St. Jude Children's Research Hospital scientists have identified a small, drug-like molecule that inhibits the function of a "disordered" protein in research that may advance a novel approach to...
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Σάββατο 12 Δεκεμβρίου 2015
Top priorities named in hearing loss research
Experts have published a list of the most urgent priorities for researching a debilitating condition that affects more than 10 million people in the UK.
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How cells in the developing ear 'practice' hearing
Before the fluid of the middle ear drains and sound waves penetrate for the first time, the inner ear cells of newborn rodents practice for their big debut.
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Sound deprivation leads to irreversible hearing loss
Researchers show that chronic conductive hearing loss leads to cochlear degeneration.
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Adding antiangiogenesis increases effectiveness of radiation against NF2-associated tumors
Vascular normalization allows reduction of radiation dosage, potentially reducing nerve damage, in animal models.
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An effective integrated reproductive strategy for hearing loss by researches from China
Hearing impairment is a major public health problem in the world, affecting over 5% of the world's population - 360 million people, including 328 million adults and 32 million children.
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New project to help tackle tinnitus
Anglia Ruskin teams up with Swedish university to develop online programme Anglia Ruskin University has launched a new internet-based project to help people suffering from a distressing and...
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Protein movement of hair bundles in the inner ear may preserve hearing for life
Hearing is made possible when hair bundles protruding from the tops of hair cells capture the energy of sound waves, converting them into electrical signals that stimulate the auditory nerve to the...
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Are faulty mitochondria to blame for hereditary hearing loss?
The search for genes involved in premature hearing loss successfully pins down another culprit. This time, the genetic miscreant was found within mitochondrial DNA.
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Noise-induced hearing loss -- genetic cause and mechanism discovered
Scientists at the Institut Pasteur, Inserm, the Collège de France and Pierre & Marie Curie University, working closely with scientists at the University of Auvergne, have recently discovered the...
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UK charity calls for more action to tackle hearing loss as number of people affected rises to 11 million
There are now 11 million people (one in six) in the UK living with hearing loss according to a new report from the national charity Action on Hearing Loss (formerly RNID), with the number...
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Chemotherapy-induced hearing loss affects cognition in pediatric brain tumor survivors
More children are surviving malignant brain tumors than in the past, thanks to the use of intense treatments using platinum-based chemotherapy (cisplatin and high-dose carboplatin).
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Can we unconsciously 'hear' distance?
Because sound travels much more slowly than light, we can often see distant events before we hear them.
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Helping kids hear better
Hearing well impacts every area of a child's life -- language and speech development, social skills, and future academic and life success.
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Inner ear gene discovery offers clues about restoring hearing, balance
A gene study of mice gives new clues to suggest it may be possible to regenerate hair cells in the inner ear, loss of which impairs hearing and balance.
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Negative feelings about aging can affect hearing and memory in older people
Older adults' feelings about getting older - often rooted in own and others' stereotypical views on aging and failing ability - affect their hearing and memory, new study shows.
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Is seeing believing? People are not good at identifying where sights, sounds originate
Study by UCLA psychologists reveals that our senses are far from flawless.Our vision and hearing aren't as reliable as we might think, according to a study by life scientists at UCLA.
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Stereotypes around aging can negatively impact memory and hearing
A study led by researchers at the University of Toronto shows that when older adults feel negatively about aging, they may lack confidence in their abilities to hear and remember things, and perform...
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Why focusing on a visual task will make us deaf to our surroundings
Concentrating attention on a visual task can render you momentarily 'deaf' to sounds at normal levels, reports a new UCL study funded by the Wellcome Trust.
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Disclosure strategies may improve communication for those with hearing loss
Massachusetts Eye and Ear researchers surveyed 337 patients with hearing loss to better understand the language they use with communication partners to disclose their disability.
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Early progress reported in designing drugs that target 'disordered' proteins
St. Jude Children's Research Hospital scientists have identified a small, drug-like molecule that inhibits the function of a "disordered" protein in research that may advance a novel approach to...
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Top priorities named in hearing loss research
Experts have published a list of the most urgent priorities for researching a debilitating condition that affects more than 10 million people in the UK.
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How cells in the developing ear 'practice' hearing
Before the fluid of the middle ear drains and sound waves penetrate for the first time, the inner ear cells of newborn rodents practice for their big debut.
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Sound deprivation leads to irreversible hearing loss
Researchers show that chronic conductive hearing loss leads to cochlear degeneration.
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Adding antiangiogenesis increases effectiveness of radiation against NF2-associated tumors
Vascular normalization allows reduction of radiation dosage, potentially reducing nerve damage, in animal models.
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An effective integrated reproductive strategy for hearing loss by researches from China
Hearing impairment is a major public health problem in the world, affecting over 5% of the world's population - 360 million people, including 328 million adults and 32 million children.
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New project to help tackle tinnitus
Anglia Ruskin teams up with Swedish university to develop online programme Anglia Ruskin University has launched a new internet-based project to help people suffering from a distressing and...
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Protein movement of hair bundles in the inner ear may preserve hearing for life
Hearing is made possible when hair bundles protruding from the tops of hair cells capture the energy of sound waves, converting them into electrical signals that stimulate the auditory nerve to the...
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Are faulty mitochondria to blame for hereditary hearing loss?
The search for genes involved in premature hearing loss successfully pins down another culprit. This time, the genetic miscreant was found within mitochondrial DNA.
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Noise-induced hearing loss -- genetic cause and mechanism discovered
Scientists at the Institut Pasteur, Inserm, the Collège de France and Pierre & Marie Curie University, working closely with scientists at the University of Auvergne, have recently discovered the...
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UK charity calls for more action to tackle hearing loss as number of people affected rises to 11 million
There are now 11 million people (one in six) in the UK living with hearing loss according to a new report from the national charity Action on Hearing Loss (formerly RNID), with the number...
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Chemotherapy-induced hearing loss affects cognition in pediatric brain tumor survivors
More children are surviving malignant brain tumors than in the past, thanks to the use of intense treatments using platinum-based chemotherapy (cisplatin and high-dose carboplatin).
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Can we unconsciously 'hear' distance?
Because sound travels much more slowly than light, we can often see distant events before we hear them.
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Helping kids hear better
Hearing well impacts every area of a child's life -- language and speech development, social skills, and future academic and life success.
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Inner ear gene discovery offers clues about restoring hearing, balance
A gene study of mice gives new clues to suggest it may be possible to regenerate hair cells in the inner ear, loss of which impairs hearing and balance.
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Hair cell regeneration or the expression of related factors that regulate the fate specification of supporting cells in the cochlear ducts of embryonic and posthatch chickens
Publication date: Available online 12 December 2015
Source:Hearing Research
Author(s): Lingling Jiang, Ran Jin, Jincao Xu, Yubin Ji, Meiguang Zhang, Xuebo Zhang, Xinwen Zhang, Zhongming Han, Shaoju Zeng
Hair cells in posthatch chickens regenerate spontaneously through mitosis or the transdifferentiation of supporting cells in response to antibiotic injury. However, how embryonic chicken cochleae respond to antibiotic treatment remains unknown. This study is the first to indicate that unlike hair cells in posthatch chickens, the auditory epithelium was free from antibiotic injury (25-250 mg gentamicin/kg) in embryonic chickens, although FITC-conjugated gentamicin actually reached embryonic hair cells. Next, we examined and counted the cells and performed labeling for BrdU, Sox2, Atoh1/Math1, PV or p27kip1 (triple or double labeling) in the injured cochlea ducts after gentamicin treatment at 2 hours (h), 15 h, 24 h, 2 days (d), 3 d and 7 d after BrdU treatment in posthatch chickens. Our results indicated that following gentamicin administration, proliferating cells (BrdU+) were labeled for Atoh1/Math1 in the damaged areas 3d after gentamicin administration, whereas hair cells (PV+) renewed through mitosis (BrdU+) or direct transdifferentiation (BrdU-) were evident only after 5 d of gentamicin administration. In addition, Sox2 expression was up-regulated in triggered supporting cells at an early stage of regeneration, but stopped at the advent of mature hair cells. Our study also indicated that p27kip1 was expressed in both hair cells and supporting cells but was down-regulated in a subgroup of the supporting cells that gave rise to hair cells. These data and the obtained dynamic changes of the cells labeled for BrdU, Sox2, Atoh1/Math1, PV or p27kip1 are useful for understanding supporting cell behaviors and their fate specification during hair cell regeneration.
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Source:Hearing Research
Author(s): Lingling Jiang, Ran Jin, Jincao Xu, Yubin Ji, Meiguang Zhang, Xuebo Zhang, Xinwen Zhang, Zhongming Han, Shaoju Zeng
Hair cells in posthatch chickens regenerate spontaneously through mitosis or the transdifferentiation of supporting cells in response to antibiotic injury. However, how embryonic chicken cochleae respond to antibiotic treatment remains unknown. This study is the first to indicate that unlike hair cells in posthatch chickens, the auditory epithelium was free from antibiotic injury (25-250 mg gentamicin/kg) in embryonic chickens, although FITC-conjugated gentamicin actually reached embryonic hair cells. Next, we examined and counted the cells and performed labeling for BrdU, Sox2, Atoh1/Math1, PV or p27kip1 (triple or double labeling) in the injured cochlea ducts after gentamicin treatment at 2 hours (h), 15 h, 24 h, 2 days (d), 3 d and 7 d after BrdU treatment in posthatch chickens. Our results indicated that following gentamicin administration, proliferating cells (BrdU+) were labeled for Atoh1/Math1 in the damaged areas 3d after gentamicin administration, whereas hair cells (PV+) renewed through mitosis (BrdU+) or direct transdifferentiation (BrdU-) were evident only after 5 d of gentamicin administration. In addition, Sox2 expression was up-regulated in triggered supporting cells at an early stage of regeneration, but stopped at the advent of mature hair cells. Our study also indicated that p27kip1 was expressed in both hair cells and supporting cells but was down-regulated in a subgroup of the supporting cells that gave rise to hair cells. These data and the obtained dynamic changes of the cells labeled for BrdU, Sox2, Atoh1/Math1, PV or p27kip1 are useful for understanding supporting cell behaviors and their fate specification during hair cell regeneration.
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Sodium salicylate potentiates the GABAB-GIRK pathway to suppress rebound depolarization in neurons of the rat's medial geniculate body
Publication date: Available online 12 December 2015
Source:Hearing Research
Author(s): Xin-Xing Wang, Yan Jin, Bin Luo, Jing-Wu Sun, Jinsheng Zhang, Ming Wang, Lin Chen
Rebound depolarization (RD) is a voltage response to the offset from pre-hyperpolarization of neuronal membrane potential, which manifests a particular form of the postsynaptic membrane potential response to inhibitory presynaptic inputs. We previously demonstrated that sodium salicylate (NaSal), a tinnitus inducer, can drastically suppress the RD in neurons of rat medial geniculate body (MGB) (Su et al, 2012, PLoS ONE 7, e46969). The purpose of the present study was to investigate the underlying cellular mechanism by using whole-cell patch-clamp recordings in rat MGB slices. NaSal (1.4 mM) had no effects on the current mediated by T-type Ca2+ channels, indicating that it does not target these channels to suppress the RD. Instead, NaSal was shown to hyperpolarize the resting membrane potential to suppress the RD. NaSal had no effects on the current mediated by hyperpolarization-activated cyclic nucleotide-gated (HCN) channels, indicating that it does not target these channels to hyperpolarize the resting membrane potential. NaSal induced an outward leak current that could be abolished by CGP55845, a GABAB receptor blocker, or respectively by Ba2+ and Tertiapin-Q, blockers for G-protein-gated inwardly rectifying potassium (GIRK) channels, indicating that NaSal potentiates the GABAB-GIRK pathway to hyperpolarize the resting membrane potential. Our study demonstrates that NaSal targets GABAB receptors to alter functional behaviors of MGB neurons, which may be implicated in NaSal-induced tinnitus.
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Source:Hearing Research
Author(s): Xin-Xing Wang, Yan Jin, Bin Luo, Jing-Wu Sun, Jinsheng Zhang, Ming Wang, Lin Chen
Rebound depolarization (RD) is a voltage response to the offset from pre-hyperpolarization of neuronal membrane potential, which manifests a particular form of the postsynaptic membrane potential response to inhibitory presynaptic inputs. We previously demonstrated that sodium salicylate (NaSal), a tinnitus inducer, can drastically suppress the RD in neurons of rat medial geniculate body (MGB) (Su et al, 2012, PLoS ONE 7, e46969). The purpose of the present study was to investigate the underlying cellular mechanism by using whole-cell patch-clamp recordings in rat MGB slices. NaSal (1.4 mM) had no effects on the current mediated by T-type Ca2+ channels, indicating that it does not target these channels to suppress the RD. Instead, NaSal was shown to hyperpolarize the resting membrane potential to suppress the RD. NaSal had no effects on the current mediated by hyperpolarization-activated cyclic nucleotide-gated (HCN) channels, indicating that it does not target these channels to hyperpolarize the resting membrane potential. NaSal induced an outward leak current that could be abolished by CGP55845, a GABAB receptor blocker, or respectively by Ba2+ and Tertiapin-Q, blockers for G-protein-gated inwardly rectifying potassium (GIRK) channels, indicating that NaSal potentiates the GABAB-GIRK pathway to hyperpolarize the resting membrane potential. Our study demonstrates that NaSal targets GABAB receptors to alter functional behaviors of MGB neurons, which may be implicated in NaSal-induced tinnitus.
Graphical abstract
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Modulation of Auditory Brainstem Responses by Serotonin and Specific Serotonin Receptors
Publication date: Available online 12 December 2015
Source:Hearing Research
Author(s): Melissa A. Papesh, Laura M. Hurley
The neuromodulator serotonin is found throughout the auditory system from the cochlea to the cortex. Although effects of serotonin have been reported at the level of single neurons in many brainstem nuclei, how these effects correspond to more integrated measures of auditory processing has not been well-explored. In the present study, we aimed to characterize the effects of serotonin on far-field auditory brainstem responses (ABR) across a wide range of stimulus frequencies and intensities. Using a mouse model, we investigated the consequences of systemic serotonin depletion, as well as the selective stimulation and suppression of the 5-HT1 and 5-HT2 receptors, on ABR latency and amplitude. Stimuli included tone pips spanning four octaves presented over a forty dB range. Depletion of serotonin reduced the ABR latencies in Wave II and later waves, suggesting that serotonergic effects occur as early as the cochlear nucleus. Further, agonists and antagonists of specific serotonergic receptors had different profiles of effects on ABR latencies and amplitudes across waves and frequencies, suggestive of distinct effects of these agents on auditory processing. Finally, most serotonergic effects were more pronounced at lower ABR frequencies, suggesting larger or more directional modulation of low-frequency processing. This is the first study to describe the effects of serotonin on ABR responses across a wide range of stimulus frequencies and amplitudes, and it presents an important step in understanding how serotonergic modulation of auditory brainstem processing may contribute to modulation of auditory perception.
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Source:Hearing Research
Author(s): Melissa A. Papesh, Laura M. Hurley
The neuromodulator serotonin is found throughout the auditory system from the cochlea to the cortex. Although effects of serotonin have been reported at the level of single neurons in many brainstem nuclei, how these effects correspond to more integrated measures of auditory processing has not been well-explored. In the present study, we aimed to characterize the effects of serotonin on far-field auditory brainstem responses (ABR) across a wide range of stimulus frequencies and intensities. Using a mouse model, we investigated the consequences of systemic serotonin depletion, as well as the selective stimulation and suppression of the 5-HT1 and 5-HT2 receptors, on ABR latency and amplitude. Stimuli included tone pips spanning four octaves presented over a forty dB range. Depletion of serotonin reduced the ABR latencies in Wave II and later waves, suggesting that serotonergic effects occur as early as the cochlear nucleus. Further, agonists and antagonists of specific serotonergic receptors had different profiles of effects on ABR latencies and amplitudes across waves and frequencies, suggestive of distinct effects of these agents on auditory processing. Finally, most serotonergic effects were more pronounced at lower ABR frequencies, suggesting larger or more directional modulation of low-frequency processing. This is the first study to describe the effects of serotonin on ABR responses across a wide range of stimulus frequencies and amplitudes, and it presents an important step in understanding how serotonergic modulation of auditory brainstem processing may contribute to modulation of auditory perception.
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Hair cell regeneration or the expression of related factors that regulate the fate specification of supporting cells in the cochlear ducts of embryonic and posthatch chickens
Publication date: Available online 12 December 2015
Source:Hearing Research
Author(s): Lingling Jiang, Ran Jin, Jincao Xu, Yubin Ji, Meiguang Zhang, Xuebo Zhang, Xinwen Zhang, Zhongming Han, Shaoju Zeng
Hair cells in posthatch chickens regenerate spontaneously through mitosis or the transdifferentiation of supporting cells in response to antibiotic injury. However, how embryonic chicken cochleae respond to antibiotic treatment remains unknown. This study is the first to indicate that unlike hair cells in posthatch chickens, the auditory epithelium was free from antibiotic injury (25-250 mg gentamicin/kg) in embryonic chickens, although FITC-conjugated gentamicin actually reached embryonic hair cells. Next, we examined and counted the cells and performed labeling for BrdU, Sox2, Atoh1/Math1, PV or p27kip1 (triple or double labeling) in the injured cochlea ducts after gentamicin treatment at 2 hours (h), 15 h, 24 h, 2 days (d), 3 d and 7 d after BrdU treatment in posthatch chickens. Our results indicated that following gentamicin administration, proliferating cells (BrdU+) were labeled for Atoh1/Math1 in the damaged areas 3d after gentamicin administration, whereas hair cells (PV+) renewed through mitosis (BrdU+) or direct transdifferentiation (BrdU-) were evident only after 5 d of gentamicin administration. In addition, Sox2 expression was up-regulated in triggered supporting cells at an early stage of regeneration, but stopped at the advent of mature hair cells. Our study also indicated that p27kip1 was expressed in both hair cells and supporting cells but was down-regulated in a subgroup of the supporting cells that gave rise to hair cells. These data and the obtained dynamic changes of the cells labeled for BrdU, Sox2, Atoh1/Math1, PV or p27kip1 are useful for understanding supporting cell behaviors and their fate specification during hair cell regeneration.
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Source:Hearing Research
Author(s): Lingling Jiang, Ran Jin, Jincao Xu, Yubin Ji, Meiguang Zhang, Xuebo Zhang, Xinwen Zhang, Zhongming Han, Shaoju Zeng
Hair cells in posthatch chickens regenerate spontaneously through mitosis or the transdifferentiation of supporting cells in response to antibiotic injury. However, how embryonic chicken cochleae respond to antibiotic treatment remains unknown. This study is the first to indicate that unlike hair cells in posthatch chickens, the auditory epithelium was free from antibiotic injury (25-250 mg gentamicin/kg) in embryonic chickens, although FITC-conjugated gentamicin actually reached embryonic hair cells. Next, we examined and counted the cells and performed labeling for BrdU, Sox2, Atoh1/Math1, PV or p27kip1 (triple or double labeling) in the injured cochlea ducts after gentamicin treatment at 2 hours (h), 15 h, 24 h, 2 days (d), 3 d and 7 d after BrdU treatment in posthatch chickens. Our results indicated that following gentamicin administration, proliferating cells (BrdU+) were labeled for Atoh1/Math1 in the damaged areas 3d after gentamicin administration, whereas hair cells (PV+) renewed through mitosis (BrdU+) or direct transdifferentiation (BrdU-) were evident only after 5 d of gentamicin administration. In addition, Sox2 expression was up-regulated in triggered supporting cells at an early stage of regeneration, but stopped at the advent of mature hair cells. Our study also indicated that p27kip1 was expressed in both hair cells and supporting cells but was down-regulated in a subgroup of the supporting cells that gave rise to hair cells. These data and the obtained dynamic changes of the cells labeled for BrdU, Sox2, Atoh1/Math1, PV or p27kip1 are useful for understanding supporting cell behaviors and their fate specification during hair cell regeneration.
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Hair cell regeneration or the expression of related factors that regulate the fate specification of supporting cells in the cochlear ducts of embryonic and posthatch chickens
Publication date: Available online 12 December 2015
Source:Hearing Research
Author(s): Lingling Jiang, Ran Jin, Jincao Xu, Yubin Ji, Meiguang Zhang, Xuebo Zhang, Xinwen Zhang, Zhongming Han, Shaoju Zeng
Hair cells in posthatch chickens regenerate spontaneously through mitosis or the transdifferentiation of supporting cells in response to antibiotic injury. However, how embryonic chicken cochleae respond to antibiotic treatment remains unknown. This study is the first to indicate that unlike hair cells in posthatch chickens, the auditory epithelium was free from antibiotic injury (25-250 mg gentamicin/kg) in embryonic chickens, although FITC-conjugated gentamicin actually reached embryonic hair cells. Next, we examined and counted the cells and performed labeling for BrdU, Sox2, Atoh1/Math1, PV or p27kip1 (triple or double labeling) in the injured cochlea ducts after gentamicin treatment at 2 hours (h), 15 h, 24 h, 2 days (d), 3 d and 7 d after BrdU treatment in posthatch chickens. Our results indicated that following gentamicin administration, proliferating cells (BrdU+) were labeled for Atoh1/Math1 in the damaged areas 3d after gentamicin administration, whereas hair cells (PV+) renewed through mitosis (BrdU+) or direct transdifferentiation (BrdU-) were evident only after 5 d of gentamicin administration. In addition, Sox2 expression was up-regulated in triggered supporting cells at an early stage of regeneration, but stopped at the advent of mature hair cells. Our study also indicated that p27kip1 was expressed in both hair cells and supporting cells but was down-regulated in a subgroup of the supporting cells that gave rise to hair cells. These data and the obtained dynamic changes of the cells labeled for BrdU, Sox2, Atoh1/Math1, PV or p27kip1 are useful for understanding supporting cell behaviors and their fate specification during hair cell regeneration.
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Source:Hearing Research
Author(s): Lingling Jiang, Ran Jin, Jincao Xu, Yubin Ji, Meiguang Zhang, Xuebo Zhang, Xinwen Zhang, Zhongming Han, Shaoju Zeng
Hair cells in posthatch chickens regenerate spontaneously through mitosis or the transdifferentiation of supporting cells in response to antibiotic injury. However, how embryonic chicken cochleae respond to antibiotic treatment remains unknown. This study is the first to indicate that unlike hair cells in posthatch chickens, the auditory epithelium was free from antibiotic injury (25-250 mg gentamicin/kg) in embryonic chickens, although FITC-conjugated gentamicin actually reached embryonic hair cells. Next, we examined and counted the cells and performed labeling for BrdU, Sox2, Atoh1/Math1, PV or p27kip1 (triple or double labeling) in the injured cochlea ducts after gentamicin treatment at 2 hours (h), 15 h, 24 h, 2 days (d), 3 d and 7 d after BrdU treatment in posthatch chickens. Our results indicated that following gentamicin administration, proliferating cells (BrdU+) were labeled for Atoh1/Math1 in the damaged areas 3d after gentamicin administration, whereas hair cells (PV+) renewed through mitosis (BrdU+) or direct transdifferentiation (BrdU-) were evident only after 5 d of gentamicin administration. In addition, Sox2 expression was up-regulated in triggered supporting cells at an early stage of regeneration, but stopped at the advent of mature hair cells. Our study also indicated that p27kip1 was expressed in both hair cells and supporting cells but was down-regulated in a subgroup of the supporting cells that gave rise to hair cells. These data and the obtained dynamic changes of the cells labeled for BrdU, Sox2, Atoh1/Math1, PV or p27kip1 are useful for understanding supporting cell behaviors and their fate specification during hair cell regeneration.
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Sodium salicylate potentiates the GABAB-GIRK pathway to suppress rebound depolarization in neurons of the rat's medial geniculate body
Publication date: Available online 12 December 2015
Source:Hearing Research
Author(s): Xin-Xing Wang, Yan Jin, Bin Luo, Jing-Wu Sun, Jinsheng Zhang, Ming Wang, Lin Chen
Rebound depolarization (RD) is a voltage response to the offset from pre-hyperpolarization of neuronal membrane potential, which manifests a particular form of the postsynaptic membrane potential response to inhibitory presynaptic inputs. We previously demonstrated that sodium salicylate (NaSal), a tinnitus inducer, can drastically suppress the RD in neurons of rat medial geniculate body (MGB) (Su et al, 2012, PLoS ONE 7, e46969). The purpose of the present study was to investigate the underlying cellular mechanism by using whole-cell patch-clamp recordings in rat MGB slices. NaSal (1.4 mM) had no effects on the current mediated by T-type Ca2+ channels, indicating that it does not target these channels to suppress the RD. Instead, NaSal was shown to hyperpolarize the resting membrane potential to suppress the RD. NaSal had no effects on the current mediated by hyperpolarization-activated cyclic nucleotide-gated (HCN) channels, indicating that it does not target these channels to hyperpolarize the resting membrane potential. NaSal induced an outward leak current that could be abolished by CGP55845, a GABAB receptor blocker, or respectively by Ba2+ and Tertiapin-Q, blockers for G-protein-gated inwardly rectifying potassium (GIRK) channels, indicating that NaSal potentiates the GABAB-GIRK pathway to hyperpolarize the resting membrane potential. Our study demonstrates that NaSal targets GABAB receptors to alter functional behaviors of MGB neurons, which may be implicated in NaSal-induced tinnitus.
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Source:Hearing Research
Author(s): Xin-Xing Wang, Yan Jin, Bin Luo, Jing-Wu Sun, Jinsheng Zhang, Ming Wang, Lin Chen
Rebound depolarization (RD) is a voltage response to the offset from pre-hyperpolarization of neuronal membrane potential, which manifests a particular form of the postsynaptic membrane potential response to inhibitory presynaptic inputs. We previously demonstrated that sodium salicylate (NaSal), a tinnitus inducer, can drastically suppress the RD in neurons of rat medial geniculate body (MGB) (Su et al, 2012, PLoS ONE 7, e46969). The purpose of the present study was to investigate the underlying cellular mechanism by using whole-cell patch-clamp recordings in rat MGB slices. NaSal (1.4 mM) had no effects on the current mediated by T-type Ca2+ channels, indicating that it does not target these channels to suppress the RD. Instead, NaSal was shown to hyperpolarize the resting membrane potential to suppress the RD. NaSal had no effects on the current mediated by hyperpolarization-activated cyclic nucleotide-gated (HCN) channels, indicating that it does not target these channels to hyperpolarize the resting membrane potential. NaSal induced an outward leak current that could be abolished by CGP55845, a GABAB receptor blocker, or respectively by Ba2+ and Tertiapin-Q, blockers for G-protein-gated inwardly rectifying potassium (GIRK) channels, indicating that NaSal potentiates the GABAB-GIRK pathway to hyperpolarize the resting membrane potential. Our study demonstrates that NaSal targets GABAB receptors to alter functional behaviors of MGB neurons, which may be implicated in NaSal-induced tinnitus.
Graphical abstract
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Sodium salicylate potentiates the GABAB-GIRK pathway to suppress rebound depolarization in neurons of the rat's medial geniculate body
Publication date: Available online 12 December 2015
Source:Hearing Research
Author(s): Xin-Xing Wang, Yan Jin, Bin Luo, Jing-Wu Sun, Jinsheng Zhang, Ming Wang, Lin Chen
Rebound depolarization (RD) is a voltage response to the offset from pre-hyperpolarization of neuronal membrane potential, which manifests a particular form of the postsynaptic membrane potential response to inhibitory presynaptic inputs. We previously demonstrated that sodium salicylate (NaSal), a tinnitus inducer, can drastically suppress the RD in neurons of rat medial geniculate body (MGB) (Su et al, 2012, PLoS ONE 7, e46969). The purpose of the present study was to investigate the underlying cellular mechanism by using whole-cell patch-clamp recordings in rat MGB slices. NaSal (1.4 mM) had no effects on the current mediated by T-type Ca2+ channels, indicating that it does not target these channels to suppress the RD. Instead, NaSal was shown to hyperpolarize the resting membrane potential to suppress the RD. NaSal had no effects on the current mediated by hyperpolarization-activated cyclic nucleotide-gated (HCN) channels, indicating that it does not target these channels to hyperpolarize the resting membrane potential. NaSal induced an outward leak current that could be abolished by CGP55845, a GABAB receptor blocker, or respectively by Ba2+ and Tertiapin-Q, blockers for G-protein-gated inwardly rectifying potassium (GIRK) channels, indicating that NaSal potentiates the GABAB-GIRK pathway to hyperpolarize the resting membrane potential. Our study demonstrates that NaSal targets GABAB receptors to alter functional behaviors of MGB neurons, which may be implicated in NaSal-induced tinnitus.
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Source:Hearing Research
Author(s): Xin-Xing Wang, Yan Jin, Bin Luo, Jing-Wu Sun, Jinsheng Zhang, Ming Wang, Lin Chen
Rebound depolarization (RD) is a voltage response to the offset from pre-hyperpolarization of neuronal membrane potential, which manifests a particular form of the postsynaptic membrane potential response to inhibitory presynaptic inputs. We previously demonstrated that sodium salicylate (NaSal), a tinnitus inducer, can drastically suppress the RD in neurons of rat medial geniculate body (MGB) (Su et al, 2012, PLoS ONE 7, e46969). The purpose of the present study was to investigate the underlying cellular mechanism by using whole-cell patch-clamp recordings in rat MGB slices. NaSal (1.4 mM) had no effects on the current mediated by T-type Ca2+ channels, indicating that it does not target these channels to suppress the RD. Instead, NaSal was shown to hyperpolarize the resting membrane potential to suppress the RD. NaSal had no effects on the current mediated by hyperpolarization-activated cyclic nucleotide-gated (HCN) channels, indicating that it does not target these channels to hyperpolarize the resting membrane potential. NaSal induced an outward leak current that could be abolished by CGP55845, a GABAB receptor blocker, or respectively by Ba2+ and Tertiapin-Q, blockers for G-protein-gated inwardly rectifying potassium (GIRK) channels, indicating that NaSal potentiates the GABAB-GIRK pathway to hyperpolarize the resting membrane potential. Our study demonstrates that NaSal targets GABAB receptors to alter functional behaviors of MGB neurons, which may be implicated in NaSal-induced tinnitus.
Graphical abstract
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Modulation of Auditory Brainstem Responses by Serotonin and Specific Serotonin Receptors
Publication date: Available online 12 December 2015
Source:Hearing Research
Author(s): Melissa A. Papesh, Laura M. Hurley
The neuromodulator serotonin is found throughout the auditory system from the cochlea to the cortex. Although effects of serotonin have been reported at the level of single neurons in many brainstem nuclei, how these effects correspond to more integrated measures of auditory processing has not been well-explored. In the present study, we aimed to characterize the effects of serotonin on far-field auditory brainstem responses (ABR) across a wide range of stimulus frequencies and intensities. Using a mouse model, we investigated the consequences of systemic serotonin depletion, as well as the selective stimulation and suppression of the 5-HT1 and 5-HT2 receptors, on ABR latency and amplitude. Stimuli included tone pips spanning four octaves presented over a forty dB range. Depletion of serotonin reduced the ABR latencies in Wave II and later waves, suggesting that serotonergic effects occur as early as the cochlear nucleus. Further, agonists and antagonists of specific serotonergic receptors had different profiles of effects on ABR latencies and amplitudes across waves and frequencies, suggestive of distinct effects of these agents on auditory processing. Finally, most serotonergic effects were more pronounced at lower ABR frequencies, suggesting larger or more directional modulation of low-frequency processing. This is the first study to describe the effects of serotonin on ABR responses across a wide range of stimulus frequencies and amplitudes, and it presents an important step in understanding how serotonergic modulation of auditory brainstem processing may contribute to modulation of auditory perception.
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Source:Hearing Research
Author(s): Melissa A. Papesh, Laura M. Hurley
The neuromodulator serotonin is found throughout the auditory system from the cochlea to the cortex. Although effects of serotonin have been reported at the level of single neurons in many brainstem nuclei, how these effects correspond to more integrated measures of auditory processing has not been well-explored. In the present study, we aimed to characterize the effects of serotonin on far-field auditory brainstem responses (ABR) across a wide range of stimulus frequencies and intensities. Using a mouse model, we investigated the consequences of systemic serotonin depletion, as well as the selective stimulation and suppression of the 5-HT1 and 5-HT2 receptors, on ABR latency and amplitude. Stimuli included tone pips spanning four octaves presented over a forty dB range. Depletion of serotonin reduced the ABR latencies in Wave II and later waves, suggesting that serotonergic effects occur as early as the cochlear nucleus. Further, agonists and antagonists of specific serotonergic receptors had different profiles of effects on ABR latencies and amplitudes across waves and frequencies, suggestive of distinct effects of these agents on auditory processing. Finally, most serotonergic effects were more pronounced at lower ABR frequencies, suggesting larger or more directional modulation of low-frequency processing. This is the first study to describe the effects of serotonin on ABR responses across a wide range of stimulus frequencies and amplitudes, and it presents an important step in understanding how serotonergic modulation of auditory brainstem processing may contribute to modulation of auditory perception.
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Modulation of Auditory Brainstem Responses by Serotonin and Specific Serotonin Receptors
Publication date: Available online 12 December 2015
Source:Hearing Research
Author(s): Melissa A. Papesh, Laura M. Hurley
The neuromodulator serotonin is found throughout the auditory system from the cochlea to the cortex. Although effects of serotonin have been reported at the level of single neurons in many brainstem nuclei, how these effects correspond to more integrated measures of auditory processing has not been well-explored. In the present study, we aimed to characterize the effects of serotonin on far-field auditory brainstem responses (ABR) across a wide range of stimulus frequencies and intensities. Using a mouse model, we investigated the consequences of systemic serotonin depletion, as well as the selective stimulation and suppression of the 5-HT1 and 5-HT2 receptors, on ABR latency and amplitude. Stimuli included tone pips spanning four octaves presented over a forty dB range. Depletion of serotonin reduced the ABR latencies in Wave II and later waves, suggesting that serotonergic effects occur as early as the cochlear nucleus. Further, agonists and antagonists of specific serotonergic receptors had different profiles of effects on ABR latencies and amplitudes across waves and frequencies, suggestive of distinct effects of these agents on auditory processing. Finally, most serotonergic effects were more pronounced at lower ABR frequencies, suggesting larger or more directional modulation of low-frequency processing. This is the first study to describe the effects of serotonin on ABR responses across a wide range of stimulus frequencies and amplitudes, and it presents an important step in understanding how serotonergic modulation of auditory brainstem processing may contribute to modulation of auditory perception.
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Source:Hearing Research
Author(s): Melissa A. Papesh, Laura M. Hurley
The neuromodulator serotonin is found throughout the auditory system from the cochlea to the cortex. Although effects of serotonin have been reported at the level of single neurons in many brainstem nuclei, how these effects correspond to more integrated measures of auditory processing has not been well-explored. In the present study, we aimed to characterize the effects of serotonin on far-field auditory brainstem responses (ABR) across a wide range of stimulus frequencies and intensities. Using a mouse model, we investigated the consequences of systemic serotonin depletion, as well as the selective stimulation and suppression of the 5-HT1 and 5-HT2 receptors, on ABR latency and amplitude. Stimuli included tone pips spanning four octaves presented over a forty dB range. Depletion of serotonin reduced the ABR latencies in Wave II and later waves, suggesting that serotonergic effects occur as early as the cochlear nucleus. Further, agonists and antagonists of specific serotonergic receptors had different profiles of effects on ABR latencies and amplitudes across waves and frequencies, suggestive of distinct effects of these agents on auditory processing. Finally, most serotonergic effects were more pronounced at lower ABR frequencies, suggesting larger or more directional modulation of low-frequency processing. This is the first study to describe the effects of serotonin on ABR responses across a wide range of stimulus frequencies and amplitudes, and it presents an important step in understanding how serotonergic modulation of auditory brainstem processing may contribute to modulation of auditory perception.
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Hair cell regeneration or the expression of related factors that regulate the fate specification of supporting cells in the cochlear ducts of embryonic and posthatch chickens
Publication date: Available online 12 December 2015
Source:Hearing Research
Author(s): Lingling Jiang, Ran Jin, Jincao Xu, Yubin Ji, Meiguang Zhang, Xuebo Zhang, Xinwen Zhang, Zhongming Han, Shaoju Zeng
Hair cells in posthatch chickens regenerate spontaneously through mitosis or the transdifferentiation of supporting cells in response to antibiotic injury. However, how embryonic chicken cochleae respond to antibiotic treatment remains unknown. This study is the first to indicate that unlike hair cells in posthatch chickens, the auditory epithelium was free from antibiotic injury (25-250 mg gentamicin/kg) in embryonic chickens, although FITC-conjugated gentamicin actually reached embryonic hair cells. Next, we examined and counted the cells and performed labeling for BrdU, Sox2, Atoh1/Math1, PV or p27kip1 (triple or double labeling) in the injured cochlea ducts after gentamicin treatment at 2 hours (h), 15 h, 24 h, 2 days (d), 3 d and 7 d after BrdU treatment in posthatch chickens. Our results indicated that following gentamicin administration, proliferating cells (BrdU+) were labeled for Atoh1/Math1 in the damaged areas 3d after gentamicin administration, whereas hair cells (PV+) renewed through mitosis (BrdU+) or direct transdifferentiation (BrdU-) were evident only after 5 d of gentamicin administration. In addition, Sox2 expression was up-regulated in triggered supporting cells at an early stage of regeneration, but stopped at the advent of mature hair cells. Our study also indicated that p27kip1 was expressed in both hair cells and supporting cells but was down-regulated in a subgroup of the supporting cells that gave rise to hair cells. These data and the obtained dynamic changes of the cells labeled for BrdU, Sox2, Atoh1/Math1, PV or p27kip1 are useful for understanding supporting cell behaviors and their fate specification during hair cell regeneration.
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Source:Hearing Research
Author(s): Lingling Jiang, Ran Jin, Jincao Xu, Yubin Ji, Meiguang Zhang, Xuebo Zhang, Xinwen Zhang, Zhongming Han, Shaoju Zeng
Hair cells in posthatch chickens regenerate spontaneously through mitosis or the transdifferentiation of supporting cells in response to antibiotic injury. However, how embryonic chicken cochleae respond to antibiotic treatment remains unknown. This study is the first to indicate that unlike hair cells in posthatch chickens, the auditory epithelium was free from antibiotic injury (25-250 mg gentamicin/kg) in embryonic chickens, although FITC-conjugated gentamicin actually reached embryonic hair cells. Next, we examined and counted the cells and performed labeling for BrdU, Sox2, Atoh1/Math1, PV or p27kip1 (triple or double labeling) in the injured cochlea ducts after gentamicin treatment at 2 hours (h), 15 h, 24 h, 2 days (d), 3 d and 7 d after BrdU treatment in posthatch chickens. Our results indicated that following gentamicin administration, proliferating cells (BrdU+) were labeled for Atoh1/Math1 in the damaged areas 3d after gentamicin administration, whereas hair cells (PV+) renewed through mitosis (BrdU+) or direct transdifferentiation (BrdU-) were evident only after 5 d of gentamicin administration. In addition, Sox2 expression was up-regulated in triggered supporting cells at an early stage of regeneration, but stopped at the advent of mature hair cells. Our study also indicated that p27kip1 was expressed in both hair cells and supporting cells but was down-regulated in a subgroup of the supporting cells that gave rise to hair cells. These data and the obtained dynamic changes of the cells labeled for BrdU, Sox2, Atoh1/Math1, PV or p27kip1 are useful for understanding supporting cell behaviors and their fate specification during hair cell regeneration.
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Sodium salicylate potentiates the GABAB-GIRK pathway to suppress rebound depolarization in neurons of the rat's medial geniculate body
Publication date: Available online 12 December 2015
Source:Hearing Research
Author(s): Xin-Xing Wang, Yan Jin, Bin Luo, Jing-Wu Sun, Jinsheng Zhang, Ming Wang, Lin Chen
Rebound depolarization (RD) is a voltage response to the offset from pre-hyperpolarization of neuronal membrane potential, which manifests a particular form of the postsynaptic membrane potential response to inhibitory presynaptic inputs. We previously demonstrated that sodium salicylate (NaSal), a tinnitus inducer, can drastically suppress the RD in neurons of rat medial geniculate body (MGB) (Su et al, 2012, PLoS ONE 7, e46969). The purpose of the present study was to investigate the underlying cellular mechanism by using whole-cell patch-clamp recordings in rat MGB slices. NaSal (1.4 mM) had no effects on the current mediated by T-type Ca2+ channels, indicating that it does not target these channels to suppress the RD. Instead, NaSal was shown to hyperpolarize the resting membrane potential to suppress the RD. NaSal had no effects on the current mediated by hyperpolarization-activated cyclic nucleotide-gated (HCN) channels, indicating that it does not target these channels to hyperpolarize the resting membrane potential. NaSal induced an outward leak current that could be abolished by CGP55845, a GABAB receptor blocker, or respectively by Ba2+ and Tertiapin-Q, blockers for G-protein-gated inwardly rectifying potassium (GIRK) channels, indicating that NaSal potentiates the GABAB-GIRK pathway to hyperpolarize the resting membrane potential. Our study demonstrates that NaSal targets GABAB receptors to alter functional behaviors of MGB neurons, which may be implicated in NaSal-induced tinnitus.
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Source:Hearing Research
Author(s): Xin-Xing Wang, Yan Jin, Bin Luo, Jing-Wu Sun, Jinsheng Zhang, Ming Wang, Lin Chen
Rebound depolarization (RD) is a voltage response to the offset from pre-hyperpolarization of neuronal membrane potential, which manifests a particular form of the postsynaptic membrane potential response to inhibitory presynaptic inputs. We previously demonstrated that sodium salicylate (NaSal), a tinnitus inducer, can drastically suppress the RD in neurons of rat medial geniculate body (MGB) (Su et al, 2012, PLoS ONE 7, e46969). The purpose of the present study was to investigate the underlying cellular mechanism by using whole-cell patch-clamp recordings in rat MGB slices. NaSal (1.4 mM) had no effects on the current mediated by T-type Ca2+ channels, indicating that it does not target these channels to suppress the RD. Instead, NaSal was shown to hyperpolarize the resting membrane potential to suppress the RD. NaSal had no effects on the current mediated by hyperpolarization-activated cyclic nucleotide-gated (HCN) channels, indicating that it does not target these channels to hyperpolarize the resting membrane potential. NaSal induced an outward leak current that could be abolished by CGP55845, a GABAB receptor blocker, or respectively by Ba2+ and Tertiapin-Q, blockers for G-protein-gated inwardly rectifying potassium (GIRK) channels, indicating that NaSal potentiates the GABAB-GIRK pathway to hyperpolarize the resting membrane potential. Our study demonstrates that NaSal targets GABAB receptors to alter functional behaviors of MGB neurons, which may be implicated in NaSal-induced tinnitus.
Graphical abstract
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Modulation of Auditory Brainstem Responses by Serotonin and Specific Serotonin Receptors
Publication date: Available online 12 December 2015
Source:Hearing Research
Author(s): Melissa A. Papesh, Laura M. Hurley
The neuromodulator serotonin is found throughout the auditory system from the cochlea to the cortex. Although effects of serotonin have been reported at the level of single neurons in many brainstem nuclei, how these effects correspond to more integrated measures of auditory processing has not been well-explored. In the present study, we aimed to characterize the effects of serotonin on far-field auditory brainstem responses (ABR) across a wide range of stimulus frequencies and intensities. Using a mouse model, we investigated the consequences of systemic serotonin depletion, as well as the selective stimulation and suppression of the 5-HT1 and 5-HT2 receptors, on ABR latency and amplitude. Stimuli included tone pips spanning four octaves presented over a forty dB range. Depletion of serotonin reduced the ABR latencies in Wave II and later waves, suggesting that serotonergic effects occur as early as the cochlear nucleus. Further, agonists and antagonists of specific serotonergic receptors had different profiles of effects on ABR latencies and amplitudes across waves and frequencies, suggestive of distinct effects of these agents on auditory processing. Finally, most serotonergic effects were more pronounced at lower ABR frequencies, suggesting larger or more directional modulation of low-frequency processing. This is the first study to describe the effects of serotonin on ABR responses across a wide range of stimulus frequencies and amplitudes, and it presents an important step in understanding how serotonergic modulation of auditory brainstem processing may contribute to modulation of auditory perception.
from #Audiology via ola Kala on Inoreader http://ift.tt/1M9fIwV
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Source:Hearing Research
Author(s): Melissa A. Papesh, Laura M. Hurley
The neuromodulator serotonin is found throughout the auditory system from the cochlea to the cortex. Although effects of serotonin have been reported at the level of single neurons in many brainstem nuclei, how these effects correspond to more integrated measures of auditory processing has not been well-explored. In the present study, we aimed to characterize the effects of serotonin on far-field auditory brainstem responses (ABR) across a wide range of stimulus frequencies and intensities. Using a mouse model, we investigated the consequences of systemic serotonin depletion, as well as the selective stimulation and suppression of the 5-HT1 and 5-HT2 receptors, on ABR latency and amplitude. Stimuli included tone pips spanning four octaves presented over a forty dB range. Depletion of serotonin reduced the ABR latencies in Wave II and later waves, suggesting that serotonergic effects occur as early as the cochlear nucleus. Further, agonists and antagonists of specific serotonergic receptors had different profiles of effects on ABR latencies and amplitudes across waves and frequencies, suggestive of distinct effects of these agents on auditory processing. Finally, most serotonergic effects were more pronounced at lower ABR frequencies, suggesting larger or more directional modulation of low-frequency processing. This is the first study to describe the effects of serotonin on ABR responses across a wide range of stimulus frequencies and amplitudes, and it presents an important step in understanding how serotonergic modulation of auditory brainstem processing may contribute to modulation of auditory perception.
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Hair cell regeneration or the expression of related factors that regulate the fate specification of supporting cells in the cochlear ducts of embryonic and posthatch chickens
Publication date: Available online 12 December 2015
Source:Hearing Research
Author(s): Lingling Jiang, Ran Jin, Jincao Xu, Yubin Ji, Meiguang Zhang, Xuebo Zhang, Xinwen Zhang, Zhongming Han, Shaoju Zeng
Hair cells in posthatch chickens regenerate spontaneously through mitosis or the transdifferentiation of supporting cells in response to antibiotic injury. However, how embryonic chicken cochleae respond to antibiotic treatment remains unknown. This study is the first to indicate that unlike hair cells in posthatch chickens, the auditory epithelium was free from antibiotic injury (25-250 mg gentamicin/kg) in embryonic chickens, although FITC-conjugated gentamicin actually reached embryonic hair cells. Next, we examined and counted the cells and performed labeling for BrdU, Sox2, Atoh1/Math1, PV or p27kip1 (triple or double labeling) in the injured cochlea ducts after gentamicin treatment at 2 hours (h), 15 h, 24 h, 2 days (d), 3 d and 7 d after BrdU treatment in posthatch chickens. Our results indicated that following gentamicin administration, proliferating cells (BrdU+) were labeled for Atoh1/Math1 in the damaged areas 3d after gentamicin administration, whereas hair cells (PV+) renewed through mitosis (BrdU+) or direct transdifferentiation (BrdU-) were evident only after 5 d of gentamicin administration. In addition, Sox2 expression was up-regulated in triggered supporting cells at an early stage of regeneration, but stopped at the advent of mature hair cells. Our study also indicated that p27kip1 was expressed in both hair cells and supporting cells but was down-regulated in a subgroup of the supporting cells that gave rise to hair cells. These data and the obtained dynamic changes of the cells labeled for BrdU, Sox2, Atoh1/Math1, PV or p27kip1 are useful for understanding supporting cell behaviors and their fate specification during hair cell regeneration.
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via IFTTT
Source:Hearing Research
Author(s): Lingling Jiang, Ran Jin, Jincao Xu, Yubin Ji, Meiguang Zhang, Xuebo Zhang, Xinwen Zhang, Zhongming Han, Shaoju Zeng
Hair cells in posthatch chickens regenerate spontaneously through mitosis or the transdifferentiation of supporting cells in response to antibiotic injury. However, how embryonic chicken cochleae respond to antibiotic treatment remains unknown. This study is the first to indicate that unlike hair cells in posthatch chickens, the auditory epithelium was free from antibiotic injury (25-250 mg gentamicin/kg) in embryonic chickens, although FITC-conjugated gentamicin actually reached embryonic hair cells. Next, we examined and counted the cells and performed labeling for BrdU, Sox2, Atoh1/Math1, PV or p27kip1 (triple or double labeling) in the injured cochlea ducts after gentamicin treatment at 2 hours (h), 15 h, 24 h, 2 days (d), 3 d and 7 d after BrdU treatment in posthatch chickens. Our results indicated that following gentamicin administration, proliferating cells (BrdU+) were labeled for Atoh1/Math1 in the damaged areas 3d after gentamicin administration, whereas hair cells (PV+) renewed through mitosis (BrdU+) or direct transdifferentiation (BrdU-) were evident only after 5 d of gentamicin administration. In addition, Sox2 expression was up-regulated in triggered supporting cells at an early stage of regeneration, but stopped at the advent of mature hair cells. Our study also indicated that p27kip1 was expressed in both hair cells and supporting cells but was down-regulated in a subgroup of the supporting cells that gave rise to hair cells. These data and the obtained dynamic changes of the cells labeled for BrdU, Sox2, Atoh1/Math1, PV or p27kip1 are useful for understanding supporting cell behaviors and their fate specification during hair cell regeneration.
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Sodium salicylate potentiates the GABAB-GIRK pathway to suppress rebound depolarization in neurons of the rat's medial geniculate body
Publication date: Available online 12 December 2015
Source:Hearing Research
Author(s): Xin-Xing Wang, Yan Jin, Bin Luo, Jing-Wu Sun, Jinsheng Zhang, Ming Wang, Lin Chen
Rebound depolarization (RD) is a voltage response to the offset from pre-hyperpolarization of neuronal membrane potential, which manifests a particular form of the postsynaptic membrane potential response to inhibitory presynaptic inputs. We previously demonstrated that sodium salicylate (NaSal), a tinnitus inducer, can drastically suppress the RD in neurons of rat medial geniculate body (MGB) (Su et al, 2012, PLoS ONE 7, e46969). The purpose of the present study was to investigate the underlying cellular mechanism by using whole-cell patch-clamp recordings in rat MGB slices. NaSal (1.4 mM) had no effects on the current mediated by T-type Ca2+ channels, indicating that it does not target these channels to suppress the RD. Instead, NaSal was shown to hyperpolarize the resting membrane potential to suppress the RD. NaSal had no effects on the current mediated by hyperpolarization-activated cyclic nucleotide-gated (HCN) channels, indicating that it does not target these channels to hyperpolarize the resting membrane potential. NaSal induced an outward leak current that could be abolished by CGP55845, a GABAB receptor blocker, or respectively by Ba2+ and Tertiapin-Q, blockers for G-protein-gated inwardly rectifying potassium (GIRK) channels, indicating that NaSal potentiates the GABAB-GIRK pathway to hyperpolarize the resting membrane potential. Our study demonstrates that NaSal targets GABAB receptors to alter functional behaviors of MGB neurons, which may be implicated in NaSal-induced tinnitus.
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Source:Hearing Research
Author(s): Xin-Xing Wang, Yan Jin, Bin Luo, Jing-Wu Sun, Jinsheng Zhang, Ming Wang, Lin Chen
Rebound depolarization (RD) is a voltage response to the offset from pre-hyperpolarization of neuronal membrane potential, which manifests a particular form of the postsynaptic membrane potential response to inhibitory presynaptic inputs. We previously demonstrated that sodium salicylate (NaSal), a tinnitus inducer, can drastically suppress the RD in neurons of rat medial geniculate body (MGB) (Su et al, 2012, PLoS ONE 7, e46969). The purpose of the present study was to investigate the underlying cellular mechanism by using whole-cell patch-clamp recordings in rat MGB slices. NaSal (1.4 mM) had no effects on the current mediated by T-type Ca2+ channels, indicating that it does not target these channels to suppress the RD. Instead, NaSal was shown to hyperpolarize the resting membrane potential to suppress the RD. NaSal had no effects on the current mediated by hyperpolarization-activated cyclic nucleotide-gated (HCN) channels, indicating that it does not target these channels to hyperpolarize the resting membrane potential. NaSal induced an outward leak current that could be abolished by CGP55845, a GABAB receptor blocker, or respectively by Ba2+ and Tertiapin-Q, blockers for G-protein-gated inwardly rectifying potassium (GIRK) channels, indicating that NaSal potentiates the GABAB-GIRK pathway to hyperpolarize the resting membrane potential. Our study demonstrates that NaSal targets GABAB receptors to alter functional behaviors of MGB neurons, which may be implicated in NaSal-induced tinnitus.
Graphical abstract
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Modulation of Auditory Brainstem Responses by Serotonin and Specific Serotonin Receptors
Publication date: Available online 12 December 2015
Source:Hearing Research
Author(s): Melissa A. Papesh, Laura M. Hurley
The neuromodulator serotonin is found throughout the auditory system from the cochlea to the cortex. Although effects of serotonin have been reported at the level of single neurons in many brainstem nuclei, how these effects correspond to more integrated measures of auditory processing has not been well-explored. In the present study, we aimed to characterize the effects of serotonin on far-field auditory brainstem responses (ABR) across a wide range of stimulus frequencies and intensities. Using a mouse model, we investigated the consequences of systemic serotonin depletion, as well as the selective stimulation and suppression of the 5-HT1 and 5-HT2 receptors, on ABR latency and amplitude. Stimuli included tone pips spanning four octaves presented over a forty dB range. Depletion of serotonin reduced the ABR latencies in Wave II and later waves, suggesting that serotonergic effects occur as early as the cochlear nucleus. Further, agonists and antagonists of specific serotonergic receptors had different profiles of effects on ABR latencies and amplitudes across waves and frequencies, suggestive of distinct effects of these agents on auditory processing. Finally, most serotonergic effects were more pronounced at lower ABR frequencies, suggesting larger or more directional modulation of low-frequency processing. This is the first study to describe the effects of serotonin on ABR responses across a wide range of stimulus frequencies and amplitudes, and it presents an important step in understanding how serotonergic modulation of auditory brainstem processing may contribute to modulation of auditory perception.
from #Audiology via ola Kala on Inoreader http://ift.tt/1M9fIwV
via IFTTT
Source:Hearing Research
Author(s): Melissa A. Papesh, Laura M. Hurley
The neuromodulator serotonin is found throughout the auditory system from the cochlea to the cortex. Although effects of serotonin have been reported at the level of single neurons in many brainstem nuclei, how these effects correspond to more integrated measures of auditory processing has not been well-explored. In the present study, we aimed to characterize the effects of serotonin on far-field auditory brainstem responses (ABR) across a wide range of stimulus frequencies and intensities. Using a mouse model, we investigated the consequences of systemic serotonin depletion, as well as the selective stimulation and suppression of the 5-HT1 and 5-HT2 receptors, on ABR latency and amplitude. Stimuli included tone pips spanning four octaves presented over a forty dB range. Depletion of serotonin reduced the ABR latencies in Wave II and later waves, suggesting that serotonergic effects occur as early as the cochlear nucleus. Further, agonists and antagonists of specific serotonergic receptors had different profiles of effects on ABR latencies and amplitudes across waves and frequencies, suggestive of distinct effects of these agents on auditory processing. Finally, most serotonergic effects were more pronounced at lower ABR frequencies, suggesting larger or more directional modulation of low-frequency processing. This is the first study to describe the effects of serotonin on ABR responses across a wide range of stimulus frequencies and amplitudes, and it presents an important step in understanding how serotonergic modulation of auditory brainstem processing may contribute to modulation of auditory perception.
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