Vascularization of the dorsal root ganglia and peripheral nerve of the mouse: Implications for chemical-induced peripheral sensory neuropathies

Persistent Link:
http://hdl.handle.net/10150/610211
Title:
Vascularization of the dorsal root ganglia and peripheral nerve of the mouse: Implications for chemical-induced peripheral sensory neuropathies
Author:
Jimenez-Andrade, Juan; Herrera, Monica; Ghilardi, Joseph; Vardanyan, Marina; Melemedjian, Ohannes; Mantyh, Patrick
Affiliation:
Department of Pharmacology, College of Medicine, University of Arizona, Tucson, AZ 85724, USA; Research Service, VA Medical Center, Minneapolis, MN 55417, USA
Issue Date:
2008
Publisher:
BioMed Central
Citation:
Molecular Pain 2008, 4:10 doi:10.1186/1744-8069-4-10
Journal:
Molecular Pain
Rights:
© 2008 Jimenez-Andrade et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0)
Collection Information:
This item is part of the UA Faculty Publications collection. For more information this item or other items in the UA Campus Repository, contact the University of Arizona Libraries at repository@u.library.arizona.edu.
Abstract:
Although a variety of industrial chemicals, as well as several chemotherapeutic agents used to treat cancer or HIV, preferentially induce a peripheral sensory neuropathy what remains unclear is why these agents induce a sensory vs. a motor or mixed neuropathy. Previous studies have shown that the endothelial cells that vascularize the dorsal root ganglion (DRG), which houses the primary afferent sensory neurons, are unique in that they have large fenestrations and are permeable to a variety of low and high molecular weight agents. In the present report we used whole-mount preparations, immunohistochemistry, and confocal laser scanning microscopy to show that the cell body-rich area of the L4 mouse DRG has a 7 fold higher density of CD31+ capillaries than cell fiber rich area of the DRG or the distal or proximal aspect of the sciatic nerve. This dense vascularization, coupled with the high permeability of these capillaries, may synergistically contribute, and in part explain, why many potentially neurotoxic agents preferentially accumulate and injure cells within the DRG. Currently, cancer survivors and HIV patients constitute the largest and most rapidly expanding groups that have chemically induced peripheral sensory neuropathy. Understanding the unique aspects of the vascularization of the DRG and closing the endothelial fenestrations of the rich vascular bed of capillaries that vascularize the DRG before intravenous administration of anti-neoplastic or anti-HIV therapies, may offer a mechanism based approach to attenuate these chemically induced peripheral neuropathies in these patients.
EISSN:
1744-8069
DOI:
10.1186/1744-8069-4-10
Version:
Final published version
Additional Links:
http://mpx.sagepub.com/content/4/1744-8069-4-10.full

Full metadata record

DC FieldValue Language
dc.contributor.authorJimenez-Andrade, Juanen
dc.contributor.authorHerrera, Monicaen
dc.contributor.authorGhilardi, Josephen
dc.contributor.authorVardanyan, Marinaen
dc.contributor.authorMelemedjian, Ohannesen
dc.contributor.authorMantyh, Patricken
dc.date.accessioned2016-05-20T09:01:11Z-
dc.date.available2016-05-20T09:01:11Z-
dc.date.issued2008en
dc.identifier.citationMolecular Pain 2008, 4:10 doi:10.1186/1744-8069-4-10en
dc.identifier.doi10.1186/1744-8069-4-10en
dc.identifier.urihttp://hdl.handle.net/10150/610211-
dc.description.abstractAlthough a variety of industrial chemicals, as well as several chemotherapeutic agents used to treat cancer or HIV, preferentially induce a peripheral sensory neuropathy what remains unclear is why these agents induce a sensory vs. a motor or mixed neuropathy. Previous studies have shown that the endothelial cells that vascularize the dorsal root ganglion (DRG), which houses the primary afferent sensory neurons, are unique in that they have large fenestrations and are permeable to a variety of low and high molecular weight agents. In the present report we used whole-mount preparations, immunohistochemistry, and confocal laser scanning microscopy to show that the cell body-rich area of the L4 mouse DRG has a 7 fold higher density of CD31+ capillaries than cell fiber rich area of the DRG or the distal or proximal aspect of the sciatic nerve. This dense vascularization, coupled with the high permeability of these capillaries, may synergistically contribute, and in part explain, why many potentially neurotoxic agents preferentially accumulate and injure cells within the DRG. Currently, cancer survivors and HIV patients constitute the largest and most rapidly expanding groups that have chemically induced peripheral sensory neuropathy. Understanding the unique aspects of the vascularization of the DRG and closing the endothelial fenestrations of the rich vascular bed of capillaries that vascularize the DRG before intravenous administration of anti-neoplastic or anti-HIV therapies, may offer a mechanism based approach to attenuate these chemically induced peripheral neuropathies in these patients.en
dc.language.isoenen
dc.publisherBioMed Centralen
dc.relation.urlhttp://mpx.sagepub.com/content/4/1744-8069-4-10.fullen
dc.rights© 2008 Jimenez-Andrade et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0)en
dc.titleVascularization of the dorsal root ganglia and peripheral nerve of the mouse: Implications for chemical-induced peripheral sensory neuropathiesen
dc.typeArticleen
dc.identifier.eissn1744-8069en
dc.contributor.departmentDepartment of Pharmacology, College of Medicine, University of Arizona, Tucson, AZ 85724, USAen
dc.contributor.departmentResearch Service, VA Medical Center, Minneapolis, MN 55417, USAen
dc.identifier.journalMolecular Painen
dc.description.collectioninformationThis item is part of the UA Faculty Publications collection. For more information this item or other items in the UA Campus Repository, contact the University of Arizona Libraries at repository@u.library.arizona.edu.en
dc.eprint.versionFinal published versionen
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