Reactive astrocytosis-induced perturbation of synaptic homeostasis is restored by nerve growth factor (484 views)
Neurobiology Of Disease (ISSN: 0969-9961), 2011 Mar; 41(3): 630-639.
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Paper type: Journal Article,
Impact factor: 5.403, 5-year impact factor: 5.271
Url: http://www.scopus.com/inward/record.url?eid=2-s2.0-79151481219&partnerID=40&md5=bfbb11267b9c39fc874eed55b3c6028a
Keywords: Nerve Growth Factor, Nerve Injury, Neuro-Glial Network, Reactive Astrocytosis, Synaptic Homeostasis, 4 Aminobutyric Acid, Calcium Binding Protein, Excitatory Amino Acid Transporter 3, Glial Fibrillary Acidic Protein, Glutamate Cysteine Ligase, Glutamate Decarboxylase 65, Glutamate Transporter, Glutamic Acid, Glutathione, Glycine Transporter, Ilomastat, Metalloproteinase, Vesicular Inhibitory Amino Acid Transporter, Animal Experiment, Animal Model, Animal Tissue, Article, Controlled Study, Enzyme Degradation, Lumbar Spinal Cord, Microglia, Nerve Cell Plasticity, Neuroprotection, Nonhuman, Peripheral Nerve Injury, Priority Journal, Protein Expression, Protein Metabolism, Sciatic Nerve, Synaptic Efficacy, Gliosis, Neural Pathways, Sprague-Dawley, Sciatic Neuropathy, Synapses,
Affiliations:
*** IBB - CNR ***
Laboratorio di Morfologia delle Reti Neuronali, Dipartimento di Medicina Pubblica Clinica e Preventiva, Seconda Università di Napoli, 80138 Naples, Italy
Laboratorio di Neuroscienze R. Levi-Montalcini and Dipartimento di Biotecnologie e Bioscienze, Università di Milano-Bicocca, Milan, Italy
Centro Interuniversitario di Ricerca sui Peptidi Bioattivi and Dipartimento delle Scienze Biologiche, Università di Napoli Federico II and Istituto di Biostrutture e Bioimmagini, Consiglio Nazionale delle Ricerche, 80138 Naples, Italy
References:
Not available.
Neurobiology Of Disease (ISSN: 0969-9961), 2011 Mar; 41(3): 630-639.
Export to BibTeX Export to EndNote
Paper type: Journal Article,
Impact factor: 5.403, 5-year impact factor: 5.271
Url: http://www.scopus.com/inward/record.url?eid=2-s2.0-79151481219&partnerID=40&md5=bfbb11267b9c39fc874eed55b3c6028a
Keywords: Nerve Growth Factor, Nerve Injury, Neuro-Glial Network, Reactive Astrocytosis, Synaptic Homeostasis, 4 Aminobutyric Acid, Calcium Binding Protein, Excitatory Amino Acid Transporter 3, Glial Fibrillary Acidic Protein, Glutamate Cysteine Ligase, Glutamate Decarboxylase 65, Glutamate Transporter, Glutamic Acid, Glutathione, Glycine Transporter, Ilomastat, Metalloproteinase, Vesicular Inhibitory Amino Acid Transporter, Animal Experiment, Animal Model, Animal Tissue, Article, Controlled Study, Enzyme Degradation, Lumbar Spinal Cord, Microglia, Nerve Cell Plasticity, Neuroprotection, Nonhuman, Peripheral Nerve Injury, Priority Journal, Protein Expression, Protein Metabolism, Sciatic Nerve, Synaptic Efficacy, Gliosis, Neural Pathways, Sprague-Dawley, Sciatic Neuropathy, Synapses,
Affiliations:
*** IBB - CNR ***
Laboratorio di Morfologia delle Reti Neuronali, Dipartimento di Medicina Pubblica Clinica e Preventiva, Seconda Università di Napoli, 80138 Naples, Italy
Laboratorio di Neuroscienze R. Levi-Montalcini and Dipartimento di Biotecnologie e Bioscienze, Università di Milano-Bicocca, Milan, Italy
Centro Interuniversitario di Ricerca sui Peptidi Bioattivi and Dipartimento delle Scienze Biologiche, Università di Napoli Federico II and Istituto di Biostrutture e Bioimmagini, Consiglio Nazionale delle Ricerche, 80138 Naples, Italy
References:
Not available.
Reactive astrocytosis-induced perturbation of synaptic homeostasis is restored by nerve growth factor
Reactive gliosis has been implicated in both inflammatory and neurodegenerative diseases. However, mechanisms by which astrocytic activation affects synaptic efficacy have been poorly elucidated. We have used the spared nerve injury (SNI) of the sciatic nerve to induce reactive astrocytosis in the lumbar spinal cord and investigate its potential role in disrupting the neuro-glial circuitry. Analysis of spinal cord sections revealed that SNI was associated with an increase of microglial (Iba1) and astrocytic (GFAP) markers. These changes, indicative of reactive gliosis, were paralleled by (i) a decrease of glial amino acid transporters (GLT1 and GlyT1) and increased levels of (ii) neuronal glutamate transporter EAAC1, (iii) neuronal vesicular GABA transporter (vGAT) and (iv) the GABAergic neuron marker GAD65/67. Besides the increase of Glutamate/GABA ratio, indicative of the perturbation of synaptic circuitry homeostasis, the boost of glutamate also compromised glial function in neuroprotection by up-regulating the xCT subunit of the glutamate-cystine antiport system and reducing glutathione (GSH) production. Finally, this study also shows that all these structural changes were linked to an alteration of endogenous NGF metabolism, as demonstrated by the decrease of endogenous NGF expression levels and increased activity of the NGF-degrading metalloproteinases. All the changes displayed by SNI-animals were reversed by a 7-days i.t. administration of NGF or GM6001, a generic metalloproteinase inhibitor, as compared to vehicle (ACSF)-treated animals. All together, these data strongly support the correlation between reactive astrogliosis and mechanisms underlying the perturbation of the synaptic circuitry in the SNI model of peripheral nerve injury, and the essential role of NGF in restoring both synaptic homeostasis and the neuroprotective function of glia. (C) 2010 Elsevier Inc. All rights reserved.
Reactive gliosis has been implicated in both inflammatory and neurodegenerative diseases. However, mechanisms by which astrocytic activation affects synaptic efficacy have been poorly elucidated. We have used the spared nerve injury (SNI) of the sciatic nerve to induce reactive astrocytosis in the lumbar spinal cord and investigate its potential role in disrupting the neuro-glial circuitry. Analysis of spinal cord sections revealed that SNI was associated with an increase of microglial (Iba1) and astrocytic (GFAP) markers. These changes, indicative of reactive gliosis, were paralleled by (i) a decrease of glial amino acid transporters (GLT1 and GlyT1) and increased levels of (ii) neuronal glutamate transporter EAAC1, (iii) neuronal vesicular GABA transporter (vGAT) and (iv) the GABAergic neuron marker GAD65/67. Besides the increase of Glutamate/GABA ratio, indicative of the perturbation of synaptic circuitry homeostasis, the boost of glutamate also compromised glial function in neuroprotection by up-regulating the xCT subunit of the glutamate-cystine antiport system and reducing glutathione (GSH) production. Finally, this study also shows that all these structural changes were linked to an alteration of endogenous NGF metabolism, as demonstrated by the decrease of endogenous NGF expression levels and increased activity of the NGF-degrading metalloproteinases. All the changes displayed by SNI-animals were reversed by a 7-days i.t. administration of NGF or GM6001, a generic metalloproteinase inhibitor, as compared to vehicle (ACSF)-treated animals. All together, these data strongly support the correlation between reactive astrogliosis and mechanisms underlying the perturbation of the synaptic circuitry in the SNI model of peripheral nerve injury, and the essential role of NGF in restoring both synaptic homeostasis and the neuroprotective function of glia. (C) 2010 Elsevier Inc. All rights reserved.
Reactive astrocytosis-induced perturbation of synaptic homeostasis is restored by nerve growth factor
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Reactive astrocytosis-induced perturbation of synaptic homeostasis is restored by nerve growth factor
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* Role of the conformational versatility of the neurotrophin N-terminal regions in their recognition by Trk receptors (527 views)
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View Export to BibTeX Export to EndNote
Bianco MR, Cirillo G, Cavaliere C, Colangelo AM, Vitagliano L, Morelli G, Sarmientos P, Martegani E, Alberghina L, Papa M
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View Export to BibTeX Export to EndNote
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15 Records (14 excluding Abstracts).
Total impact factor: 70.47 (63.834 excluding Abstracts).
Total 5 year impact factor: 72.135 (68.267 excluding Abstracts).
Total impact factor: 70.47 (63.834 excluding Abstracts).
Total 5 year impact factor: 72.135 (68.267 excluding Abstracts).
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