The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform
V R King - One of the best experts on this subject based on the ideXlab platform.
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changes in truncated trkb and p75 Receptor Expression in the rat spinal cord following spinal cord hemisection and spinal cord hemisection plus neurotrophin treatment
Experimental Neurology, 2000Co-Authors: V R King, Elizabeth J Bradbury, Stephen B. Mcmahon, John V PriestleyAbstract:Although numerous studies have examined the effects of neurotrophin treatment following spinal cord injury, few have examined the changes that occur in the neurotrophin Receptors following either such damage or neurotrophin treatment. To determine what changes occur in neurotrophin Receptor Expression following spinal cord damage, adult rats received a midthoracic spinal cord hemisection alone or in combination with intrathecal application of brain-derived neurotrophic factor (BDNF) or neurotrophin-3 (NT-3). Using immunohistochemical and in situ hybridization techniques, p75, trkA, trkB, and trkC Receptor Expression was examined throughout the spinal cord. Results showed that trkA, full-length trkB, and trkC Receptors were not present in the lesion site but had a normal Expression pattern in uninjured parts of the spinal cord. In contrast, p75 Receptor Expression occurred on Schwann cells throughout the lesion site. BDNF and NT-3 (but not saline) applied to the lesion site increased this Expression. In addition, the truncated trkB Receptor was expressed in the border between the lesion and intact spinal cord. Truncated trkB Receptor Expression was also increased throughout the white matter ipsilateral to the lesion and BDNF (but not NT-3 or saline) prevented this increase. The study is the first to show changes in truncated trkB Receptor Expression that extend beyond the site of a spinal cord lesion and is one of the first to show that BDNF and NT-3 affect Schwann cells and/or p75 Expression following spinal cord damage. These results indicate that changes in neurotrophin Receptor Expression following spinal cord injury could influence the availability of neurotrophins at the lesion site. In addition, neurotrophins may affect their own availability to damaged neurons by altering the Expression of the p75 and truncated trkB Receptor.
John V Priestley - One of the best experts on this subject based on the ideXlab platform.
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changes in truncated trkb and p75 Receptor Expression in the rat spinal cord following spinal cord hemisection and spinal cord hemisection plus neurotrophin treatment
Experimental Neurology, 2000Co-Authors: V R King, Elizabeth J Bradbury, Stephen B. Mcmahon, John V PriestleyAbstract:Although numerous studies have examined the effects of neurotrophin treatment following spinal cord injury, few have examined the changes that occur in the neurotrophin Receptors following either such damage or neurotrophin treatment. To determine what changes occur in neurotrophin Receptor Expression following spinal cord damage, adult rats received a midthoracic spinal cord hemisection alone or in combination with intrathecal application of brain-derived neurotrophic factor (BDNF) or neurotrophin-3 (NT-3). Using immunohistochemical and in situ hybridization techniques, p75, trkA, trkB, and trkC Receptor Expression was examined throughout the spinal cord. Results showed that trkA, full-length trkB, and trkC Receptors were not present in the lesion site but had a normal Expression pattern in uninjured parts of the spinal cord. In contrast, p75 Receptor Expression occurred on Schwann cells throughout the lesion site. BDNF and NT-3 (but not saline) applied to the lesion site increased this Expression. In addition, the truncated trkB Receptor was expressed in the border between the lesion and intact spinal cord. Truncated trkB Receptor Expression was also increased throughout the white matter ipsilateral to the lesion and BDNF (but not NT-3 or saline) prevented this increase. The study is the first to show changes in truncated trkB Receptor Expression that extend beyond the site of a spinal cord lesion and is one of the first to show that BDNF and NT-3 affect Schwann cells and/or p75 Expression following spinal cord damage. These results indicate that changes in neurotrophin Receptor Expression following spinal cord injury could influence the availability of neurotrophins at the lesion site. In addition, neurotrophins may affect their own availability to damaged neurons by altering the Expression of the p75 and truncated trkB Receptor.
Elliot L. Chaikof - One of the best experts on this subject based on the ideXlab platform.
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efferocytosis as a regulator of macrophage chemokine Receptor Expression and polarization
European Journal of Immunology, 2016Co-Authors: Julianty Angsana, Carolyn A. Haller, Elliot L. Chaikof, Jiaxuan ChenAbstract:Efferocytosis has been suggested to promote macrophage resolution programs that are dependent on motility and emigration, however, few studies have addressed directed migration in resolving macrophages. In this report, we hypothesized that efferocytosis would induce differential chemokine Receptor Expression. Polarized macrophage populations, including macrophages actively engaged in efferocytosis, were characterized by PCR array and traditional transwell motility assays. We identified specific up-regulation of chemokine Receptor CXCR4 on both mouse and human macrophages and characterized in vivo Expression of CXCR4 in a resolving model of murine peritonitis. Using adoptive transfer and AMD3100 blocking, we confirmed a role for CXCR4 in macrophage egress to draining lymphatics. Collectively these data provide an important mechanistic link between efferocytosis and macrophage emigration.
James H Meadorwoodruff - One of the best experts on this subject based on the ideXlab platform.
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abnormal glutamate Receptor Expression in the medial temporal lobe in schizophrenia and mood disorders
Neuropsychopharmacology, 2007Co-Authors: Monica Beneyto, Lars V Kristiansen, Akinwunmi Oniorisan, Robert E Mccullumsmith, James H MeadorwoodruffAbstract:Pharmacological and anatomical evidence suggests that abnormal glutamate neurotransmission may be associated with the pathophysiology of schizophrenia and mood disorders. Medial temporal lobe structural alterations have been implicated in schizophrenia and to a lesser extent in mood disorders. To comprehensively examine the ionotropic glutamate Receptors in these illnesses, we used in situ hybridization to determine transcript Expression of N-methyl-D-aspartate (NMDA), α-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA), and kainate Receptor subunits in the medial temporal lobe of subjects with schizophrenia, bipolar disorder (BD), or major depression (MDD). We used Receptor autoradiography to assess changes in glutamate Receptor binding in the same subjects. Our results indicate that there are region- and disorder-specific abnormalities in the Expression of ionotropic glutamate Receptor subunits in schizophrenia and mood disorders. We did not find any changes in transcript Expression in the hippocampus. In the entorhinal cortex, most changes in glutamate Receptor Expression were associated with BD, with decreased GluR2, GluR3, and GluR6 mRNA Expression. In the perirhinal cortex we detected decreased Expression of GluR5 in all three diagnoses, of GluR1, GluR3, NR2B in both BD and MDD, and decreased NR1 and NR2A in BD and MDD, respectively. Receptor binding showed NMDA Receptor subsites particularly affected in the hippocampus, where MK801 binding was reduced in schizophrenia and BD, and MDL105,519 and CGP39653 binding were increased in BD and MDD, respectively. In the hippocampus AMPA and kainate binding were not changed. We found no changes in the entorhinal and perirhinal cortices. These data suggest that glutamate Receptor Expression is altered in the medial temporal lobe in schizophrenia and the mood disorders. We propose that disturbances in glutamate-mediated synaptic transmission in the medial temporal lobe are important factors in the pathophysiology of these severe psychiatric illnesses.
Elizabeth J Bradbury - One of the best experts on this subject based on the ideXlab platform.
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changes in truncated trkb and p75 Receptor Expression in the rat spinal cord following spinal cord hemisection and spinal cord hemisection plus neurotrophin treatment
Experimental Neurology, 2000Co-Authors: V R King, Elizabeth J Bradbury, Stephen B. Mcmahon, John V PriestleyAbstract:Although numerous studies have examined the effects of neurotrophin treatment following spinal cord injury, few have examined the changes that occur in the neurotrophin Receptors following either such damage or neurotrophin treatment. To determine what changes occur in neurotrophin Receptor Expression following spinal cord damage, adult rats received a midthoracic spinal cord hemisection alone or in combination with intrathecal application of brain-derived neurotrophic factor (BDNF) or neurotrophin-3 (NT-3). Using immunohistochemical and in situ hybridization techniques, p75, trkA, trkB, and trkC Receptor Expression was examined throughout the spinal cord. Results showed that trkA, full-length trkB, and trkC Receptors were not present in the lesion site but had a normal Expression pattern in uninjured parts of the spinal cord. In contrast, p75 Receptor Expression occurred on Schwann cells throughout the lesion site. BDNF and NT-3 (but not saline) applied to the lesion site increased this Expression. In addition, the truncated trkB Receptor was expressed in the border between the lesion and intact spinal cord. Truncated trkB Receptor Expression was also increased throughout the white matter ipsilateral to the lesion and BDNF (but not NT-3 or saline) prevented this increase. The study is the first to show changes in truncated trkB Receptor Expression that extend beyond the site of a spinal cord lesion and is one of the first to show that BDNF and NT-3 affect Schwann cells and/or p75 Expression following spinal cord damage. These results indicate that changes in neurotrophin Receptor Expression following spinal cord injury could influence the availability of neurotrophins at the lesion site. In addition, neurotrophins may affect their own availability to damaged neurons by altering the Expression of the p75 and truncated trkB Receptor.
