The Experts below are selected from a list of 204 Experts worldwide ranked by ideXlab platform

Francisco Aboitiz - One of the best experts on this subject based on the ideXlab platform.

  • chronic stress induces dendritic atrophy in the rat Medial Geniculate Nucleus effects on auditory conditioning
    Behavioural Brain Research, 2009
    Co-Authors: Alexies Dagninosubiabre, Gonzalo Terreros, Ursula Wyneken, Benjamin A. Porter, Michael P. Kilgard, Marco Atzori, Pablo Munozllancao, Gabriela Diazveliz, Francisco Aboitiz
    Abstract:

    Chronic stress induces dendritic atrophy in the inferior colliculus (IC, auditory mesencephalon) and impairs auditory avoidance conditioning. The aim of this study was to determine in Golgi preparations and in cued fear conditioning whether stress affects other auditory components, like the thalamic Medial Geniculate Nucleus (MG) or the posterior thalamic Nucleus (PO), in Sprague-Dawley rats. Chronic restraint stress produced a significant dendritic atrophy in the MG (stress: 407+/-55 microm; control: 808+/-120 microm; p<0.01) but did not affect auditory fear conditioning. The last result was in apparent contrast with the fact that stress impairs both the acquisition of auditory avoidance conditioned responses and the dendritic structure in two major nuclei of the auditory system. In order to analyze this disagreement, we investigated whether the stress-related freezing to tone occurring in the fear conditioning protocol corresponded to a conditioned or an unconditioned fear response, using changes in tone instead of light throughout conditioning trials. Chronic stress significantly enhanced visual fear conditioning in stressed animals compared to controls (stress: 58.9+/-8.42%, control: 23.31+/-8.01%; p<0.05), but this fear enhancement was related to unconditioned fear. Conversely, chronic stress did not affect the morphology of the PO (subserving both auditory and somatosensory information) or the corresponding auditory and somatosensory unconditioned responses (acoustic startle response and escape behavior). Our results suggest that the auditory conditioned stimulus can be processed in part independently of the IC and MG in the stressed animals, and sent to the amygdala via the PO inducing unconditioned fear. Comparable alterations could be produced in major depression.

  • Chronic stress induces dendritic atrophy in the rat Medial Geniculate Nucleus: effects on auditory conditioning.
    Behavioural brain research, 2009
    Co-Authors: Alexies Dagnino-subiabre, Pablo Muñoz-llancao, Gonzalo Terreros, Ursula Wyneken, Gabriela Díaz-véliz, Benjamin A. Porter, Michael P. Kilgard, Marco Atzori, Francisco Aboitiz
    Abstract:

    Chronic stress induces dendritic atrophy in the inferior colliculus (IC, auditory mesencephalon) and impairs auditory avoidance conditioning. The aim of this study was to determine in Golgi preparations and in cued fear conditioning whether stress affects other auditory components, like the thalamic Medial Geniculate Nucleus (MG) or the posterior thalamic Nucleus (PO), in Sprague-Dawley rats. Chronic restraint stress produced a significant dendritic atrophy in the MG (stress: 407+/-55 microm; control: 808+/-120 microm; p

Jay Kalra - One of the best experts on this subject based on the ideXlab platform.

  • Superoxide dismutase, catalase, and U78517F attenuate neuronal damage in gerbils with repeated brief ischemic insults
    Neurochemical Research, 1994
    Co-Authors: Debbie Truelove, Ashfaq Shuaib, Sadiq Ijaz, Steve Richardson, Jay Kalra
    Abstract:

    Repeated ischemic insults at one hour intervals result in more severe neuronal damage than a single similar duration insult. The mechanism for the more severe damage with repetitive ischemia is not fully understood. We hypothesized that the prolonged reperfusion periods between the relatively short ischemic insults may result in a pronounced generation of oxygen free radicals (OFRs). In this study, we tested the protective effects of superoxide dismutase (SOD) and catalase (alone or in combination), and U78517F in a gerbil model of repetitive ischemia. Three episodes (two min each) of bilateral carotid occlusion were used at one hour intervals to produce repetitive ischemia. Superoxide dismutase and catalase were infused via osmotic pumps into the lateral ventricles. Two doses of U78517F were given three times per animal, one half hour prior to each occlusion. Neuronal damage was assessed 7 days later in several brain regions using the silver staining technique. The Mann-Whitney U test was used for statistical comparison. Superoxide dismutase showed significant protection in the hippocampus (CA4), striatum, thalamus and the Medial Geniculate Nucleus (MGN). Catalase showed significant protection in the striatum, hippocampus, thalamus, and MGN and the substantia nigra reticulata. Combination of the two resulted in additional protection in the cerebral cortex. Compared to the controls, there was little protection with a dose of 3 mg/kg of U78517F. There was significant protection with a dose of 10 mg/kg in the hippocampus (CA4), striatum, thalamus, Medial Geniculate Nucleus and the substantia nigra reticulata. The significant protection noted with SOD, catalase or U78517F with repeated ischemia supports, the hypothesis that OFRs may play a role in neuronal damage in repeated cerebral ischemia.

  • Neuronal protection with superoxide dismutase in repetitive forebrain ischemia in gerbils
    Free radical biology & medicine, 1994
    Co-Authors: Debbie Truelove, Ashfaq Shuaib, Sadiq Ijaz, Rahmat Ishaqzay, Jay Kalra
    Abstract:

    The underlying mechanism for severe damage with repetitive ischemia is not fully understood. Because of prolonged periods of reperfusions between the brief insults, we speculated that the severe damage may be secondary to excessive generation of oxygen free radicals. In this study we tested the efficacy of peg-superoxide dismutase (SOD) in a model of repeated ischemia in gerbils. Superoxide dismutase (SOD) or vehicle (saline) was delivered through osmotic pumps into the lateral ventricles continuously from the onset of the insult until the gerbils were sacrificed 6 days later. Threee doses of SOD were used in the experiments (110, 150, and 190 units per μl). Damage was assessed using a 0–4 point scoring system and statistical comparisons were done using the Mann-Whitney U-test. There was significant protection in the hippocampus (p < 0.05), striatum (p < 0.001), and substantia nigra reticulata (p < 0.05) in the lowest dose SOD-treated group (110 units per μl). Animals treated with 150 units showed lesser (but significant) protection in the thalamus, Medial Geniculate Nucleus, and striatum. In the animals treated with the higher dose of SOD (190 units per μl), the extent of damage was no different than vehicle-treated controls in the cortex, striatum, and hippocampus. Compared to controls, neuronal damage was, however, significantly more severe in the Medial Geniculate Nucleus and the thalamus in the high-dose SOD-treated animals (p < 0.05). Our experimetns suggest that the SOD may have a small therapeutic window. Higher doses may either have no neuroprotective effects or may be harmful.

  • Repetitive transient forebrain ischemia in gerbils: delayed neuronal damage in the substantia nigra reticulata
    Brain Research, 1992
    Co-Authors: Ashfaq Shuaib, Sadiq Ijaz, Jay Kalra, William E. Code
    Abstract:

    Repetitive cerebral ischemia results in severe neuronal damage in multiple regions of the brain including the hippocampus, striatum, thalamus, Medial Geniculate Nucleus and the substantia nigra reticulata (SNr). We postulated that the damage in the SNr was delayed, resulting from a loss of striatal inhibitory input. We used the gerbil model of repetitive ischemia (3 min times 2 and 3 min times 3) to evaluate the extent of neuronal damage at 2, 3, 5 and 7 days after the ischemic insult. Silver degeneration stain was used for histological evaluation. Our results indicate that damage in the SNr begins after 48 h and is maximum at 7 days. This delay in onset of damage offers a window for pharmacological protection.

Daniel S. Barth - One of the best experts on this subject based on the ideXlab platform.

  • A horseradish peroxidase study of parallel thalamocortical projections responsible for the generation of mid-latency auditory-evoked potentials.
    Brain Research, 1994
    Co-Authors: Barbara Brett, Shi Di, Linda R Watkins, Daniel S. Barth
    Abstract:

    Abstract Mid-latency auditory-evoked potentials (MAEP) were recorded from the parietotemporal region of the rat using a high spatial resolution epicortical multielectrode array. Horseradish peroxidase was injected into regions of primary and secondary auditory cortex which generate spatially and temporally distinct components of the MAEP complex to retrogradely label their thalamocortical projections. These data provide anatomical evidence for three parallel thalamocortical projection systems, originating in the ventral, dorsal and Medial subdivisions of the Medial Geniculate Nucleus, which may be responsible for the asynchronous activation of three distinct subpopulations of cortical neurons giving rise to components of the MAEP complex. Specific and non-specific characteristics of the thalamocortical projections are discussed.

  • A horseradish peroxidase study of parallel thalamocortical projections responsible for the generation of mid-latency auditory-evoked potentials.
    Brain Research, 1994
    Co-Authors: Barbara Brett, Shi Di, Linda R Watkins, Daniel S. Barth
    Abstract:

    Abstract Mid-latency auditory-evoked potentials (MAEP) were recorded from the parietotemporal region of the rat using a high spatial resolution epicortical multielectrode array. Horseradish peroxidase was injected into regions of primary and secondary auditory cortex which generate spatially and temporally distinct components of the MAEP complex to retrogradely label their thalamocortical projections. These data provide anatomical evidence for three parallel thalamocortical projection systems, originating in the ventral, dorsal and Medial subdivisions of the Medial Geniculate Nucleus, which may be responsible for the asynchronous activation of three distinct subpopulations of cortical neurons giving rise to components of the MAEP complex. Specific and non-specific characteristics of the thalamocortical projections are discussed.

Ursula Wyneken - One of the best experts on this subject based on the ideXlab platform.

  • chronic stress induces dendritic atrophy in the rat Medial Geniculate Nucleus effects on auditory conditioning
    Behavioural Brain Research, 2009
    Co-Authors: Alexies Dagninosubiabre, Gonzalo Terreros, Ursula Wyneken, Benjamin A. Porter, Michael P. Kilgard, Marco Atzori, Pablo Munozllancao, Gabriela Diazveliz, Francisco Aboitiz
    Abstract:

    Chronic stress induces dendritic atrophy in the inferior colliculus (IC, auditory mesencephalon) and impairs auditory avoidance conditioning. The aim of this study was to determine in Golgi preparations and in cued fear conditioning whether stress affects other auditory components, like the thalamic Medial Geniculate Nucleus (MG) or the posterior thalamic Nucleus (PO), in Sprague-Dawley rats. Chronic restraint stress produced a significant dendritic atrophy in the MG (stress: 407+/-55 microm; control: 808+/-120 microm; p<0.01) but did not affect auditory fear conditioning. The last result was in apparent contrast with the fact that stress impairs both the acquisition of auditory avoidance conditioned responses and the dendritic structure in two major nuclei of the auditory system. In order to analyze this disagreement, we investigated whether the stress-related freezing to tone occurring in the fear conditioning protocol corresponded to a conditioned or an unconditioned fear response, using changes in tone instead of light throughout conditioning trials. Chronic stress significantly enhanced visual fear conditioning in stressed animals compared to controls (stress: 58.9+/-8.42%, control: 23.31+/-8.01%; p<0.05), but this fear enhancement was related to unconditioned fear. Conversely, chronic stress did not affect the morphology of the PO (subserving both auditory and somatosensory information) or the corresponding auditory and somatosensory unconditioned responses (acoustic startle response and escape behavior). Our results suggest that the auditory conditioned stimulus can be processed in part independently of the IC and MG in the stressed animals, and sent to the amygdala via the PO inducing unconditioned fear. Comparable alterations could be produced in major depression.

  • Chronic stress induces dendritic atrophy in the rat Medial Geniculate Nucleus: effects on auditory conditioning.
    Behavioural brain research, 2009
    Co-Authors: Alexies Dagnino-subiabre, Pablo Muñoz-llancao, Gonzalo Terreros, Ursula Wyneken, Gabriela Díaz-véliz, Benjamin A. Porter, Michael P. Kilgard, Marco Atzori, Francisco Aboitiz
    Abstract:

    Chronic stress induces dendritic atrophy in the inferior colliculus (IC, auditory mesencephalon) and impairs auditory avoidance conditioning. The aim of this study was to determine in Golgi preparations and in cued fear conditioning whether stress affects other auditory components, like the thalamic Medial Geniculate Nucleus (MG) or the posterior thalamic Nucleus (PO), in Sprague-Dawley rats. Chronic restraint stress produced a significant dendritic atrophy in the MG (stress: 407+/-55 microm; control: 808+/-120 microm; p

Gonzalo Terreros - One of the best experts on this subject based on the ideXlab platform.

  • chronic stress induces dendritic atrophy in the rat Medial Geniculate Nucleus effects on auditory conditioning
    Behavioural Brain Research, 2009
    Co-Authors: Alexies Dagninosubiabre, Gonzalo Terreros, Ursula Wyneken, Benjamin A. Porter, Michael P. Kilgard, Marco Atzori, Pablo Munozllancao, Gabriela Diazveliz, Francisco Aboitiz
    Abstract:

    Chronic stress induces dendritic atrophy in the inferior colliculus (IC, auditory mesencephalon) and impairs auditory avoidance conditioning. The aim of this study was to determine in Golgi preparations and in cued fear conditioning whether stress affects other auditory components, like the thalamic Medial Geniculate Nucleus (MG) or the posterior thalamic Nucleus (PO), in Sprague-Dawley rats. Chronic restraint stress produced a significant dendritic atrophy in the MG (stress: 407+/-55 microm; control: 808+/-120 microm; p<0.01) but did not affect auditory fear conditioning. The last result was in apparent contrast with the fact that stress impairs both the acquisition of auditory avoidance conditioned responses and the dendritic structure in two major nuclei of the auditory system. In order to analyze this disagreement, we investigated whether the stress-related freezing to tone occurring in the fear conditioning protocol corresponded to a conditioned or an unconditioned fear response, using changes in tone instead of light throughout conditioning trials. Chronic stress significantly enhanced visual fear conditioning in stressed animals compared to controls (stress: 58.9+/-8.42%, control: 23.31+/-8.01%; p<0.05), but this fear enhancement was related to unconditioned fear. Conversely, chronic stress did not affect the morphology of the PO (subserving both auditory and somatosensory information) or the corresponding auditory and somatosensory unconditioned responses (acoustic startle response and escape behavior). Our results suggest that the auditory conditioned stimulus can be processed in part independently of the IC and MG in the stressed animals, and sent to the amygdala via the PO inducing unconditioned fear. Comparable alterations could be produced in major depression.

  • Chronic stress induces dendritic atrophy in the rat Medial Geniculate Nucleus: effects on auditory conditioning.
    Behavioural brain research, 2009
    Co-Authors: Alexies Dagnino-subiabre, Pablo Muñoz-llancao, Gonzalo Terreros, Ursula Wyneken, Gabriela Díaz-véliz, Benjamin A. Porter, Michael P. Kilgard, Marco Atzori, Francisco Aboitiz
    Abstract:

    Chronic stress induces dendritic atrophy in the inferior colliculus (IC, auditory mesencephalon) and impairs auditory avoidance conditioning. The aim of this study was to determine in Golgi preparations and in cued fear conditioning whether stress affects other auditory components, like the thalamic Medial Geniculate Nucleus (MG) or the posterior thalamic Nucleus (PO), in Sprague-Dawley rats. Chronic restraint stress produced a significant dendritic atrophy in the MG (stress: 407+/-55 microm; control: 808+/-120 microm; p