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P K Sarkar - One of the best experts on this subject based on the ideXlab platform.
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Delayed detyrosination of alpha-tubulin from parallel fibre axons and its correlation with impaired Synaptogenesis in hypothyroid rat cerebellum.
Brain research, 1993Co-Authors: R Poddar, P K SarkarAbstract:The biochemical basis of retarded differentiation and maturation of microtubules and impaired Synaptogenesis in hypothyroidism has been investigated by studying the temporal and spatial relationship between alpha-tubulin detyrosination in the parallel fibre axons of rat cerebellum and alterations in the activity of the detyrosinating enzyme, TTCP (tubulinyl tyrosine carboxypeptidase) with the progress of Synaptogenesis in the molecular layer. Detyrosination was monitored by following the disappearance of stain from cerebellar sections, immunocytochemically labeled with a monoclonal antibody (20C6) specific for alpha-tubulin, tyrosinated at the C-terminal end. With respect to normal controls, detyrosination of alpha-tubulin from the parallel fibres of the molecular layer during Synaptogenesis was not only delayed by about 5 days but also prolonged in the hypothyroid cerebellum. Correspondingly, the increase of TTCP activity in the developing thyroid deficient cerebellum was also delayed by about 1 week. Comparison of the developmental profile of TTCP activity in the normal and hypothyroid cerebellum during Synaptogenesis revealed that the overall activity of the enzyme in the thyroid deficient cerebellum was reduced to almost half of that of the normal controls. These results establish that thyroid hormones are essential for the induction of TTCP, which catalyses detyrosination during the normal ontogenic development of rat cerebellum. Since our data also suggest that detyrosination precedes synaptic contacts to generate a class of differentiated microtubules functionally competent for Synaptogenesis, the delayed detyrosination in the hypothyroid cerebellum may desynchronize the normal developmental program resulting in incomplete Synaptogenesis.
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Delayed detyrosination of α-tubulin from parallel fibre axons and its correlation with impaired Synaptogenesis in hypothyroid rat cerebellum
Brain Research, 1993Co-Authors: R Poddar, P K SarkarAbstract:The biochemical basis of retarded differentiation and maturation of microtubules and impaired Synaptogenesis in hypothyroidism has been investigated by studying the temporal and spatial relationship between α-tubulin detyrosination in the parallel fibre axons of rat cerebellum and alterations in the activity of the detyrosinating enzyme, TTCP (tubulinyl tyrosine carboxypeptidase) with the progress of Synaptogenesis in the molecular layer. Detyrosination was monitored by following the disappearance of stain from cerebellar sections, immunocytochemically labeled with a monoclonal antibody (20C6) specific for α-tubulin, tyrosinated at the C-terminal end. With respect to normal controls, detyrosination of α-tubulin from the parallel fibres of the molecular layer during Synaptogenesis was not only delayed by about 5 days but also prolonged in the hypothyroid cerebellum. Correspondingly, the increase of TTCP activity in the developing thyroid deficient cerebellum was also delayed by about 1 week. Comparison of the developmental profile of TTCP activity in the normal and hypothyroid cerebellum during Synaptogenesis revealed that the overall activity of the enzyme in the thyroid deficient cerebellum was reduced to almost half of that of the normal controls. These results establish that thyroid hormones are essential for the induction of TTCP, which catalyses detyrosination during the normal ontogenic development of rat cerebellum. Since our data also suggest that detyrosination preceeds synaptic contacts to generate a class of differentiated microtubules functionally competent for Synaptogenesis, the delayed detyrosination in the hypothyroid cerebellum may desynchronize the normal developmental program resulting in incomplete Synaptogenesis.
R Poddar - One of the best experts on this subject based on the ideXlab platform.
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Delayed detyrosination of alpha-tubulin from parallel fibre axons and its correlation with impaired Synaptogenesis in hypothyroid rat cerebellum.
Brain research, 1993Co-Authors: R Poddar, P K SarkarAbstract:The biochemical basis of retarded differentiation and maturation of microtubules and impaired Synaptogenesis in hypothyroidism has been investigated by studying the temporal and spatial relationship between alpha-tubulin detyrosination in the parallel fibre axons of rat cerebellum and alterations in the activity of the detyrosinating enzyme, TTCP (tubulinyl tyrosine carboxypeptidase) with the progress of Synaptogenesis in the molecular layer. Detyrosination was monitored by following the disappearance of stain from cerebellar sections, immunocytochemically labeled with a monoclonal antibody (20C6) specific for alpha-tubulin, tyrosinated at the C-terminal end. With respect to normal controls, detyrosination of alpha-tubulin from the parallel fibres of the molecular layer during Synaptogenesis was not only delayed by about 5 days but also prolonged in the hypothyroid cerebellum. Correspondingly, the increase of TTCP activity in the developing thyroid deficient cerebellum was also delayed by about 1 week. Comparison of the developmental profile of TTCP activity in the normal and hypothyroid cerebellum during Synaptogenesis revealed that the overall activity of the enzyme in the thyroid deficient cerebellum was reduced to almost half of that of the normal controls. These results establish that thyroid hormones are essential for the induction of TTCP, which catalyses detyrosination during the normal ontogenic development of rat cerebellum. Since our data also suggest that detyrosination precedes synaptic contacts to generate a class of differentiated microtubules functionally competent for Synaptogenesis, the delayed detyrosination in the hypothyroid cerebellum may desynchronize the normal developmental program resulting in incomplete Synaptogenesis.
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Delayed detyrosination of α-tubulin from parallel fibre axons and its correlation with impaired Synaptogenesis in hypothyroid rat cerebellum
Brain Research, 1993Co-Authors: R Poddar, P K SarkarAbstract:The biochemical basis of retarded differentiation and maturation of microtubules and impaired Synaptogenesis in hypothyroidism has been investigated by studying the temporal and spatial relationship between α-tubulin detyrosination in the parallel fibre axons of rat cerebellum and alterations in the activity of the detyrosinating enzyme, TTCP (tubulinyl tyrosine carboxypeptidase) with the progress of Synaptogenesis in the molecular layer. Detyrosination was monitored by following the disappearance of stain from cerebellar sections, immunocytochemically labeled with a monoclonal antibody (20C6) specific for α-tubulin, tyrosinated at the C-terminal end. With respect to normal controls, detyrosination of α-tubulin from the parallel fibres of the molecular layer during Synaptogenesis was not only delayed by about 5 days but also prolonged in the hypothyroid cerebellum. Correspondingly, the increase of TTCP activity in the developing thyroid deficient cerebellum was also delayed by about 1 week. Comparison of the developmental profile of TTCP activity in the normal and hypothyroid cerebellum during Synaptogenesis revealed that the overall activity of the enzyme in the thyroid deficient cerebellum was reduced to almost half of that of the normal controls. These results establish that thyroid hormones are essential for the induction of TTCP, which catalyses detyrosination during the normal ontogenic development of rat cerebellum. Since our data also suggest that detyrosination preceeds synaptic contacts to generate a class of differentiated microtubules functionally competent for Synaptogenesis, the delayed detyrosination in the hypothyroid cerebellum may desynchronize the normal developmental program resulting in incomplete Synaptogenesis.
D.f. Luthy - One of the best experts on this subject based on the ideXlab platform.
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Terminal dendritic sprouting and reactive Synaptogenesis in the postnatal organ of Corti in culture.
The Journal of Comparative Neurology, 1998Co-Authors: Hanna M. Sobkowicz, Benjamin K. August, S. M. Slapnick, D.f. LuthyAbstract:Synaptogenesis in the organ of Corti between the primary receptors, the inner hair cells, and the peripheral processes of their afferent spiral ganglion neurons in the mouse lasts for 5 days postnatally (Sobkowicz et al. [1986] J. Neurocytol. 15:693-714). The transplantation of the organ into culture at the fifth postnatal day induces a reactive sprouting of dendritic terminals and an extensive formation of new ribbon synapses within 24 hours. This reactive Synaptogenesis differs strikingly from the primary Synaptogenesis and has been seen thus far only in the inner hair cells. The synaptically engaged neuronal endings sprout a multitude of filopodia that intussuscept the inner hair cells. The filopodial tips contain a heavy electron-dense matter that appears to attract the synaptic ribbons, which form new synaptic contacts with the growing processes. The intensity of the filopodial growth and Synaptogenesis subsides in about 3 days; the filopodia undergo resorption, leaving behind fibrous cytoplasmic plaques mostly stored in the supranuclear part of the hair cells. However, occasional filopodial growth and formation of new synaptic connections continued. The data demonstrate that any disruption or disturbance of the initial synaptic contacts between the inner hair cells and their afferent neurons caused by transplantation results in prompt synaptic reacquisition. Furthermore, we suggest that the transitory phase of terminal sprouting and multiribbon synapse formation manifests a trophic dependence that develops postnatally between the synaptic cells.
Kazuyoshi Tsutsui - One of the best experts on this subject based on the ideXlab platform.
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mode of action and functional significance of estrogen inducing dendritic growth spinogenesis and Synaptogenesis in the developing purkinje cell
The Journal of Neuroscience, 2007Co-Authors: Katsunori Sasahara, Hanako Shikimi, Shogo Haraguchi, Hirotaka Sakamoto, Shinichiro Honda, Nobuhiro Harada, Kazuyoshi TsutsuiAbstract:Neurosteroids are synthesized de novo from cholesterol in the brain. To understand neurosteroid action in the brain, data on the regio- and temporal-specific synthesis of neurosteroids are needed. Recently, we identified the Purkinje cell as an active neurosteroidogenic cell. In rodents, this neuron actively produces several neurosteroids including estradiol during neonatal life, when cerebellar neuronal circuit formation occurs. Estradiol may be involved in cerebellar neuronal circuit formation through promoting neuronal growth and neuronal synaptic contact, because the Purkinje cell expresses estrogen receptor-β (ERβ). To test this hypothesis, in this study we examined the effects of estradiol on dendritic growth, spinogenesis, and Synaptogenesis in the Purkinje cell using neonatal wild-type (WT) mice or cytochrome P450 aromatase knock-out (ArKO) mice. Administration of estradiol to neonatal WT or ArKO mice increased dendritic growth, spinogenesis, and Synaptogenesis in the Purkinje cell. In contrast, WT mice treated with tamoxifen, an ER antagonist, or ArKO mice exhibited decreased Purkinje dendritic growth, spinogenesis, and Synaptogenesis at the same neonatal period. To elucidate the mode of action of estradiol, we further examined the expression of brain-derived neurotrophic factor (BDNF) in response to estrogen actions in the neonate. Estrogen administration to neonatal WT or ArKO mice increased the BDNF level in the cerebellum, whereas tamoxifen decreased the BDNF level in WT mice similar to ArKO mice. BDNF administration to tamoxifen-treated WT mice increased Purkinje dendritic growth. These results indicate that estradiol induces dendritic growth, spinogenesis, and Synaptogenesis in the developing Purkinje cell via BDNF action during neonatal life.
W. Christopher Risher - One of the best experts on this subject based on the ideXlab platform.
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Thrombospondin receptor α2δ-1 promotes Synaptogenesis and spinogenesis via postsynaptic Rac1.
Journal of Cell Biology, 2018Co-Authors: W. Christopher Risher, Nam Soo Kim, Sehwon Koh, Ji-eun Choi, Petar Mitev, Erin F. Spence, Louis-jan Pilaz, Dongqing Wang, Guoping Feng, Debra L. SilverAbstract:Astrocytes control excitatory Synaptogenesis by secreting thrombospondins (TSPs), which function via their neuronal receptor, the calcium channel subunit α2δ-1. α2δ-1 is a drug target for epilepsy and neuropathic pain; thus the TSP–α2δ-1 interaction is implicated in both synaptic development and disease pathogenesis. However, the mechanism by which this interaction promotes Synaptogenesis and the requirement for α2δ-1 for connectivity of the developing mammalian brain are unknown. In this study, we show that global or cell-specific loss of α2δ-1 yields profound deficits in excitatory synapse numbers, ultrastructure, and activity and severely stunts spinogenesis in the mouse cortex. Postsynaptic but not presynaptic α2δ-1 is required and sufficient for TSP-induced Synaptogenesis in vitro and spine formation in vivo, but an α2δ-1 mutant linked to autism cannot rescue these Synaptogenesis defects. Finally, we reveal that TSP–α2δ-1 interactions control Synaptogenesis postsynaptically via Rac1, suggesting potential molecular mechanisms that underlie both synaptic development and pathology.
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Thrombospondins as key regulators of Synaptogenesis in the central nervous system
Matrix Biology, 2012Co-Authors: W. Christopher Risher, Cagla ErogluAbstract:Thrombospondins (TSPs) are a family of large, oligomeric multidomain glycoproteins that participate in a variety of biological functions as part of the extracellular matrix (ECM). Through their associations with a number of binding partners, TSPs mediate complex cell-cell and cell-matrix interactions in such diverse processes as angiogenesis, inflammation, osteogenesis, cell proliferation, and apoptosis. It was recently shown in the developing central nervous system (CNS) that TSPs promote the formation of new synapses, which are the unique cell-cell adhesions between neurons in the brain. This increase in Synaptogenesis is mediated by the interaction between astrocyte-secreted TSPs and their neuronal receptor, calcium channel subunit α2δ-1. The cellular and molecular mechanisms that underlie induction of Synaptogenesis via this interaction are yet to be fully elucidated. This review will focus on what is known about TSP and synapse formation during development, possible roles for TSP following brain injury, and what the previously established actions of TSP in other biological tissues may tell us about the mechanisms underlying TSP's functions in CNS Synaptogenesis.
