The Experts below are selected from a list of 237 Experts worldwide ranked by ideXlab platform
Dorothy G Flood - One of the best experts on this subject based on the ideXlab platform.
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synaptic loss in the Central Nucleus of the inferior colliculus correlates with sensorineural hearing loss in the c57bl 6 mouse model of presbycusis
Hearing Research, 1995Co-Authors: Ann Marie Kazee, Vlasta P Spong, Joseph P Walto, Richard Salvi, Dorothy G FloodAbstract:Between 3 and 25 months of age, light and electron microscopic features of principal neurons in the Central Nucleus of the inferior colliculus of the C57BL/6 mouse were quantitated. This mouse strain has a genetic defect producing progressive sensorineural hearing loss which starts during young adulthood (2 months of age) with high-frequency sounds. During the second year of life, hearing is severely impaired, progressively involving all frequencies. The hearing loss was documented in the present study by auditory brainstem recordings of the mice at various ages. The cochleas from many of the same animals showed massive loss of both inner and outer hair cells beginning at the base (high-frequency region) and progressing with age along the entire length to the apex (low-frequency region). In the inferior colliculi, there was a significant decrease in the size of principal neurons in the Central Nucleus. There was a dramatic decrease in the number of synapses of all morphologic types on principal neuronal somas. The percentage of somatic membrane covered by synapses decreased by 67%. A ventral (high frequency) to dorsal (low frequency) gradient of synaptic loss could not be identified within the Central Nucleus. These synaptic changes may be related to the equally dramatic physiologic changes which have been noted in the Central Nucleus of the inferior colliculus, in which response properties of neurons normally sensitive to high-frequency sounds become more sensitive to low-frequency sounds. The synaptic loss noted in this study may be due to more than the loss of primary afferent pathways. It may represent alterations of the complex synaptic circuitry related to the Central deficits of presbycusis.
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Synaptic loss in the Central Nucleus of the inferior colliculus correlates with sensorineural hearing loss in the C57BL/6 mouse model of presbycusis
Hearing research, 1995Co-Authors: Ann Marie Kazee, Richard Salvi, Li Ying Han, Vlasta P. Spongr, Joseph P. Walton, Dorothy G FloodAbstract:Between 3 and 25 months of age, light and electron microscopic features of principal neurons in the Central Nucleus of the inferior colliculus of the C57BL/6 mouse were quantitated. This mouse strain has a genetic defect producing progressive sensorineural hearing loss which starts during young adulthood (2 months of age) with high-frequency sounds. During the second year of life, hearing is severely impaired, progressively involving all frequencies. The hearing loss was documented in the present study by auditory brainstem recordings of the mice at various ages. The cochleas from many of the same animals showed massive loss of both inner and outer hair cells beginning at the base (high-frequency region) and progressing with age along the entire length to the apex (low-frequency region). In the inferior colliculi, there was a significant decrease in the size of principal neurons in the Central Nucleus. There was a dramatic decrease in the number of synapses of all morphologic types on principal neuronal somas. The percentage of somatic membrane covered by synapses decreased by 67%. A ventral (high frequency) to dorsal (low frequency) gradient of synaptic loss could not be identified within the Central Nucleus. These synaptic changes may be related to the equally dramatic physiologic changes which have been noted in the Central Nucleus of the inferior colliculus, in which response properties of neurons normally sensitive to high-frequency sounds become more sensitive to low-frequency sounds. The synaptic loss noted in this study may be due to more than the loss of primary afferent pathways. It may represent alterations of the complex synaptic circuitry related to the Central deficits of presbycusis.
Ann Marie Kazee - One of the best experts on this subject based on the ideXlab platform.
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synaptic loss in the Central Nucleus of the inferior colliculus correlates with sensorineural hearing loss in the c57bl 6 mouse model of presbycusis
Hearing Research, 1995Co-Authors: Ann Marie Kazee, Vlasta P Spong, Joseph P Walto, Richard Salvi, Dorothy G FloodAbstract:Between 3 and 25 months of age, light and electron microscopic features of principal neurons in the Central Nucleus of the inferior colliculus of the C57BL/6 mouse were quantitated. This mouse strain has a genetic defect producing progressive sensorineural hearing loss which starts during young adulthood (2 months of age) with high-frequency sounds. During the second year of life, hearing is severely impaired, progressively involving all frequencies. The hearing loss was documented in the present study by auditory brainstem recordings of the mice at various ages. The cochleas from many of the same animals showed massive loss of both inner and outer hair cells beginning at the base (high-frequency region) and progressing with age along the entire length to the apex (low-frequency region). In the inferior colliculi, there was a significant decrease in the size of principal neurons in the Central Nucleus. There was a dramatic decrease in the number of synapses of all morphologic types on principal neuronal somas. The percentage of somatic membrane covered by synapses decreased by 67%. A ventral (high frequency) to dorsal (low frequency) gradient of synaptic loss could not be identified within the Central Nucleus. These synaptic changes may be related to the equally dramatic physiologic changes which have been noted in the Central Nucleus of the inferior colliculus, in which response properties of neurons normally sensitive to high-frequency sounds become more sensitive to low-frequency sounds. The synaptic loss noted in this study may be due to more than the loss of primary afferent pathways. It may represent alterations of the complex synaptic circuitry related to the Central deficits of presbycusis.
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Synaptic loss in the Central Nucleus of the inferior colliculus correlates with sensorineural hearing loss in the C57BL/6 mouse model of presbycusis
Hearing research, 1995Co-Authors: Ann Marie Kazee, Richard Salvi, Li Ying Han, Vlasta P. Spongr, Joseph P. Walton, Dorothy G FloodAbstract:Between 3 and 25 months of age, light and electron microscopic features of principal neurons in the Central Nucleus of the inferior colliculus of the C57BL/6 mouse were quantitated. This mouse strain has a genetic defect producing progressive sensorineural hearing loss which starts during young adulthood (2 months of age) with high-frequency sounds. During the second year of life, hearing is severely impaired, progressively involving all frequencies. The hearing loss was documented in the present study by auditory brainstem recordings of the mice at various ages. The cochleas from many of the same animals showed massive loss of both inner and outer hair cells beginning at the base (high-frequency region) and progressing with age along the entire length to the apex (low-frequency region). In the inferior colliculi, there was a significant decrease in the size of principal neurons in the Central Nucleus. There was a dramatic decrease in the number of synapses of all morphologic types on principal neuronal somas. The percentage of somatic membrane covered by synapses decreased by 67%. A ventral (high frequency) to dorsal (low frequency) gradient of synaptic loss could not be identified within the Central Nucleus. These synaptic changes may be related to the equally dramatic physiologic changes which have been noted in the Central Nucleus of the inferior colliculus, in which response properties of neurons normally sensitive to high-frequency sounds become more sensitive to low-frequency sounds. The synaptic loss noted in this study may be due to more than the loss of primary afferent pathways. It may represent alterations of the complex synaptic circuitry related to the Central deficits of presbycusis.
Michael Davis - One of the best experts on this subject based on the ideXlab platform.
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involvement of the Central Nucleus and basolateral complex of the amygdala in fear conditioning measured with fear potentiated startle in rats trained concurrently with auditory and visual conditioned stimuli
The Journal of Neuroscience, 1995Co-Authors: Serge Campeau, Michael DavisAbstract:The goal of this work was to test the involvement of the Central Nucleus and basolateral complex of the amygdala in fear conditioning, using auditory and visual conditioned stimuli (CSs). The acoustic startle reflex in rats was used as the behavioral index of conditioning because startle is reliably enhanced in the presence of a conditioned stimulus (CS) previously paired with a footshock. Initially, differential conditioning procedures indicated reliable discrimination between a noise CS and a visual CS. Subsequently, the effects of amygdala lesions were evaluated when both modalities were paired with shocks in the same rats. Electrolytic or ibotenic acid lesions of the Central Nucleus of the amygdala blocked fear-potentiated startle to both auditory and visual CSs, consistent with the idea that the Central Nucleus serves as a response independent, final common relay for fear conditioning. Similarly, pre- or post-training electrolytic or NMDA- induced lesions of the basolateral complex of the amygdala, which damaged the lateral Nucleus, and most of the basolateral Nucleus, disrupted fear-potentiated startle to both CS modalities. This finding is consistent with the suggestion that, in fear conditioning, the basolateral complex of the amygdala serves as an obligatory relay of sensory information from subcortical and cortical sensory areas to the Central Nucleus of the amygdala.
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Lesions of the Central Nucleus of the amygdala block the excitatory effects of septal ablation on the acoustic startle reflex.
Physiology & behavior, 1992Co-Authors: Kathleen R. Melia, Catherine B Sananes, Michael DavisAbstract:Many studies have investigated the role of the septum and the amygdala in emotional behavior. While the literature is somewhat inconsistent, most studies suggest a role for the septal nuclei in the inhibition of fear and stress responses (at the behavioral, autonomic and hormonal levels) while the Central Nucleus of the amygdala is involved in the production of such responses. The present study examined the ability of lesions of the Central Nucleus of the amygdala to block the excitatory effects of complete septal ablation on the acoustic startle reflex. Septal ablation produced a significant increase in startle amplitude which was blocked by concomitant lesions of the Central Nucleus of the amygdala. These results suggest that the increase in startle amplitude resulting from septal damage might be due to a disinhibition of neuronal activity in the Central Nucleus of the amygdala, a structure known to mediate the increase in startle associated with conditioned and unconditioned fear, or from antagonistic interactions at other target sites which themselves modulate startle.
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A direct projection from the Central Nucleus of the amygdala to the acoustic startle pathway: anterograde and retrograde tracing studies.
Behavioral neuroscience, 1991Co-Authors: Jeffrey B. Rosen, Janice M Hitchcock, Catherine B Sananes, Mindy J.d. Miserendino, Michael DavisAbstract:Previous work has shown that lesions of the Central Nucleus of the amygdala block fear-potentiated acoustic startle and that electrical simulation of the Central Nucleus enhances acoustic startle in rats. In the present study, the anterograde tracer Phaseolus vulgaris-leucoagglutinin was used to identify and delineate the course of a direct projection from the Central Nucleus of the amygdala to the Nucleus reticularis pontis caudalis, a Nucleus in the acoustic startle circuit. Experiments using the retrograde tracer Fluoro-Gold confirmed this and indicated that the rostral part of the medial subdivision of the Central Nucleus of the amygdala contains the cells that project to the startle circuit. With this information, lesion studies (see companion article Hitchcock & Davis, 1991) may be used to determine whether this projection plays a role in fear-potentiated startle.
Richard Salvi - One of the best experts on this subject based on the ideXlab platform.
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synaptic loss in the Central Nucleus of the inferior colliculus correlates with sensorineural hearing loss in the c57bl 6 mouse model of presbycusis
Hearing Research, 1995Co-Authors: Ann Marie Kazee, Vlasta P Spong, Joseph P Walto, Richard Salvi, Dorothy G FloodAbstract:Between 3 and 25 months of age, light and electron microscopic features of principal neurons in the Central Nucleus of the inferior colliculus of the C57BL/6 mouse were quantitated. This mouse strain has a genetic defect producing progressive sensorineural hearing loss which starts during young adulthood (2 months of age) with high-frequency sounds. During the second year of life, hearing is severely impaired, progressively involving all frequencies. The hearing loss was documented in the present study by auditory brainstem recordings of the mice at various ages. The cochleas from many of the same animals showed massive loss of both inner and outer hair cells beginning at the base (high-frequency region) and progressing with age along the entire length to the apex (low-frequency region). In the inferior colliculi, there was a significant decrease in the size of principal neurons in the Central Nucleus. There was a dramatic decrease in the number of synapses of all morphologic types on principal neuronal somas. The percentage of somatic membrane covered by synapses decreased by 67%. A ventral (high frequency) to dorsal (low frequency) gradient of synaptic loss could not be identified within the Central Nucleus. These synaptic changes may be related to the equally dramatic physiologic changes which have been noted in the Central Nucleus of the inferior colliculus, in which response properties of neurons normally sensitive to high-frequency sounds become more sensitive to low-frequency sounds. The synaptic loss noted in this study may be due to more than the loss of primary afferent pathways. It may represent alterations of the complex synaptic circuitry related to the Central deficits of presbycusis.
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Synaptic loss in the Central Nucleus of the inferior colliculus correlates with sensorineural hearing loss in the C57BL/6 mouse model of presbycusis
Hearing research, 1995Co-Authors: Ann Marie Kazee, Richard Salvi, Li Ying Han, Vlasta P. Spongr, Joseph P. Walton, Dorothy G FloodAbstract:Between 3 and 25 months of age, light and electron microscopic features of principal neurons in the Central Nucleus of the inferior colliculus of the C57BL/6 mouse were quantitated. This mouse strain has a genetic defect producing progressive sensorineural hearing loss which starts during young adulthood (2 months of age) with high-frequency sounds. During the second year of life, hearing is severely impaired, progressively involving all frequencies. The hearing loss was documented in the present study by auditory brainstem recordings of the mice at various ages. The cochleas from many of the same animals showed massive loss of both inner and outer hair cells beginning at the base (high-frequency region) and progressing with age along the entire length to the apex (low-frequency region). In the inferior colliculi, there was a significant decrease in the size of principal neurons in the Central Nucleus. There was a dramatic decrease in the number of synapses of all morphologic types on principal neuronal somas. The percentage of somatic membrane covered by synapses decreased by 67%. A ventral (high frequency) to dorsal (low frequency) gradient of synaptic loss could not be identified within the Central Nucleus. These synaptic changes may be related to the equally dramatic physiologic changes which have been noted in the Central Nucleus of the inferior colliculus, in which response properties of neurons normally sensitive to high-frequency sounds become more sensitive to low-frequency sounds. The synaptic loss noted in this study may be due to more than the loss of primary afferent pathways. It may represent alterations of the complex synaptic circuitry related to the Central deficits of presbycusis.
Peter C Holland - One of the best experts on this subject based on the ideXlab platform.
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Amygdala Central Nucleus function is necessary for learning, but not expression, of conditioned auditory orienting.
Behavioral neuroscience, 2005Co-Authors: Frank Groshek, Michela Gallagher, Erin C. Kerfoot, Vanessa Mckenna, Alan S. Polackwich, Peter C HollandAbstract:When exposed to pairings of a visual stimulus with food delivery, rats normally acquire both conditioned orienting responses directed toward the visual stimulus and conditioned food-related responses. Consistent with the results of previous lesion studies, reversible inactivation of amygdala Central Nucleus function before each conditioning session prevented the acquisition of conditioned orienting responses, whereas food-related behaviors were acquired normally. By contrast, neither inactivation nor neurotoxic lesions of Central Nucleus affected the expression of previously-acquired conditioned orienting responses. Thus, the Central Nucleus is apparently not critical to the maintenance of information required for conditioned orienting, but instead is necessary for memory storage elsewhere. Specialized roles for components of a circuit for conditioned orienting, which includes the Central Nucleus, the substantia nigra, and dorsolateral striatum, are discussed.
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Amygdala Central Nucleus function is necessary for learning but not expression of conditioned visual orienting
The European journal of neuroscience, 2004Co-Authors: Michael A. Mcdannald, Michela Gallagher, Erin C. Kerfoot, Peter C HollandAbstract:When exposed to pairings of a visual stimulus with food delivery, rats normally acquire both conditioned orienting responses directed toward the visual stimulus and conditioned food-related responses. Consistent with the results of previous lesion studies, reversible inactivation of amygdala Central Nucleus function before each conditioning session prevented the acquisition of conditioned orienting responses, whereas food-related behaviors were acquired normally. By contrast, neither inactivation nor neurotoxic lesions of Central Nucleus affected the expression of previously acquired conditioned orienting responses. Thus, the Central Nucleus is apparently not critical to the maintenance of information required for conditioned orienting, but instead is necessary for memory storage elsewhere. Specialized roles for components of a circuit for conditioned orienting, which includes the Central Nucleus, the substantia nigra, and dorsolateral striatum, are discussed.
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Inhibitory learning tests of conditioned stimulus associability in rats with lesions of the amygdala Central Nucleus.
Behavioral neuroscience, 2001Co-Authors: Peter C Holland, Yolanda Chik, Qui ZhangAbstract:Normal rats showed faster inhibitory learning about a light conditioned stimulus (CS) if it had previously been an inconsistent predictor of a tone CS than if it had been a consistent predictor of the tone. In contrast, the inhibitory learning of rats with ibotenic acid lesions of the amygdala Central Nucleus (CN) was unaffected by the prior predictive value of the light. These results support claims that the CN is critical to surprise-induced enhancement of attentional processing of CSs.
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Amygdala Central Nucleus lesions disrupt increments, but not decrements, in conditioned stimulus processing.
Behavioral Neuroscience, 1993Co-Authors: Peter C Holland, Michela GallagherAbstract:: The effects of neurotoxic lesions of the amygdala Central Nucleus (CN) on changes in the associability of a conditioned stimulus (CS) in appetitive Pavlovian conditioning were examined in 2 experiments with rats. In Experiment 1, CN lesions had no effect on the reduction in the associability of a CS produced by preexposure to that cue (latent inhibition). In Experiment 2, CN lesions prevented the enhancement of the associability of a CS that is normally observed when an inconsistent predictive relation is arranged between that CS and another cue. The results support previous claims that the amygdala CN is involved in broad-based incremental, but not decremental, changes in the processing of CSs in Pavlovian conditioning.
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Effects of amygdala Central Nucleus lesions on blocking and unblocking.
Behavioral neuroscience, 1993Co-Authors: Peter C Holland, Michela GallagherAbstract:The effects of lesions of the amygdala Central Nucleus (CN) on blocking and unblocking of appetitive Pavlovian conditioning were examined in 2 experiments with rats. In both lesioned and unlesioned rats, prior pairing of one conditioned stimulus (CS) with a food unconditioned stimulus (US) blocked the acquisition of conditioning to a second CS when a compound of both stimuli was paired with that same US. If the value of the US was increased or decreased when the second CS was added, unlesioned rats acquired substantial conditioning to the second cue (unblocking). Unblocking occurred in lesioned rats only when the US value was increased. In both lesioned and unlesioned rats, unblocking was prevented if the compound cue was paired with the original US prior to the change in US value. These data suggest that the CN is involved in increasing attention to signals for significant events but not in tuning out redundant cues.