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OtoRhinoLaryngology by Sfakianakis G.Alexandros Sfakianakis G.Alexandros,Anapafseos 5 Agios Nikolaos 72100 Crete Greece,tel : 00302841026182,00306932607174
Σάββατο 23 Ιουλίου 2016
Traumatic Cochlear Nerve Avulsion Following Otic-Capsule Sparing Temporal Bone Fracture.
Long-term effects of adolescent concussion history on gait, across age
Publication date: Available online 22 July 2016
Source:Gait & Posture
Author(s): Douglas N. Martini, Grant C. Goulet, Deanna H. Gates, Steven P. Broglio
The aim of this study was to examine the possible long-term effects of high school concussion history on gait performance across the lifespan. Individuals with and without a concussion history were grouped into 20-year-old (yo) (n=40), 40yo (n=19), and 60yo (n=18) age groups. Participants completed five trials of four walking conditions: a normal walk, a dual task walk, an obstructed walk, and an obstructed, dual task walk. Spatiotemporal gait parameters for gait analyses during single and dual task conditions. Gait velocity, step width, stride length, percent of time in double support, and obstacle toe clearance were the gait variables assessed along with number correct from dual task. Gait was analyzed via optical motion capture. Data were analyzed by two-factor, multivariate ANOVAs and significant interactions were explored using post hoc contrasts. A significant (F=2.62, p=0.03) interaction was observed for the obstructed walk condition. Further analyses yielded no significant concussion history and control group differences, within age. The data indicate that an adolescent concussion history has a non-observable effect on gait across the lifespan.
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Source:Gait & Posture
Author(s): Douglas N. Martini, Grant C. Goulet, Deanna H. Gates, Steven P. Broglio
The aim of this study was to examine the possible long-term effects of high school concussion history on gait performance across the lifespan. Individuals with and without a concussion history were grouped into 20-year-old (yo) (n=40), 40yo (n=19), and 60yo (n=18) age groups. Participants completed five trials of four walking conditions: a normal walk, a dual task walk, an obstructed walk, and an obstructed, dual task walk. Spatiotemporal gait parameters for gait analyses during single and dual task conditions. Gait velocity, step width, stride length, percent of time in double support, and obstacle toe clearance were the gait variables assessed along with number correct from dual task. Gait was analyzed via optical motion capture. Data were analyzed by two-factor, multivariate ANOVAs and significant interactions were explored using post hoc contrasts. A significant (F=2.62, p=0.03) interaction was observed for the obstructed walk condition. Further analyses yielded no significant concussion history and control group differences, within age. The data indicate that an adolescent concussion history has a non-observable effect on gait across the lifespan.
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Long-term effects of adolescent concussion history on gait, across age
Publication date: Available online 22 July 2016
Source:Gait & Posture
Author(s): Douglas N. Martini, Grant C. Goulet, Deanna H. Gates, Steven P. Broglio
The aim of this study was to examine the possible long-term effects of high school concussion history on gait performance across the lifespan. Individuals with and without a concussion history were grouped into 20-year-old (yo) (n=40), 40yo (n=19), and 60yo (n=18) age groups. Participants completed five trials of four walking conditions: a normal walk, a dual task walk, an obstructed walk, and an obstructed, dual task walk. Spatiotemporal gait parameters for gait analyses during single and dual task conditions. Gait velocity, step width, stride length, percent of time in double support, and obstacle toe clearance were the gait variables assessed along with number correct from dual task. Gait was analyzed via optical motion capture. Data were analyzed by two-factor, multivariate ANOVAs and significant interactions were explored using post hoc contrasts. A significant (F=2.62, p=0.03) interaction was observed for the obstructed walk condition. Further analyses yielded no significant concussion history and control group differences, within age. The data indicate that an adolescent concussion history has a non-observable effect on gait across the lifespan.
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Source:Gait & Posture
Author(s): Douglas N. Martini, Grant C. Goulet, Deanna H. Gates, Steven P. Broglio
The aim of this study was to examine the possible long-term effects of high school concussion history on gait performance across the lifespan. Individuals with and without a concussion history were grouped into 20-year-old (yo) (n=40), 40yo (n=19), and 60yo (n=18) age groups. Participants completed five trials of four walking conditions: a normal walk, a dual task walk, an obstructed walk, and an obstructed, dual task walk. Spatiotemporal gait parameters for gait analyses during single and dual task conditions. Gait velocity, step width, stride length, percent of time in double support, and obstacle toe clearance were the gait variables assessed along with number correct from dual task. Gait was analyzed via optical motion capture. Data were analyzed by two-factor, multivariate ANOVAs and significant interactions were explored using post hoc contrasts. A significant (F=2.62, p=0.03) interaction was observed for the obstructed walk condition. Further analyses yielded no significant concussion history and control group differences, within age. The data indicate that an adolescent concussion history has a non-observable effect on gait across the lifespan.
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Long-term effects of adolescent concussion history on gait, across age
Publication date: Available online 22 July 2016
Source:Gait & Posture
Author(s): Douglas N. Martini, Grant C. Goulet, Deanna H. Gates, Steven P. Broglio
The aim of this study was to examine the possible long-term effects of high school concussion history on gait performance across the lifespan. Individuals with and without a concussion history were grouped into 20-year-old (yo) (n=40), 40yo (n=19), and 60yo (n=18) age groups. Participants completed five trials of four walking conditions: a normal walk, a dual task walk, an obstructed walk, and an obstructed, dual task walk. Spatiotemporal gait parameters for gait analyses during single and dual task conditions. Gait velocity, step width, stride length, percent of time in double support, and obstacle toe clearance were the gait variables assessed along with number correct from dual task. Gait was analyzed via optical motion capture. Data were analyzed by two-factor, multivariate ANOVAs and significant interactions were explored using post hoc contrasts. A significant (F=2.62, p=0.03) interaction was observed for the obstructed walk condition. Further analyses yielded no significant concussion history and control group differences, within age. The data indicate that an adolescent concussion history has a non-observable effect on gait across the lifespan.
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Source:Gait & Posture
Author(s): Douglas N. Martini, Grant C. Goulet, Deanna H. Gates, Steven P. Broglio
The aim of this study was to examine the possible long-term effects of high school concussion history on gait performance across the lifespan. Individuals with and without a concussion history were grouped into 20-year-old (yo) (n=40), 40yo (n=19), and 60yo (n=18) age groups. Participants completed five trials of four walking conditions: a normal walk, a dual task walk, an obstructed walk, and an obstructed, dual task walk. Spatiotemporal gait parameters for gait analyses during single and dual task conditions. Gait velocity, step width, stride length, percent of time in double support, and obstacle toe clearance were the gait variables assessed along with number correct from dual task. Gait was analyzed via optical motion capture. Data were analyzed by two-factor, multivariate ANOVAs and significant interactions were explored using post hoc contrasts. A significant (F=2.62, p=0.03) interaction was observed for the obstructed walk condition. Further analyses yielded no significant concussion history and control group differences, within age. The data indicate that an adolescent concussion history has a non-observable effect on gait across the lifespan.
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Adjustments of the amplitude mapping function: Sensitivity of cochlear implant users and effects on subjective preference and speech recognition
10.1080/14992027.2016.1202454<br/>Femke L. Theelen–van den Hoek
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Adjustments of the amplitude mapping function: Sensitivity of cochlear implant users and effects on subjective preference and speech recognition
10.1080/14992027.2016.1202454<br/>Femke L. Theelen–van den Hoek
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Adjustments of the amplitude mapping function: Sensitivity of cochlear implant users and effects on subjective preference and speech recognition
10.1080/14992027.2016.1202454<br/>Femke L. Theelen–van den Hoek
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Adjustments of the amplitude mapping function: Sensitivity of cochlear implant users and effects on subjective preference and speech recognition
10.1080/14992027.2016.1202454<br/>Femke L. Theelen–van den Hoek
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Adjustments of the amplitude mapping function: Sensitivity of cochlear implant users and effects on subjective preference and speech recognition
10.1080/14992027.2016.1202454<br/>Femke L. Theelen–van den Hoek
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Neurofilament heavy chain expression and neuroplasticity in rat auditory cortex after unilateral and bilateral deafness
Publication date: Available online 22 July 2016
Source:Hearing Research
Author(s): Min-Hyun Park, Jeong Hun Jang, Jae-Jin Song, Ho Sun Lee, Seung Ha Oh
Deafness induces many plastic changes in the auditory neural system. For instance, dendritic changes cause synaptic changes in neural cells. SMI-32, a monoclonal antibody reveals auditory areas and recognizes non-phosphorylated epitopes on medium- and high-molecular-weight subunits of neurofilament proteins in cortical pyramidal neuron dendrites. We investigated SMI-32-immunoreactive (-ir) protein levels in the auditory cortices of rats with induced unilateral and bilateral deafness. Adult male Sprague–Dawley rats were divided into unilateral deafness (UD), bilateral deafness (BD), and control groups. Deafness was induced by cochlear ablation. All rats were sacrificed, and the auditory cortices were harvested for real-time quantitative polymerase chain reaction (RT-qPCR) and western blot analyses at 2, 4, 6, and 12 weeks after deafness was induced. Immunohistochemical staining was performed to evaluate the location of SMI-32-ir neurons. Neurofilament heavy chain (NEFH) mRNA expression and SMI-32-ir protein levels were increased in the BD group. In particular, SMI-32-ir protein levels increased significantly 6 and 12 weeks after deafness was induced. In contrast, no significant changes in protein level were detected in the right or left auditory cortices at any time point in the UD group. NEFH mRNA level decreased at 4 weeks after deafness was induced in the UD group, but recovered thereafter. Taken together, BD induced plastic changes in the auditory cortex, whereas UD did not affect the auditory neural system sufficiently to show plastic changes, as measured by neurofilament protein level.
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Source:Hearing Research
Author(s): Min-Hyun Park, Jeong Hun Jang, Jae-Jin Song, Ho Sun Lee, Seung Ha Oh
Deafness induces many plastic changes in the auditory neural system. For instance, dendritic changes cause synaptic changes in neural cells. SMI-32, a monoclonal antibody reveals auditory areas and recognizes non-phosphorylated epitopes on medium- and high-molecular-weight subunits of neurofilament proteins in cortical pyramidal neuron dendrites. We investigated SMI-32-immunoreactive (-ir) protein levels in the auditory cortices of rats with induced unilateral and bilateral deafness. Adult male Sprague–Dawley rats were divided into unilateral deafness (UD), bilateral deafness (BD), and control groups. Deafness was induced by cochlear ablation. All rats were sacrificed, and the auditory cortices were harvested for real-time quantitative polymerase chain reaction (RT-qPCR) and western blot analyses at 2, 4, 6, and 12 weeks after deafness was induced. Immunohistochemical staining was performed to evaluate the location of SMI-32-ir neurons. Neurofilament heavy chain (NEFH) mRNA expression and SMI-32-ir protein levels were increased in the BD group. In particular, SMI-32-ir protein levels increased significantly 6 and 12 weeks after deafness was induced. In contrast, no significant changes in protein level were detected in the right or left auditory cortices at any time point in the UD group. NEFH mRNA level decreased at 4 weeks after deafness was induced in the UD group, but recovered thereafter. Taken together, BD induced plastic changes in the auditory cortex, whereas UD did not affect the auditory neural system sufficiently to show plastic changes, as measured by neurofilament protein level.
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Neurofilament heavy chain expression and neuroplasticity in rat auditory cortex after unilateral and bilateral deafness
Publication date: Available online 22 July 2016
Source:Hearing Research
Author(s): Min-Hyun Park, Jeong Hun Jang, Jae-Jin Song, Ho Sun Lee, Seung Ha Oh
Deafness induces many plastic changes in the auditory neural system. For instance, dendritic changes cause synaptic changes in neural cells. SMI-32, a monoclonal antibody reveals auditory areas and recognizes non-phosphorylated epitopes on medium- and high-molecular-weight subunits of neurofilament proteins in cortical pyramidal neuron dendrites. We investigated SMI-32-immunoreactive (-ir) protein levels in the auditory cortices of rats with induced unilateral and bilateral deafness. Adult male Sprague–Dawley rats were divided into unilateral deafness (UD), bilateral deafness (BD), and control groups. Deafness was induced by cochlear ablation. All rats were sacrificed, and the auditory cortices were harvested for real-time quantitative polymerase chain reaction (RT-qPCR) and western blot analyses at 2, 4, 6, and 12 weeks after deafness was induced. Immunohistochemical staining was performed to evaluate the location of SMI-32-ir neurons. Neurofilament heavy chain (NEFH) mRNA expression and SMI-32-ir protein levels were increased in the BD group. In particular, SMI-32-ir protein levels increased significantly 6 and 12 weeks after deafness was induced. In contrast, no significant changes in protein level were detected in the right or left auditory cortices at any time point in the UD group. NEFH mRNA level decreased at 4 weeks after deafness was induced in the UD group, but recovered thereafter. Taken together, BD induced plastic changes in the auditory cortex, whereas UD did not affect the auditory neural system sufficiently to show plastic changes, as measured by neurofilament protein level.
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Source:Hearing Research
Author(s): Min-Hyun Park, Jeong Hun Jang, Jae-Jin Song, Ho Sun Lee, Seung Ha Oh
Deafness induces many plastic changes in the auditory neural system. For instance, dendritic changes cause synaptic changes in neural cells. SMI-32, a monoclonal antibody reveals auditory areas and recognizes non-phosphorylated epitopes on medium- and high-molecular-weight subunits of neurofilament proteins in cortical pyramidal neuron dendrites. We investigated SMI-32-immunoreactive (-ir) protein levels in the auditory cortices of rats with induced unilateral and bilateral deafness. Adult male Sprague–Dawley rats were divided into unilateral deafness (UD), bilateral deafness (BD), and control groups. Deafness was induced by cochlear ablation. All rats were sacrificed, and the auditory cortices were harvested for real-time quantitative polymerase chain reaction (RT-qPCR) and western blot analyses at 2, 4, 6, and 12 weeks after deafness was induced. Immunohistochemical staining was performed to evaluate the location of SMI-32-ir neurons. Neurofilament heavy chain (NEFH) mRNA expression and SMI-32-ir protein levels were increased in the BD group. In particular, SMI-32-ir protein levels increased significantly 6 and 12 weeks after deafness was induced. In contrast, no significant changes in protein level were detected in the right or left auditory cortices at any time point in the UD group. NEFH mRNA level decreased at 4 weeks after deafness was induced in the UD group, but recovered thereafter. Taken together, BD induced plastic changes in the auditory cortex, whereas UD did not affect the auditory neural system sufficiently to show plastic changes, as measured by neurofilament protein level.
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Neurofilament heavy chain expression and neuroplasticity in rat auditory cortex after unilateral and bilateral deafness
Publication date: Available online 22 July 2016
Source:Hearing Research
Author(s): Min-Hyun Park, Jeong Hun Jang, Jae-Jin Song, Ho Sun Lee, Seung Ha Oh
Deafness induces many plastic changes in the auditory neural system. For instance, dendritic changes cause synaptic changes in neural cells. SMI-32, a monoclonal antibody reveals auditory areas and recognizes non-phosphorylated epitopes on medium- and high-molecular-weight subunits of neurofilament proteins in cortical pyramidal neuron dendrites. We investigated SMI-32-immunoreactive (-ir) protein levels in the auditory cortices of rats with induced unilateral and bilateral deafness. Adult male Sprague–Dawley rats were divided into unilateral deafness (UD), bilateral deafness (BD), and control groups. Deafness was induced by cochlear ablation. All rats were sacrificed, and the auditory cortices were harvested for real-time quantitative polymerase chain reaction (RT-qPCR) and western blot analyses at 2, 4, 6, and 12 weeks after deafness was induced. Immunohistochemical staining was performed to evaluate the location of SMI-32-ir neurons. Neurofilament heavy chain (NEFH) mRNA expression and SMI-32-ir protein levels were increased in the BD group. In particular, SMI-32-ir protein levels increased significantly 6 and 12 weeks after deafness was induced. In contrast, no significant changes in protein level were detected in the right or left auditory cortices at any time point in the UD group. NEFH mRNA level decreased at 4 weeks after deafness was induced in the UD group, but recovered thereafter. Taken together, BD induced plastic changes in the auditory cortex, whereas UD did not affect the auditory neural system sufficiently to show plastic changes, as measured by neurofilament protein level.
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Source:Hearing Research
Author(s): Min-Hyun Park, Jeong Hun Jang, Jae-Jin Song, Ho Sun Lee, Seung Ha Oh
Deafness induces many plastic changes in the auditory neural system. For instance, dendritic changes cause synaptic changes in neural cells. SMI-32, a monoclonal antibody reveals auditory areas and recognizes non-phosphorylated epitopes on medium- and high-molecular-weight subunits of neurofilament proteins in cortical pyramidal neuron dendrites. We investigated SMI-32-immunoreactive (-ir) protein levels in the auditory cortices of rats with induced unilateral and bilateral deafness. Adult male Sprague–Dawley rats were divided into unilateral deafness (UD), bilateral deafness (BD), and control groups. Deafness was induced by cochlear ablation. All rats were sacrificed, and the auditory cortices were harvested for real-time quantitative polymerase chain reaction (RT-qPCR) and western blot analyses at 2, 4, 6, and 12 weeks after deafness was induced. Immunohistochemical staining was performed to evaluate the location of SMI-32-ir neurons. Neurofilament heavy chain (NEFH) mRNA expression and SMI-32-ir protein levels were increased in the BD group. In particular, SMI-32-ir protein levels increased significantly 6 and 12 weeks after deafness was induced. In contrast, no significant changes in protein level were detected in the right or left auditory cortices at any time point in the UD group. NEFH mRNA level decreased at 4 weeks after deafness was induced in the UD group, but recovered thereafter. Taken together, BD induced plastic changes in the auditory cortex, whereas UD did not affect the auditory neural system sufficiently to show plastic changes, as measured by neurofilament protein level.
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Neurofilament heavy chain expression and neuroplasticity in rat auditory cortex after unilateral and bilateral deafness
Publication date: Available online 22 July 2016
Source:Hearing Research
Author(s): Min-Hyun Park, Jeong Hun Jang, Jae-Jin Song, Ho Sun Lee, Seung Ha Oh
Deafness induces many plastic changes in the auditory neural system. For instance, dendritic changes cause synaptic changes in neural cells. SMI-32, a monoclonal antibody reveals auditory areas and recognizes non-phosphorylated epitopes on medium- and high-molecular-weight subunits of neurofilament proteins in cortical pyramidal neuron dendrites. We investigated SMI-32-immunoreactive (-ir) protein levels in the auditory cortices of rats with induced unilateral and bilateral deafness. Adult male Sprague–Dawley rats were divided into unilateral deafness (UD), bilateral deafness (BD), and control groups. Deafness was induced by cochlear ablation. All rats were sacrificed, and the auditory cortices were harvested for real-time quantitative polymerase chain reaction (RT-qPCR) and western blot analyses at 2, 4, 6, and 12 weeks after deafness was induced. Immunohistochemical staining was performed to evaluate the location of SMI-32-ir neurons. Neurofilament heavy chain (NEFH) mRNA expression and SMI-32-ir protein levels were increased in the BD group. In particular, SMI-32-ir protein levels increased significantly 6 and 12 weeks after deafness was induced. In contrast, no significant changes in protein level were detected in the right or left auditory cortices at any time point in the UD group. NEFH mRNA level decreased at 4 weeks after deafness was induced in the UD group, but recovered thereafter. Taken together, BD induced plastic changes in the auditory cortex, whereas UD did not affect the auditory neural system sufficiently to show plastic changes, as measured by neurofilament protein level.
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via IFTTT
Source:Hearing Research
Author(s): Min-Hyun Park, Jeong Hun Jang, Jae-Jin Song, Ho Sun Lee, Seung Ha Oh
Deafness induces many plastic changes in the auditory neural system. For instance, dendritic changes cause synaptic changes in neural cells. SMI-32, a monoclonal antibody reveals auditory areas and recognizes non-phosphorylated epitopes on medium- and high-molecular-weight subunits of neurofilament proteins in cortical pyramidal neuron dendrites. We investigated SMI-32-immunoreactive (-ir) protein levels in the auditory cortices of rats with induced unilateral and bilateral deafness. Adult male Sprague–Dawley rats were divided into unilateral deafness (UD), bilateral deafness (BD), and control groups. Deafness was induced by cochlear ablation. All rats were sacrificed, and the auditory cortices were harvested for real-time quantitative polymerase chain reaction (RT-qPCR) and western blot analyses at 2, 4, 6, and 12 weeks after deafness was induced. Immunohistochemical staining was performed to evaluate the location of SMI-32-ir neurons. Neurofilament heavy chain (NEFH) mRNA expression and SMI-32-ir protein levels were increased in the BD group. In particular, SMI-32-ir protein levels increased significantly 6 and 12 weeks after deafness was induced. In contrast, no significant changes in protein level were detected in the right or left auditory cortices at any time point in the UD group. NEFH mRNA level decreased at 4 weeks after deafness was induced in the UD group, but recovered thereafter. Taken together, BD induced plastic changes in the auditory cortex, whereas UD did not affect the auditory neural system sufficiently to show plastic changes, as measured by neurofilament protein level.
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Neurofilament heavy chain expression and neuroplasticity in rat auditory cortex after unilateral and bilateral deafness
Publication date: Available online 22 July 2016
Source:Hearing Research
Author(s): Min-Hyun Park, Jeong Hun Jang, Jae-Jin Song, Ho Sun Lee, Seung Ha Oh
Deafness induces many plastic changes in the auditory neural system. For instance, dendritic changes cause synaptic changes in neural cells. SMI-32, a monoclonal antibody reveals auditory areas and recognizes non-phosphorylated epitopes on medium- and high-molecular-weight subunits of neurofilament proteins in cortical pyramidal neuron dendrites. We investigated SMI-32-immunoreactive (-ir) protein levels in the auditory cortices of rats with induced unilateral and bilateral deafness. Adult male Sprague–Dawley rats were divided into unilateral deafness (UD), bilateral deafness (BD), and control groups. Deafness was induced by cochlear ablation. All rats were sacrificed, and the auditory cortices were harvested for real-time quantitative polymerase chain reaction (RT-qPCR) and western blot analyses at 2, 4, 6, and 12 weeks after deafness was induced. Immunohistochemical staining was performed to evaluate the location of SMI-32-ir neurons. Neurofilament heavy chain (NEFH) mRNA expression and SMI-32-ir protein levels were increased in the BD group. In particular, SMI-32-ir protein levels increased significantly 6 and 12 weeks after deafness was induced. In contrast, no significant changes in protein level were detected in the right or left auditory cortices at any time point in the UD group. NEFH mRNA level decreased at 4 weeks after deafness was induced in the UD group, but recovered thereafter. Taken together, BD induced plastic changes in the auditory cortex, whereas UD did not affect the auditory neural system sufficiently to show plastic changes, as measured by neurofilament protein level.
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via IFTTT
Source:Hearing Research
Author(s): Min-Hyun Park, Jeong Hun Jang, Jae-Jin Song, Ho Sun Lee, Seung Ha Oh
Deafness induces many plastic changes in the auditory neural system. For instance, dendritic changes cause synaptic changes in neural cells. SMI-32, a monoclonal antibody reveals auditory areas and recognizes non-phosphorylated epitopes on medium- and high-molecular-weight subunits of neurofilament proteins in cortical pyramidal neuron dendrites. We investigated SMI-32-immunoreactive (-ir) protein levels in the auditory cortices of rats with induced unilateral and bilateral deafness. Adult male Sprague–Dawley rats were divided into unilateral deafness (UD), bilateral deafness (BD), and control groups. Deafness was induced by cochlear ablation. All rats were sacrificed, and the auditory cortices were harvested for real-time quantitative polymerase chain reaction (RT-qPCR) and western blot analyses at 2, 4, 6, and 12 weeks after deafness was induced. Immunohistochemical staining was performed to evaluate the location of SMI-32-ir neurons. Neurofilament heavy chain (NEFH) mRNA expression and SMI-32-ir protein levels were increased in the BD group. In particular, SMI-32-ir protein levels increased significantly 6 and 12 weeks after deafness was induced. In contrast, no significant changes in protein level were detected in the right or left auditory cortices at any time point in the UD group. NEFH mRNA level decreased at 4 weeks after deafness was induced in the UD group, but recovered thereafter. Taken together, BD induced plastic changes in the auditory cortex, whereas UD did not affect the auditory neural system sufficiently to show plastic changes, as measured by neurofilament protein level.
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