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Charles M Liberman - One of the best experts on this subject based on the ideXlab platform.
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cochlear synaptopathy changes sound evoked activity without changing spontaneous discharge in the mouse inferior colliculus
Frontiers in Systems Neuroscience, 2018Co-Authors: Luke A Shaheen, Charles M LibermanAbstract:Tinnitus and hyperacusis are life-disrupting perceptual abnormalities that are often preceded by acoustic Overexposure. Animal models of Overexposure have suggested a link between these phenomena and neural hyperactivity, i.e. elevated spontaneous rates (SRs) and sound-evoked responses. Prior work has focused on changes in central auditory responses, with less attention paid to the exact nature of the associated cochlear damage. The demonstration that acoustic Overexposure can cause cochlear neuropathy without permanent threshold elevation suggests cochlear neuropathy per se may be a key elicitor of neural hyperactivity. We addressed this hypothesis by recording responses in the mouse inferior colliculus (IC) following a bilateral, neuropathic noise exposure. One to three wks post-exposure, mean SRs were unchanged in mice recorded while awake, or under anesthesia. SRs were also unaffected by more intense, or unilateral exposures. These results suggest that neither neuropathy nor hair cell loss are sufficient to raise SRs in the IC, at least in 7-wk-old mice, one to three wks post exposure. However, it’s not clear whether our mice had tinnitus. Tone-evoked rate-level functions at the CF were steeper following exposure, specifically in the region of maximal neuropathy. Furthermore, suppression driven by off-CF tones and by ipsilateral noise were also reduced. Both changes were especially pronounced in neurons of awake mice. This neural hypersensitivity may manifest as behavioral hypersensitivity to sound - prior work reports that this same exposure causes elevated acoustic startle. Together, these results indicate that neuropathy may initiate a compensatory response in the central auditory system leading to the genesis of hyperacusis.
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effects of cochlear synaptopathy on spontaneous and sound evoked activity in the mouse inferior colliculus
bioRxiv, 2018Co-Authors: Luke A Shaheen, Charles M LibermanAbstract:Tinnitus and hyperacusis are life-disrupting perceptual abnormalities that are often preceded by acoustic Overexposure. Animal models of Overexposure have suggested a link between these phenomena and neural hyperactivity, i.e. elevated spontaneous rates (SRs) and sound-evoked responses. Prior work has focused on changes in central auditory responses, with less attention paid to the exact nature of the associated peripheral damage. The demonstration that acoustic Overexposure can cause cochlear nerve damage without permanent threshold elevation suggests this type of peripheral damage may be a key elicitor of tinnitus and hyperacusis in humans with normal audiograms. We addressed this idea by recording responses in the mouse inferior colliculus (IC) following a bilateral, neuropathic noise exposure. Two weeks post-exposure, mean SRs were unchanged in mice recorded while awake, or under anesthesia. SRs were also unaffected by more intense, or unilateral exposures. These results suggest that neither neuropathy nor hair cell loss are sufficient to raise SRs in the IC, at least in mice. However, it is not clear whether our mice had tinnitus. Tone-evoked rate-level functions at the CF were steeper following exposure, specifically in the region of maximal neuropathy. Furthermore, inhibition driven by off-CF tones and by ipsilateral noise were also reduced. Both changes were especially pronounced in neurons of awake mice. These findings align with prior reports of elevated acoustic startle in neuropathic mice, and indicate that neuropathy may initiate a compensatory response in the central auditory system leading to the genesis of hyperacusis.
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Image_2_Cochlear Synaptopathy Changes Sound-Evoked Activity Without Changing Spontaneous Discharge in the Mouse Inferior Colliculus.TIF
2018Co-Authors: Luke A Shaheen, Charles M LibermanAbstract:Tinnitus and hyperacusis are life-disrupting perceptual abnormalities that are often preceded by acoustic Overexposure. Animal models of Overexposure have suggested a link between these phenomena and neural hyperactivity, i.e., elevated spontaneous rates (SRs) and sound-evoked responses. Prior work has focused on changes in central auditory responses, with less attention paid to the exact nature of the associated cochlear damage. The demonstration that acoustic Overexposure can cause cochlear neuropathy without permanent threshold elevation suggests cochlear neuropathy per se may be a key elicitor of neural hyperactivity. We addressed this hypothesis by recording responses in the mouse inferior colliculus (IC) following a bilateral, neuropathic noise exposure. One to three weeks post-exposure, mean SRs were unchanged in mice recorded while awake, or under anesthesia. SRs were also unaffected by more intense, or unilateral exposures. These results suggest that neither neuropathy nor hair cell loss are sufficient to raise SRs in the IC, at least in 7-week-old mice, 1–3 weeks post exposure. However, it is not clear whether our mice had tinnitus. Tone-evoked rate-level functions at the CF were steeper following exposure, specifically in the region of maximal neuropathy. Furthermore, suppression driven by off-CF tones and by ipsilateral noise were reduced. Both changes were especially pronounced in neurons of awake mice. This neural hypersensitivity may manifest as behavioral hypersensitivity to sound – prior work reports that this same exposure causes elevated acoustic startle. Together, these results indicate that neuropathy may initiate a compensatory response in the central auditory system leading to the genesis of hyperacusis.
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Cochlear Synaptopathy Changes Sound-Evoked Activity Without Changing Spontaneous Discharge in the Mouse Inferior Colliculus
Frontiers Media S.A., 2018Co-Authors: Luke A Shaheen, Charles M LibermanAbstract:Tinnitus and hyperacusis are life-disrupting perceptual abnormalities that are often preceded by acoustic Overexposure. Animal models of Overexposure have suggested a link between these phenomena and neural hyperactivity, i.e., elevated spontaneous rates (SRs) and sound-evoked responses. Prior work has focused on changes in central auditory responses, with less attention paid to the exact nature of the associated cochlear damage. The demonstration that acoustic Overexposure can cause cochlear neuropathy without permanent threshold elevation suggests cochlear neuropathy per se may be a key elicitor of neural hyperactivity. We addressed this hypothesis by recording responses in the mouse inferior colliculus (IC) following a bilateral, neuropathic noise exposure. One to three weeks post-exposure, mean SRs were unchanged in mice recorded while awake, or under anesthesia. SRs were also unaffected by more intense, or unilateral exposures. These results suggest that neither neuropathy nor hair cell loss are sufficient to raise SRs in the IC, at least in 7-week-old mice, 1–3 weeks post exposure. However, it is not clear whether our mice had tinnitus. Tone-evoked rate-level functions at the CF were steeper following exposure, specifically in the region of maximal neuropathy. Furthermore, suppression driven by off-CF tones and by ipsilateral noise were reduced. Both changes were especially pronounced in neurons of awake mice. This neural hypersensitivity may manifest as behavioral hypersensitivity to sound – prior work reports that this same exposure causes elevated acoustic startle. Together, these results indicate that neuropathy may initiate a compensatory response in the central auditory system leading to the genesis of hyperacusis
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round window delivery of neurotrophin 3 regenerates cochlear synapses after acoustic Overexposure
Scientific Reports, 2016Co-Authors: Charles M Liberman, Jun Suzuki, Gabriel CorfasAbstract:In acquired sensorineural hearing loss, such as that produced by noise or aging, there can be massive loss of the synaptic connections between cochlear sensory cells and primary sensory neurons, without loss of the sensory cells themselves. Because the cell bodies and central projections of these cochlear neurons survive for months to years, there is a long therapeutic window in which to re-establish functional connections and improve hearing ability. Here we show in noise-exposed mice that local delivery of neurotrophin-3 (NT-3) to the round window niche, 24 hours after an exposure that causes an immediate loss of up to 50% loss of synapses in the cochlear basal region, can regenerate pre- and post-synaptic elements at the hair cell / cochlear nerve interface. This synaptic regeneration, as documented by confocal microscopy of immunostained cochlear sensory epithelia, was coupled with a corresponding functional recovery, as seen in the suprathreshold amplitude of auditory brainstem response Wave 1. Cochlear delivery of neurotrophins in humans is likely achievable as an office procedure via transtympanic injection, making our results highly significant in a translational context.
Kyung Chul Yoon - One of the best experts on this subject based on the ideXlab platform.
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influence of light emitting diode derived blue light Overexposure on mouse ocular surface
PLOS ONE, 2016Co-Authors: Hyo Seok Lee, Lian Cui, Ji Suk Choi, Joohee Choi, Ga Eon Kim, Won Choi, Kyung Chul YoonAbstract:Purpose To investigate the influence of Overexposure to light emitting diode (LED)-derived light with various wavelengths on mouse ocular surface. Methods LEDs with various wavelengths were used to irradiate C57BL/6 mice at an energy dose of 50 J/cm2, twice a day, for 10 consecutive days. The red, green, and blue groups represented wavelengths of 630 nm, 525 nm, and 410 nm, respectively. The untouched group (UT) was not exposed to LED light and served as the untreated control. Tear volume, tear film break-up time (TBUT), and corneal fluorescein staining scores were measured on days 1, 3, 5, 7, and 10. Levels of interferon (IFN)-γ, interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α were measured in the cornea and conjunctiva using a multiplex immunobead assay at day 10. Levels of malondialdehyde (MDA) were measured with an enzyme-linked immunosorbent assay. Flow cytometry, 2’7’-dichlorofluorescein diacetate (DCF-DA) assay, histologic analysis, immunohistochemistry with 4-hydroxynonenal, and terminal deoxynucleotidyl transferase-mediated dUTP-nick end labeling (TUNEL) staining were also performed. Results TBUT of the blue group showed significant decreases at days 7 and 10, compared with the UT and red groups. Corneal fluorescein staining scores significantly increased in the blue group when compared with UT, red, and green groups at days 5, 7, and 10. A significant increase in the corneal levels of IL-1β and IL-6 was observed in the blue group, compared with the other groups. The blue group showed significantly increased reactive oxygen species production in the DCF-DA assay and increased inflammatory T cells in the flow cytometry. A significantly increased TUNEL positive cells was identified in the blue group. Conclusions Overexposure to blue light with short wavelengths can induce oxidative damage and apoptosis to the cornea, which may manifest as increased ocular surface inflammation and resultant dry eye.
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Influence of Light Emitting Diode-Derived Blue Light Overexposure on Mouse Ocular Surface.
Public Library of Science (PLoS), 2024Co-Authors: Hyo Seok Lee, Lian Cui, Ji Suk Choi, Joohee Choi, Ga Eon Kim, Won Choi, Kyung Chul YoonAbstract:To investigate the influence of Overexposure to light emitting diode (LED)-derived light with various wavelengths on mouse ocular surface.LEDs with various wavelengths were used to irradiate C57BL/6 mice at an energy dose of 50 J/cm2, twice a day, for 10 consecutive days. The red, green, and blue groups represented wavelengths of 630 nm, 525 nm, and 410 nm, respectively. The untouched group (UT) was not exposed to LED light and served as the untreated control. Tear volume, tear film break-up time (TBUT), and corneal fluorescein staining scores were measured on days 1, 3, 5, 7, and 10. Levels of interferon (IFN)-γ, interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α were measured in the cornea and conjunctiva using a multiplex immunobead assay at day 10. Levels of malondialdehyde (MDA) were measured with an enzyme-linked immunosorbent assay. Flow cytometry, 2'7'-dichlorofluorescein diacetate (DCF-DA) assay, histologic analysis, immunohistochemistry with 4-hydroxynonenal, and terminal deoxynucleotidyl transferase-mediated dUTP-nick end labeling (TUNEL) staining were also performed.TBUT of the blue group showed significant decreases at days 7 and 10, compared with the UT and red groups. Corneal fluorescein staining scores significantly increased in the blue group when compared with UT, red, and green groups at days 5, 7, and 10. A significant increase in the corneal levels of IL-1β and IL-6 was observed in the blue group, compared with the other groups. The blue group showed significantly increased reactive oxygen species production in the DCF-DA assay and increased inflammatory T cells in the flow cytometry. A significantly increased TUNEL positive cells was identified in the blue group.Overexposure to blue light with short wavelengths can induce oxidative damage and apoptosis to the cornea, which may manifest as increased ocular surface inflammation and resultant dry eye
A L Fowden - One of the best experts on this subject based on the ideXlab platform.
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neonatal glucocorticoid Overexposure programs pituitary adrenal function in ponies
Domestic Animal Endocrinology, 2015Co-Authors: Juanita K Jellyman, O A Valenzuela, V L Allen, A J Forhead, N B Holdstock, A L FowdenAbstract:The present study tested the hypothesis that Overexposure to endogenous glucocorticoids in neonatal life alters the reactivity of the hypothalamic-pituitary-adrenal (HPA) axis in ponies at 1 and 2 yr of age. Newborn foals received saline (0.9% NaCl, n = 8, control) or long-acting adrenocorticotropic hormone (ACTH1-24) (Depot Synacthen 0.125 mg intramuscularly twice daily, n = 9) for 5 d after birth to raise cortisol concentrations 5- to 6-fold. At 1 and 2 yr of age, HPA axis function was assessed by bolus administration of short-acting ACTH1-24 (1 μg/kg intravenous) and insulin (0.5 U/kg intravenous) to induce hypoglycemic on separate days. Arterial blood samples were taken at 5 to 30-min intervals before and after drug administration to measure plasma ACTH and/or cortisol concentrations. There were no differences in the basal plasma ACTH or cortisol concentrations or in the cortisol response to exogenous ACTH1-24 with neonatal treatment or age. At 1 and 2 yr of age, the increment in plasma ACTH but not cortisol at 60 min in response to insulin-induced hypoglycemia was greater in ponies treated neonatally with ACTH than saline (P < 0.05). Neonatal cortisol Overexposure induced by neonatal ACTH treatment, therefore, alters functioning of the HPA axis in adult ponies.
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hypothalamic pituitary adrenal axis function in pony foals after neonatal acth induced glucocorticoid Overexposure
Equine Veterinary Journal, 2012Co-Authors: Juanita K Jellyman, V L Allen, A J Forhead, N B Holdstock, A L FowdenAbstract:Summary Reasons for performing the study: The effects of Overexposure to glucocorticoids during early life of the foal on the subsequent HPA programming of the hypothalamic–pituitary–adrenal axis are unknown. Objectives: To test the hypotheses that excess glucocorticoid exposure in early life subsequently increases both basal plasma concentrations of cortisol and the adrenocortical responsiveness to exogenous adrenocorticotropic hormone (ACTH). Methods: Foals received either saline (0.9% NaCl, n = 9) or long-acting ACTH (0.125 mg i.m. b.i.d., n = 6) for 5 days from Day 1 to increase endogenous cortisol concentrations. Long-term indwelling catheters were inserted under local anaesthesia into the jugular veins of foals aged 2 and 12 weeks. After recovery, short-acting ACTH1-24 was given as a single i.v. injection (2 µg/kg bwt) and blood samples were taken at 5–30 min intervals before and after ACTH administration to measure plasma cortisol concentrations. Results: Basal plasma cortisol concentrations were higher in ACTH- than in saline-treated foals at age 3 weeks, but not at 13 weeks. There were no significant differences in either the time profile or the area under the cortisol curve in response to ACTH between the 2 groups. Conclusions: These data suggest that ACTH-induced Overexposure to glucocorticoids during early post natal life of the foal does not have a programming effect on HPA axis function at 13 weeks. In foals, the effects of ACTH-induced Overexposure to glucocorticoids, if any, may not become apparent until much later in life in a long-lived species such as the horse. Potential relevance: These studies suggest that clinical and other stressful conditions that raise plasma cortisol concentrations during early life are unlikely to programme cardiovascular and metabolic function in horses in the short term.
Hyo Seok Lee - One of the best experts on this subject based on the ideXlab platform.
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influence of light emitting diode derived blue light Overexposure on mouse ocular surface
PLOS ONE, 2016Co-Authors: Hyo Seok Lee, Lian Cui, Ji Suk Choi, Joohee Choi, Ga Eon Kim, Won Choi, Kyung Chul YoonAbstract:Purpose To investigate the influence of Overexposure to light emitting diode (LED)-derived light with various wavelengths on mouse ocular surface. Methods LEDs with various wavelengths were used to irradiate C57BL/6 mice at an energy dose of 50 J/cm2, twice a day, for 10 consecutive days. The red, green, and blue groups represented wavelengths of 630 nm, 525 nm, and 410 nm, respectively. The untouched group (UT) was not exposed to LED light and served as the untreated control. Tear volume, tear film break-up time (TBUT), and corneal fluorescein staining scores were measured on days 1, 3, 5, 7, and 10. Levels of interferon (IFN)-γ, interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α were measured in the cornea and conjunctiva using a multiplex immunobead assay at day 10. Levels of malondialdehyde (MDA) were measured with an enzyme-linked immunosorbent assay. Flow cytometry, 2’7’-dichlorofluorescein diacetate (DCF-DA) assay, histologic analysis, immunohistochemistry with 4-hydroxynonenal, and terminal deoxynucleotidyl transferase-mediated dUTP-nick end labeling (TUNEL) staining were also performed. Results TBUT of the blue group showed significant decreases at days 7 and 10, compared with the UT and red groups. Corneal fluorescein staining scores significantly increased in the blue group when compared with UT, red, and green groups at days 5, 7, and 10. A significant increase in the corneal levels of IL-1β and IL-6 was observed in the blue group, compared with the other groups. The blue group showed significantly increased reactive oxygen species production in the DCF-DA assay and increased inflammatory T cells in the flow cytometry. A significantly increased TUNEL positive cells was identified in the blue group. Conclusions Overexposure to blue light with short wavelengths can induce oxidative damage and apoptosis to the cornea, which may manifest as increased ocular surface inflammation and resultant dry eye.
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Influence of Light Emitting Diode-Derived Blue Light Overexposure on Mouse Ocular Surface.
Public Library of Science (PLoS), 2024Co-Authors: Hyo Seok Lee, Lian Cui, Ji Suk Choi, Joohee Choi, Ga Eon Kim, Won Choi, Kyung Chul YoonAbstract:To investigate the influence of Overexposure to light emitting diode (LED)-derived light with various wavelengths on mouse ocular surface.LEDs with various wavelengths were used to irradiate C57BL/6 mice at an energy dose of 50 J/cm2, twice a day, for 10 consecutive days. The red, green, and blue groups represented wavelengths of 630 nm, 525 nm, and 410 nm, respectively. The untouched group (UT) was not exposed to LED light and served as the untreated control. Tear volume, tear film break-up time (TBUT), and corneal fluorescein staining scores were measured on days 1, 3, 5, 7, and 10. Levels of interferon (IFN)-γ, interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α were measured in the cornea and conjunctiva using a multiplex immunobead assay at day 10. Levels of malondialdehyde (MDA) were measured with an enzyme-linked immunosorbent assay. Flow cytometry, 2'7'-dichlorofluorescein diacetate (DCF-DA) assay, histologic analysis, immunohistochemistry with 4-hydroxynonenal, and terminal deoxynucleotidyl transferase-mediated dUTP-nick end labeling (TUNEL) staining were also performed.TBUT of the blue group showed significant decreases at days 7 and 10, compared with the UT and red groups. Corneal fluorescein staining scores significantly increased in the blue group when compared with UT, red, and green groups at days 5, 7, and 10. A significant increase in the corneal levels of IL-1β and IL-6 was observed in the blue group, compared with the other groups. The blue group showed significantly increased reactive oxygen species production in the DCF-DA assay and increased inflammatory T cells in the flow cytometry. A significantly increased TUNEL positive cells was identified in the blue group.Overexposure to blue light with short wavelengths can induce oxidative damage and apoptosis to the cornea, which may manifest as increased ocular surface inflammation and resultant dry eye
Huigao Duan - One of the best experts on this subject based on the ideXlab platform.
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preparing patterned carbonaceous nanostructures directly by Overexposure of pmma using electron beam lithography
Nanotechnology, 2009Co-Authors: Huigao Duan, Jianguo Zhao, Yongzhe Zhang, Erqing Xie, Li HanAbstract:The Overexposure process of poly(methyl methacrylate) (PMMA) was studied in detail using electron-beam lithography. It was found that PMMA films could be directly patterned without development due to the electron-beam-induced collapse of PMMA macromolecular chains. By analyzing the evolution of surface morphologies and compositions of the overexposed PMMA films, it was also found that the transformation of PMMA from positive to negative resist was a carbonization process, so patterned carbonaceous nanostructures could be prepared directly by Overexposure of PMMA using electron-beam lithography. This simple one-step process for directly obtaining patterned carbonaceous nanostructures has promising potential application as a tool to make masks and templates, nanoelectrodes, and building blocks for MEMS and nanophotonic devices.
