The Experts below are selected from a list of 177 Experts worldwide ranked by ideXlab platform
Bruce T. Volpe - One of the best experts on this subject based on the ideXlab platform.
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dizocilpine maleate mk 801 but not 2 3 dihydroxy 6 nitro 7 sulfamoyl benzo f quinoxaline nbqx prevents Transneuronal Degeneration of nigral neurons after neurotoxic striatal pallidal lesion
Neuroscience, 1999Co-Authors: Lorraine A. Degiorgio, N Degiorgio, Bruce T. VolpeAbstract:Abstract Unilateral neurotoxin lesion of rat caudate–putamen and globus pallidus resulted in delayed, Transneuronal Degeneration of GABAergic substantia nigra pars reticulata neurons. To explore whether the disinhibition of endogenous glutamate excitatory input played a role in the Degeneration of substantia nigra pars reticulata neurons, animals with unilateral striatal–pallidal lesions received three daily intraperitoneal injections of either dizocilpine maleate (MK-801, 1 or 10 mg/kg), an N-methyl- d -aspartate glutamate receptor blocker, or 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(f)quinoxaline (NBQX, 30 mg/kg), an α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptor blocker, that began 24 h after the striatal–pallidal neurotoxin lesion. Drug treatment affected neither the volume of the initial lesion nor the volume of striatal–pallidal glial fibrillary acidic protein immunoreactivity. Neuron number in the substantia nigra pars reticulata ipsilateral to the lesioned striatopallidum was reduced on average by 37% in untreated control rats, in low dose MK-801, and NBQX-treated rats (P These data demonstrate that dose-related treatment with N-methyl- d -aspartate glutamate receptor blockers protects substantia nigra pars reticulata neurons, and suggests that glutamatergic mechanisms play a role in delayed Transneuronal Degeneration.
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Histological and temporal characteristics of nigral Transneuronal Degeneration after striatal injury
Brain Research, 1998Co-Authors: Lorraine A. Degiorgio, Christine Dibinis, Teresa A. Milner, Makoto Saji, Bruce T. VolpeAbstract:Neurotoxic injury of the caudate-putamen and lateral globus pallidus unilaterally initiated Transneuronal Degeneration of neurons in the ipsilateral substantia nigra reticulata (SNR). Quantification of SNR neurons using unbiased stereology demonstrated that neuron loss began 4 days after the initial striatal lesion, followed by significant loss (50%) at 6 days and a plateau at 8 days. Analysis at the light and ultrastructural levels revealed morphological changes consistent with a type of programmed cell death. These temporal and histological results refine an in vivo model in which to explore mechanisms of delayed neuronal Degeneration.
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behavioral correlates of Transneuronal Degeneration of substantia nigra reticulata neurons are reversed by ablation of the subthalamic nucleus
Behavioural Brain Research, 1997Co-Authors: Makoto Saii, Bruce T. Volpe, Yukio Endo, Tatsuya Miyanishi, Kousaku OhnoAbstract:In rats, acute injury of neurons in the caudate nucleus (CN) and globus pallidus (GP) by local injection of ibotenic acid (IA) or by transient forebrain ischemia has caused Transneuronal cell death of neurons in the substantia nigra reticulata (SNr) weeks after the initial injury. Recently transient expression of an immediate early gene c-fos was induced specifically in neurons of the subthalamic nucleus (STN) and SNr at 36-48 h after the IA-lesions, prior to the delayed Degeneration of SNr neurons. These cellular and molecular events may alter the level of inhibitory output from the basal ganglia and lead to movement disorders. To test (i) whether movement disorders occur in the early period after unilateral lesions of the CN and GP by IA-injection, and (ii) whether ablation of the STN reverses the early movement disorders, we used a modified version of Porsolt forced swim test in which the lesion-induced asymmetry of motor function becomes apparent as rotation when the animals are forced to swim. Following unilateral IA-lesions of the right CN and GP in rats, rapid contraversive rotation appeared transiently 36-48 h after the lesions, and, in turn, slow ipsiversive rotation appeared at 3-5 days postlesion. Prior ablation of the ipsilateral STN reversed these early movement disorders produced by the unilateral IA-lesions of the CN and GP and instead created persistent contraversive rotation 7-10 days after the lesions. Each phase of the dominant rotation behavior was dependent on asymmetrical limb motor activity; decreased left limb activity caused contraversive rotation, and increased left limb activity caused ipsiversive rotation. Reversal of these early movement disorders suggests that ablatin of the STN prevents the Transneuronal Degeneration of the SNr.
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prevention of Transneuronal Degeneration of neurons in the substantia nigra reticulata by ablation of the subthalamic nucleus
Experimental Neurology, 1996Co-Authors: Makoto Saji, Alan D Blau, Bruce T. VolpeAbstract:Transneuronal Degeneration (TND) of neurons in the substantia nigra reticulata (SNR) occurs after initial ischemic or neurotoxin damage to the striatum. The mechanism is incompletely understood. In rats ibotenic acid (IBO) lesion of the caudate nucleus (CN) and the globus pallidus (GP) caused, 3 weeks later, a 47% loss of neurons (P < 0.001) in the SNR. Rats with IBO lesion confined to either the CN or the GP had SNR neuron numbers comparable to control. The volume of the SNR was decreased, as expected, in all groups with striatal lesions. To test whether the subthalamic nucleus (STN) played a role in the demise of SNR neurons, the STN was lesioned 1 week before animals were exposed to CN and GP injury. STN ablation prevented the expected SNR neuron loss. Based on the current information about basal ganglia anatomy, an imbalance between GABAergic and glutamatergic afferents may have caused TND in the SNR. These results suggest that the potential for the release of intrinsic excitotoxicity exists within certain anatomic networks.
Fusahiro Ikuta - One of the best experts on this subject based on the ideXlab platform.
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evidence for Transneuronal Degeneration in the spinal cord in man a quantitative investigation of neurons in the intermediate zone after long term amputation of the unilateral upper arm
Acta Neuropathologica, 1995Co-Authors: Hiroshi Suzuki, Kiyomitsu Oyanagi, Hitoshi Takahashi, Fusahiro IkutaAbstract:Does Transneuronal Degeneration occur in the neurons of the spinal intermediate zone following Degeneration of the anterior horn cells in man? To investigate this possibility, we carried out a quantitative examination of neurons in the cervical intermediate zone of a 56-yearold man who had suffered accidental amputation of the right upper arm 38 years prior to death. Recently, we reported that the cervical anterior horn cells of this patient were reduced in number not only on the amputation side but also on the spared side. The present study revealed that medium-sized neurons in the cervical intermediate zone, which were considered to be internuncial neurons, were decreased in number on both the amputation and the spared sides, but less so on the spared side. These findings indicate that retrograde Transneuronal Degeneration occurs in the internuncial neurons following Degeneration of the anterior horn cells caused by amputation. Sequentially to this, Degeneration of the commissural neurons in the intermediate zone secondary to that of the internuncial neurons may induce Degeneration of the neurons in the intermediate zone and the anterior horn cells on the spared side.
Lorraine A. Degiorgio - One of the best experts on this subject based on the ideXlab platform.
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dizocilpine maleate mk 801 but not 2 3 dihydroxy 6 nitro 7 sulfamoyl benzo f quinoxaline nbqx prevents Transneuronal Degeneration of nigral neurons after neurotoxic striatal pallidal lesion
Neuroscience, 1999Co-Authors: Lorraine A. Degiorgio, N Degiorgio, Bruce T. VolpeAbstract:Abstract Unilateral neurotoxin lesion of rat caudate–putamen and globus pallidus resulted in delayed, Transneuronal Degeneration of GABAergic substantia nigra pars reticulata neurons. To explore whether the disinhibition of endogenous glutamate excitatory input played a role in the Degeneration of substantia nigra pars reticulata neurons, animals with unilateral striatal–pallidal lesions received three daily intraperitoneal injections of either dizocilpine maleate (MK-801, 1 or 10 mg/kg), an N-methyl- d -aspartate glutamate receptor blocker, or 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(f)quinoxaline (NBQX, 30 mg/kg), an α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptor blocker, that began 24 h after the striatal–pallidal neurotoxin lesion. Drug treatment affected neither the volume of the initial lesion nor the volume of striatal–pallidal glial fibrillary acidic protein immunoreactivity. Neuron number in the substantia nigra pars reticulata ipsilateral to the lesioned striatopallidum was reduced on average by 37% in untreated control rats, in low dose MK-801, and NBQX-treated rats (P These data demonstrate that dose-related treatment with N-methyl- d -aspartate glutamate receptor blockers protects substantia nigra pars reticulata neurons, and suggests that glutamatergic mechanisms play a role in delayed Transneuronal Degeneration.
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Histological and temporal characteristics of nigral Transneuronal Degeneration after striatal injury
Brain Research, 1998Co-Authors: Lorraine A. Degiorgio, Christine Dibinis, Teresa A. Milner, Makoto Saji, Bruce T. VolpeAbstract:Neurotoxic injury of the caudate-putamen and lateral globus pallidus unilaterally initiated Transneuronal Degeneration of neurons in the ipsilateral substantia nigra reticulata (SNR). Quantification of SNR neurons using unbiased stereology demonstrated that neuron loss began 4 days after the initial striatal lesion, followed by significant loss (50%) at 6 days and a plateau at 8 days. Analysis at the light and ultrastructural levels revealed morphological changes consistent with a type of programmed cell death. These temporal and histological results refine an in vivo model in which to explore mechanisms of delayed neuronal Degeneration.
Makoto Saji - One of the best experts on this subject based on the ideXlab platform.
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Histological and temporal characteristics of nigral Transneuronal Degeneration after striatal injury
Brain Research, 1998Co-Authors: Lorraine A. Degiorgio, Christine Dibinis, Teresa A. Milner, Makoto Saji, Bruce T. VolpeAbstract:Neurotoxic injury of the caudate-putamen and lateral globus pallidus unilaterally initiated Transneuronal Degeneration of neurons in the ipsilateral substantia nigra reticulata (SNR). Quantification of SNR neurons using unbiased stereology demonstrated that neuron loss began 4 days after the initial striatal lesion, followed by significant loss (50%) at 6 days and a plateau at 8 days. Analysis at the light and ultrastructural levels revealed morphological changes consistent with a type of programmed cell death. These temporal and histological results refine an in vivo model in which to explore mechanisms of delayed neuronal Degeneration.
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prevention of Transneuronal Degeneration of neurons in the substantia nigra reticulata by ablation of the subthalamic nucleus
Experimental Neurology, 1996Co-Authors: Makoto Saji, Alan D Blau, Bruce T. VolpeAbstract:Transneuronal Degeneration (TND) of neurons in the substantia nigra reticulata (SNR) occurs after initial ischemic or neurotoxin damage to the striatum. The mechanism is incompletely understood. In rats ibotenic acid (IBO) lesion of the caudate nucleus (CN) and the globus pallidus (GP) caused, 3 weeks later, a 47% loss of neurons (P < 0.001) in the SNR. Rats with IBO lesion confined to either the CN or the GP had SNR neuron numbers comparable to control. The volume of the SNR was decreased, as expected, in all groups with striatal lesions. To test whether the subthalamic nucleus (STN) played a role in the demise of SNR neurons, the STN was lesioned 1 week before animals were exposed to CN and GP injury. STN ablation prevented the expected SNR neuron loss. Based on the current information about basal ganglia anatomy, an imbalance between GABAergic and glutamatergic afferents may have caused TND in the SNR. These results suggest that the potential for the release of intrinsic excitotoxicity exists within certain anatomic networks.
James A Bourne - One of the best experts on this subject based on the ideXlab platform.
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retrograde Transneuronal Degeneration in the retina and lateral geniculate nucleus of the v1 lesioned marmoset monkey
Brain Structure & Function, 2015Co-Authors: Anita E Hendrickson, Claire E Warner, Daniel E Possin, Jing Huang, William C Kwan, James A BourneAbstract:Retrograde Transneuronal Degeneration (RTD) of retinal ganglion cells and dorsal lateral geniculate (LGN) neurons are well described following a lesion of the primary visual cortex (V1) in both Old World monkeys and humans. Based on previous studies of New World monkeys and prosimians, it was suggested that these species displayed no RTD following a lesion of V1. In this study of the New World marmoset monkey, 1 year after a unilateral V1 lesion either in adults or at 14 days after birth, we observed ~20 % ganglion cell (GC) loss in adult but ~70 % in infants. This finding is similar to the RTD previously described for Old World Macaca monkeys. Furthermore, in infants we find a similar amount of RTD at 3 weeks and 1 year following lesion, demonstrating that RTD is very rapid in neonates. This highlights the importance of trying to prevent the rapid onset of RTD following a lesion of V1 in early life as a strategy for improved functional recovery. Despite differences in GC loss, there was little difference between LGN Degeneration in infant versus adult lesions. A wedge on the horizontal meridian corresponding to the LGN foveal representation revealed extensive neuronal loss. Retinal afferent input was labeled by cholera toxin B subunit. Input to the degenerated parvocellular layers was difficult to detect, while input to magnocellular and koniocellular layers was reduced but still apparent. Our demonstration that the New World marmoset monkey shares many of the features of neuroplasticity with Old World Macaca monkeys and humans emphasizes the opportunity and benefit of marmosets as models of visual cortical injury.
