Rod microglia: elongation, alignment, and coupling to form trains across the somatosensory cortex after experimental diffuse brain injury

Persistent Link:
http://hdl.handle.net/10150/610191
Title:
Rod microglia: elongation, alignment, and coupling to form trains across the somatosensory cortex after experimental diffuse brain injury
Author:
Ziebell, Jenna; Taylor, Samuel; Cao, Tuoxin; Harrison, Jordan; Lifshitz, Jonathan
Affiliation:
Department of Child Health, University of Arizona College of Medicine - Phoenix, Phoenix, AZ, USA; Barrow Neurological Institute at Phoenix Children’s Hospital, Phoenix, AZ, USA; Spinal Cord & Brain Injury Research Center, Department of Anatomy & Neurobiology, Department of Physical Medicine & Rehabilitation, University of Kentucky College of Medicine, Lexington, KY, USA; Department of Biology and Biochemistry, University of Bath, Bath, England; Neuroscience Program, Arizona State University, Tempe, AZ, USA; Phoenix VA Healthcare System, Phoenix, AZ, USA
Issue Date:
2012
Publisher:
BioMed Central
Citation:
Ziebell et al. Journal of Neuroinflammation 2012, 9:247 http://www.jneuroinflammation.com/content/9/1/247
Journal:
Journal of Neuroinflammation
Rights:
© 2012 Ziebell 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:
BACKGROUND:Since their discovery, the morphology of microglia has been interpreted to mirror their function, with ramified microglia constantly surveying the micro-environment and rapidly activating when changes occur. In 1899, Franz Nissl discovered what we now recognize as a distinct microglial activation state, microglial rod cells (Stabchenzellen), which he observed adjacent to neurons. These rod-shaped microglia are typically found in human autopsy cases of paralysis of the insane, a disease of the pre-penicillin era, and best known today from HIV-1-infected brains. Microglial rod cells have been implicated in cortical 'synaptic stripping' but their exact role has remained unclear. This is due at least in part to a scarcity of experimental models. Now we have noted these rod microglia after experimental diffuse brain injury in brain regions that have an associated sensory sensitivity. Here, we describe the time course, location, and surrounding architecture associated with rod microglia following experimental diffuse traumatic brain injury (TBI).METHODS:Rats were subjected to a moderate midline fluid percussion injury (mFPI), which resulted in transient suppression of their righting reflex (6 to 10 min). Multiple immunohistochemistry protocols targeting microglia with Iba1 and other known microglia markers were undertaken to identify the morphological activation of microglia. Additionally, labeling with Iba1 and cell markers for neurons and astrocytes identified the architecture that surrounds these rod cells.RESULTS:We identified an abundance of Iba1-positive microglia with rod morphology in the primary sensory barrel fields (S1BF). Although present for at least 4 weeks post mFPI, they developed over the first week, peaking at 7 days post-injury. In the absence of contusion, Iba1-positive microglia appear to elongate with their processes extending from the apical and basal ends. These cells then abut one another and lay adjacent to cytoarchitecture of dendrites and axons, with no alignment with astrocytes and oligodendrocytes. Iba1-positive rod microglial cells differentially express other known markers for reactive microglia including OX-6 and CD68.CONCLUSION:Diffuse traumatic brain injury induces a distinct rod microglia morphology, unique phenotype, and novel association between cells; these observations entice further investigation for impact on neurological outcome.
EISSN:
1742-2094
DOI:
10.1186/1742-2094-9-247
Keywords:
Brain injury; Microglial rod cells; Rod microglia; Inflammation
Version:
Final published version
Additional Links:
http://www.jneuroinflammation.com/content/9/1/247

Full metadata record

DC FieldValue Language
dc.contributor.authorZiebell, Jennaen
dc.contributor.authorTaylor, Samuelen
dc.contributor.authorCao, Tuoxinen
dc.contributor.authorHarrison, Jordanen
dc.contributor.authorLifshitz, Jonathanen
dc.date.accessioned2016-05-20T09:00:40Z-
dc.date.available2016-05-20T09:00:40Z-
dc.date.issued2012en
dc.identifier.citationZiebell et al. Journal of Neuroinflammation 2012, 9:247 http://www.jneuroinflammation.com/content/9/1/247en
dc.identifier.doi10.1186/1742-2094-9-247en
dc.identifier.urihttp://hdl.handle.net/10150/610191-
dc.description.abstractBACKGROUND:Since their discovery, the morphology of microglia has been interpreted to mirror their function, with ramified microglia constantly surveying the micro-environment and rapidly activating when changes occur. In 1899, Franz Nissl discovered what we now recognize as a distinct microglial activation state, microglial rod cells (Stabchenzellen), which he observed adjacent to neurons. These rod-shaped microglia are typically found in human autopsy cases of paralysis of the insane, a disease of the pre-penicillin era, and best known today from HIV-1-infected brains. Microglial rod cells have been implicated in cortical 'synaptic stripping' but their exact role has remained unclear. This is due at least in part to a scarcity of experimental models. Now we have noted these rod microglia after experimental diffuse brain injury in brain regions that have an associated sensory sensitivity. Here, we describe the time course, location, and surrounding architecture associated with rod microglia following experimental diffuse traumatic brain injury (TBI).METHODS:Rats were subjected to a moderate midline fluid percussion injury (mFPI), which resulted in transient suppression of their righting reflex (6 to 10 min). Multiple immunohistochemistry protocols targeting microglia with Iba1 and other known microglia markers were undertaken to identify the morphological activation of microglia. Additionally, labeling with Iba1 and cell markers for neurons and astrocytes identified the architecture that surrounds these rod cells.RESULTS:We identified an abundance of Iba1-positive microglia with rod morphology in the primary sensory barrel fields (S1BF). Although present for at least 4 weeks post mFPI, they developed over the first week, peaking at 7 days post-injury. In the absence of contusion, Iba1-positive microglia appear to elongate with their processes extending from the apical and basal ends. These cells then abut one another and lay adjacent to cytoarchitecture of dendrites and axons, with no alignment with astrocytes and oligodendrocytes. Iba1-positive rod microglial cells differentially express other known markers for reactive microglia including OX-6 and CD68.CONCLUSION:Diffuse traumatic brain injury induces a distinct rod microglia morphology, unique phenotype, and novel association between cellsen
dc.description.abstractthese observations entice further investigation for impact on neurological outcome.en
dc.language.isoenen
dc.publisherBioMed Centralen
dc.relation.urlhttp://www.jneuroinflammation.com/content/9/1/247en
dc.rights© 2012 Ziebell 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.subjectBrain injuryen
dc.subjectMicroglial rod cellsen
dc.subjectRod microgliaen
dc.subjectInflammationen
dc.titleRod microglia: elongation, alignment, and coupling to form trains across the somatosensory cortex after experimental diffuse brain injuryen
dc.typeArticleen
dc.identifier.eissn1742-2094en
dc.contributor.departmentDepartment of Child Health, University of Arizona College of Medicine - Phoenix, Phoenix, AZ, USAen
dc.contributor.departmentBarrow Neurological Institute at Phoenix Children’s Hospital, Phoenix, AZ, USAen
dc.contributor.departmentSpinal Cord & Brain Injury Research Center, Department of Anatomy & Neurobiology, Department of Physical Medicine & Rehabilitation, University of Kentucky College of Medicine, Lexington, KY, USAen
dc.contributor.departmentDepartment of Biology and Biochemistry, University of Bath, Bath, Englanden
dc.contributor.departmentNeuroscience Program, Arizona State University, Tempe, AZ, USAen
dc.contributor.departmentPhoenix VA Healthcare System, Phoenix, AZ, USAen
dc.identifier.journalJournal of Neuroinflammationen
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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