyword(s):  
Receptive Fields ◽  
Natural Sounds ◽  
Auditory Neurons
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