The Experts below are selected from a list of 252 Experts worldwide ranked by ideXlab platform
M. P. Stryker - One of the best experts on this subject based on the ideXlab platform.
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INFUSION OF NERVE GROWTH FACTOR (NGF) INTO KITTEN VISUAL CORTEX INCREASES IMMUNOREACTIVITY FOR NGF, NGF RECEPTORS, AND CHOLINE ACETYLTRANSFERASE IN BASAL FOREBRAIN WITHOUT AFFECTING OCULAR DOMINANCE PLASTICITY OR COLUMN DEVELOPMENT
2013Co-Authors: M. A. Silver, M. Fagiolini, D. C. Gillespie, C. L. Howe, M. G. Frank, N. P. Issa, A. Antonini, M. P. StrykerAbstract:AbstractöIntracerebroventricular or intracortical administration of nerve growth factor (NGF) has been shown to block or attenuate visual cortical plasticity in the rat. In cats and ferrets, the e¡ects of exogenous NGF on development and plasticity of visual cortex have been reported to be small or nonexistent. To determine whether locally delivered NGF a¡ects ocular dominance column formation or the plasticity produced by monocular deprivation in cats at the height of the critical period, we infused recombinant human NGF into the primary visual cortex of kittens using an implanted cannula Minipump. NGF had no e¡ect on the normal developmental segregation of geniculocortical a¡erents into ocular dominance columns as determined both physiologically and anatomically. The plasticity of binocular visual cortical responses induced by monocular deprivation was also normal in regions of immunohistochemically detectable NGF infusion, as measured using intrinsic signal optical imaging and single-unit electrophysiology. Immunohistochemical analysis of the basal forebrain regions of the same animals demonstrated that the NGF infused into cortex was biologically active, producing an increase in the number of NGF-, TrkA-, p75NTR-, and choline acetyltransferase-positive neurons in basal forebrain nuclei in the hemisphere ipsilateral to the NGF Minipump compared to the contralateral basal forebrain neurons
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infusion of nerve growth factor ngf into kitten visual cortex increases immunoreactivity for ngf ngf receptors and choline acetyltransferase in basal forebrain without affecting ocular dominance plasticity or column development
Neuroscience, 2001Co-Authors: M. A. Silver, M. Fagiolini, D. C. Gillespie, C. L. Howe, M. G. Frank, N. P. Issa, A. Antonini, M. P. StrykerAbstract:Intracerebroventricular or intracortical administration of nerve growth factor (NGF) has been shown to block or attenuate visual cortical plasticity in the rat. In cats and ferrets, the effects of exogenous NGF on development and plasticity of visual cortex have been reported to be small or nonexistent. To determine whether locally delivered NGF affects ocular dominance column formation or the plasticity produced by monocular deprivation in cats at the height of the critical period, we infused recombinant human NGF into the primary visual cortex of kittens using an implanted cannula Minipump. NGF had no effect on the normal developmental segregation of geniculocortical afferents into ocular dominance columns as determined both physiologically and anatomically. The plasticity of binocular visual cortical responses induced by monocular deprivation was also normal in regions of immunohistochemically detectable NGF infusion, as measured using intrinsic signal optical imaging and single-unit electrophysiology. Immunohistochemical analysis of the basal forebrain regions of the same animals demonstrated that the NGF infused into cortex was biologically active, producing an increase in the number of NGF-, TrkA-, p75NTR-, and choline acetyltransferase-positive neurons in basal forebrain nuclei in the hemisphere ipsilateral to the NGF Minipump compared to the contralateral basal forebrain neurons. We conclude that NGF delivered locally to axon terminals of cholinergic basal forebrain neurons resulted in increases in protein expression at the cell body through retrograde signaling.
Byron C. Yoburn - One of the best experts on this subject based on the ideXlab platform.
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μ-Opioid receptor downregulation contributes to opioid tolerance in vivo
Pharmacology Biochemistry and Behavior, 2001Co-Authors: Kristi Stafford, A. Benedict Gomes, Ji Shen, Byron C. YoburnAbstract:The present study examined the contribution of downregulation of μ-opioid receptors to opioid tolerance in an intact animal model. Mice were implanted subcutaneously with osmotic Minipumps that infused etorphine (50–250 μg/kg/day) for 7 days. Other mice were implanted subcutaneously with a morphine pellet (25 mg) or a morphine pellet plus an osmotic Minipump that infused morphine (5–40 mg/kg/day) for 7 days. Controls were implanted with an inert placebo pellet. At the end of treatment, pumps and pellets were removed, and saturation binding studies were conducted in whole brain ([3H]DAMGO) or morphine and etorphine analgesic ED50s were determined (tail-flick). Morphine tolerance increased linearly with the infusion dose of morphine (ED50 shift at highest infusion dose, 4.76). No significant downregulation of μ-receptors in whole brain was observed at the highest morphine treatment dose. Etorphine produced dose-dependent downregulation of μ-opioid receptor density and tolerance (ED50 shift at highest infusion dose, 6.97). Downregulation of μ-receptors only occurred at the higher etorphine infusion doses (≥150 μg/kg/day). Unlike morphine tolerance, the magnitude of etorphine tolerance was a nonlinear function of the dose and increased markedly at infusion doses that produced downregulation. These results suggest that μ-opioid receptor downregulation contributes to opioid tolerance in vivo. Therefore, opioid tolerance appears to rely upon both “receptor density-dependent” and “ receptor density-independent” mechanisms.
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mu-Opioid receptor downregulation contributes to opioid tolerance in vivo.
Pharmacology Biochemistry and Behavior, 2001Co-Authors: Kristi Stafford, A. Benedict Gomes, Ji Shen, Byron C. YoburnAbstract:The present study examined the contribution of downregulation of mu-opioid receptors to opioid tolerance in an intact animal model. Mice were implanted subcutaneously with osmotic Minipumps that infused etorphine (50-250 microg/kg/day) for 7 days. Other mice were implanted subcutaneously with a morphine pellet (25 mg) or a morphine pellet plus an osmotic Minipump that infused morphine (5-40 mg/kg/day) for 7 days. Controls were implanted with an inert placebo pellet. At the end of treatment, pumps and pellets were removed, and saturation binding studies were conducted in whole brain ([3H]DAMGO) or morphine and etorphine analgesic ED(50)s were determined (tail-flick). Morphine tolerance increased linearly with the infusion dose of morphine (ED(50) shift at highest infusion dose, 4.76). No significant downregulation of mu-receptors in whole brain was observed at the highest morphine treatment dose. Etorphine produced dose-dependent downregulation of mu-opioid receptor density and tolerance (ED(50) shift at highest infusion dose, 6.97). Downregulation of mu-receptors only occurred at the higher etorphine infusion doses (> or =150 microg/kg/day). Unlike morphine tolerance, the magnitude of etorphine tolerance was a nonlinear function of the dose and increased markedly at infusion doses that produced downregulation. These results suggest that mu-opioid receptor downregulation contributes to opioid tolerance in vivo. Therefore, opioid tolerance appears to rely upon both "receptor density-dependent" and " receptor density-independent" mechanisms.
M. A. Silver - One of the best experts on this subject based on the ideXlab platform.
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INFUSION OF NERVE GROWTH FACTOR (NGF) INTO KITTEN VISUAL CORTEX INCREASES IMMUNOREACTIVITY FOR NGF, NGF RECEPTORS, AND CHOLINE ACETYLTRANSFERASE IN BASAL FOREBRAIN WITHOUT AFFECTING OCULAR DOMINANCE PLASTICITY OR COLUMN DEVELOPMENT
2013Co-Authors: M. A. Silver, M. Fagiolini, D. C. Gillespie, C. L. Howe, M. G. Frank, N. P. Issa, A. Antonini, M. P. StrykerAbstract:AbstractöIntracerebroventricular or intracortical administration of nerve growth factor (NGF) has been shown to block or attenuate visual cortical plasticity in the rat. In cats and ferrets, the e¡ects of exogenous NGF on development and plasticity of visual cortex have been reported to be small or nonexistent. To determine whether locally delivered NGF a¡ects ocular dominance column formation or the plasticity produced by monocular deprivation in cats at the height of the critical period, we infused recombinant human NGF into the primary visual cortex of kittens using an implanted cannula Minipump. NGF had no e¡ect on the normal developmental segregation of geniculocortical a¡erents into ocular dominance columns as determined both physiologically and anatomically. The plasticity of binocular visual cortical responses induced by monocular deprivation was also normal in regions of immunohistochemically detectable NGF infusion, as measured using intrinsic signal optical imaging and single-unit electrophysiology. Immunohistochemical analysis of the basal forebrain regions of the same animals demonstrated that the NGF infused into cortex was biologically active, producing an increase in the number of NGF-, TrkA-, p75NTR-, and choline acetyltransferase-positive neurons in basal forebrain nuclei in the hemisphere ipsilateral to the NGF Minipump compared to the contralateral basal forebrain neurons
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infusion of nerve growth factor ngf into kitten visual cortex increases immunoreactivity for ngf ngf receptors and choline acetyltransferase in basal forebrain without affecting ocular dominance plasticity or column development
Neuroscience, 2001Co-Authors: M. A. Silver, M. Fagiolini, D. C. Gillespie, C. L. Howe, M. G. Frank, N. P. Issa, A. Antonini, M. P. StrykerAbstract:Intracerebroventricular or intracortical administration of nerve growth factor (NGF) has been shown to block or attenuate visual cortical plasticity in the rat. In cats and ferrets, the effects of exogenous NGF on development and plasticity of visual cortex have been reported to be small or nonexistent. To determine whether locally delivered NGF affects ocular dominance column formation or the plasticity produced by monocular deprivation in cats at the height of the critical period, we infused recombinant human NGF into the primary visual cortex of kittens using an implanted cannula Minipump. NGF had no effect on the normal developmental segregation of geniculocortical afferents into ocular dominance columns as determined both physiologically and anatomically. The plasticity of binocular visual cortical responses induced by monocular deprivation was also normal in regions of immunohistochemically detectable NGF infusion, as measured using intrinsic signal optical imaging and single-unit electrophysiology. Immunohistochemical analysis of the basal forebrain regions of the same animals demonstrated that the NGF infused into cortex was biologically active, producing an increase in the number of NGF-, TrkA-, p75NTR-, and choline acetyltransferase-positive neurons in basal forebrain nuclei in the hemisphere ipsilateral to the NGF Minipump compared to the contralateral basal forebrain neurons. We conclude that NGF delivered locally to axon terminals of cholinergic basal forebrain neurons resulted in increases in protein expression at the cell body through retrograde signaling.
Kristi Stafford - One of the best experts on this subject based on the ideXlab platform.
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μ-Opioid receptor downregulation contributes to opioid tolerance in vivo
Pharmacology Biochemistry and Behavior, 2001Co-Authors: Kristi Stafford, A. Benedict Gomes, Ji Shen, Byron C. YoburnAbstract:The present study examined the contribution of downregulation of μ-opioid receptors to opioid tolerance in an intact animal model. Mice were implanted subcutaneously with osmotic Minipumps that infused etorphine (50–250 μg/kg/day) for 7 days. Other mice were implanted subcutaneously with a morphine pellet (25 mg) or a morphine pellet plus an osmotic Minipump that infused morphine (5–40 mg/kg/day) for 7 days. Controls were implanted with an inert placebo pellet. At the end of treatment, pumps and pellets were removed, and saturation binding studies were conducted in whole brain ([3H]DAMGO) or morphine and etorphine analgesic ED50s were determined (tail-flick). Morphine tolerance increased linearly with the infusion dose of morphine (ED50 shift at highest infusion dose, 4.76). No significant downregulation of μ-receptors in whole brain was observed at the highest morphine treatment dose. Etorphine produced dose-dependent downregulation of μ-opioid receptor density and tolerance (ED50 shift at highest infusion dose, 6.97). Downregulation of μ-receptors only occurred at the higher etorphine infusion doses (≥150 μg/kg/day). Unlike morphine tolerance, the magnitude of etorphine tolerance was a nonlinear function of the dose and increased markedly at infusion doses that produced downregulation. These results suggest that μ-opioid receptor downregulation contributes to opioid tolerance in vivo. Therefore, opioid tolerance appears to rely upon both “receptor density-dependent” and “ receptor density-independent” mechanisms.
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mu-Opioid receptor downregulation contributes to opioid tolerance in vivo.
Pharmacology Biochemistry and Behavior, 2001Co-Authors: Kristi Stafford, A. Benedict Gomes, Ji Shen, Byron C. YoburnAbstract:The present study examined the contribution of downregulation of mu-opioid receptors to opioid tolerance in an intact animal model. Mice were implanted subcutaneously with osmotic Minipumps that infused etorphine (50-250 microg/kg/day) for 7 days. Other mice were implanted subcutaneously with a morphine pellet (25 mg) or a morphine pellet plus an osmotic Minipump that infused morphine (5-40 mg/kg/day) for 7 days. Controls were implanted with an inert placebo pellet. At the end of treatment, pumps and pellets were removed, and saturation binding studies were conducted in whole brain ([3H]DAMGO) or morphine and etorphine analgesic ED(50)s were determined (tail-flick). Morphine tolerance increased linearly with the infusion dose of morphine (ED(50) shift at highest infusion dose, 4.76). No significant downregulation of mu-receptors in whole brain was observed at the highest morphine treatment dose. Etorphine produced dose-dependent downregulation of mu-opioid receptor density and tolerance (ED(50) shift at highest infusion dose, 6.97). Downregulation of mu-receptors only occurred at the higher etorphine infusion doses (> or =150 microg/kg/day). Unlike morphine tolerance, the magnitude of etorphine tolerance was a nonlinear function of the dose and increased markedly at infusion doses that produced downregulation. These results suggest that mu-opioid receptor downregulation contributes to opioid tolerance in vivo. Therefore, opioid tolerance appears to rely upon both "receptor density-dependent" and " receptor density-independent" mechanisms.
D. C. Gillespie - One of the best experts on this subject based on the ideXlab platform.
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INFUSION OF NERVE GROWTH FACTOR (NGF) INTO KITTEN VISUAL CORTEX INCREASES IMMUNOREACTIVITY FOR NGF, NGF RECEPTORS, AND CHOLINE ACETYLTRANSFERASE IN BASAL FOREBRAIN WITHOUT AFFECTING OCULAR DOMINANCE PLASTICITY OR COLUMN DEVELOPMENT
2013Co-Authors: M. A. Silver, M. Fagiolini, D. C. Gillespie, C. L. Howe, M. G. Frank, N. P. Issa, A. Antonini, M. P. StrykerAbstract:AbstractöIntracerebroventricular or intracortical administration of nerve growth factor (NGF) has been shown to block or attenuate visual cortical plasticity in the rat. In cats and ferrets, the e¡ects of exogenous NGF on development and plasticity of visual cortex have been reported to be small or nonexistent. To determine whether locally delivered NGF a¡ects ocular dominance column formation or the plasticity produced by monocular deprivation in cats at the height of the critical period, we infused recombinant human NGF into the primary visual cortex of kittens using an implanted cannula Minipump. NGF had no e¡ect on the normal developmental segregation of geniculocortical a¡erents into ocular dominance columns as determined both physiologically and anatomically. The plasticity of binocular visual cortical responses induced by monocular deprivation was also normal in regions of immunohistochemically detectable NGF infusion, as measured using intrinsic signal optical imaging and single-unit electrophysiology. Immunohistochemical analysis of the basal forebrain regions of the same animals demonstrated that the NGF infused into cortex was biologically active, producing an increase in the number of NGF-, TrkA-, p75NTR-, and choline acetyltransferase-positive neurons in basal forebrain nuclei in the hemisphere ipsilateral to the NGF Minipump compared to the contralateral basal forebrain neurons
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infusion of nerve growth factor ngf into kitten visual cortex increases immunoreactivity for ngf ngf receptors and choline acetyltransferase in basal forebrain without affecting ocular dominance plasticity or column development
Neuroscience, 2001Co-Authors: M. A. Silver, M. Fagiolini, D. C. Gillespie, C. L. Howe, M. G. Frank, N. P. Issa, A. Antonini, M. P. StrykerAbstract:Intracerebroventricular or intracortical administration of nerve growth factor (NGF) has been shown to block or attenuate visual cortical plasticity in the rat. In cats and ferrets, the effects of exogenous NGF on development and plasticity of visual cortex have been reported to be small or nonexistent. To determine whether locally delivered NGF affects ocular dominance column formation or the plasticity produced by monocular deprivation in cats at the height of the critical period, we infused recombinant human NGF into the primary visual cortex of kittens using an implanted cannula Minipump. NGF had no effect on the normal developmental segregation of geniculocortical afferents into ocular dominance columns as determined both physiologically and anatomically. The plasticity of binocular visual cortical responses induced by monocular deprivation was also normal in regions of immunohistochemically detectable NGF infusion, as measured using intrinsic signal optical imaging and single-unit electrophysiology. Immunohistochemical analysis of the basal forebrain regions of the same animals demonstrated that the NGF infused into cortex was biologically active, producing an increase in the number of NGF-, TrkA-, p75NTR-, and choline acetyltransferase-positive neurons in basal forebrain nuclei in the hemisphere ipsilateral to the NGF Minipump compared to the contralateral basal forebrain neurons. We conclude that NGF delivered locally to axon terminals of cholinergic basal forebrain neurons resulted in increases in protein expression at the cell body through retrograde signaling.