Rod microglia: a morphological definition.
Brain microglial morphology relates to function, with ramified microglia surveying the micro-environment and amoeboid microglia engulfing debris. One subgroup of microglia, rod microglia, have been observed in a number of pathological conditions, however neither a function nor specific morphology has been defined. Historically, rod microglia have been described intermittently as cells with a sausage-shaped soma and long, thin processes, which align adjacent to neurons. More recently, our group has described rod microglia aligning end-to-end with one another to form trains adjacent to neuronal processes. Confusion in the literature regarding rod microglia arises from some reports referring to the sausage-shaped cell body, while ignoring the spatial distribution of processes. Here, we systematically define the morphological characteristics of rod microglia that form after diffuse brain injury in the rat, which differ morphologically from the spurious rod microglia found in uninjured sham. Rod microglia in the diffuse-injured rat brain show a ratio of 1.79 ± 0.03 cell length:cell width at day 1 post-injury, which increases to 3.35 ± 0.05 at day 7, compared to sham (1.17 ± 0.02). The soma length:width differs only at day 7 post-injury (2.92 ± 0.07 length:width), compared to sham (2.49 ± 0.05). Further analysis indicated that rod microglia may not elongate in cell length but rather narrow in cell width, and retract planar (side) processes. These morphological characteristics serve as a tool for distinguishing rod microglia from other morphologies. The function of rod microglia remains enigmatic; based on morphology we propose origins and functions for rod microglia after acute neurological insult, which may provide biomarkers or therapeutic targets.
BARROW Neurological Institute at Phoenix Children's Hospital, Phoenix, Arizona, United States of America; Department of Child Health, University of Arizona College of Medicine - Phoenix, Phoenix, Arizona, United States of America; Department of Biology and Biochemistry, University of Bath, Bath, United Kingdom.
Samuel E
SE
Taylor
BARROW Neurological Institute at Phoenix Children's Hospital, Phoenix, Arizona, United States of America; Department of Child Health, University of Arizona College of Medicine - Phoenix, Phoenix, Arizona, United States of America.
Cristina
C
Morganti-Kossmann
BARROW Neurological Institute at Phoenix Children's Hospital, Phoenix, Arizona, United States of America; Department of Child Health, University of Arizona College of Medicine - Phoenix, Phoenix, Arizona, United States of America; Phoenix VA Healthcare System, Phoenix, Arizona, United States of America; Neuroscience Program, Department of Psychology, Arizona State University, Tempe, Arizona, United States of America.
Jonathan
J
Lifshitz
BARROW Neurological Institute at Phoenix Children's Hospital, Phoenix, Arizona, United States of America; Department of Child Health, University of Arizona College of Medicine - Phoenix, Phoenix, Arizona, United States of America.
Jenna M
JM
Ziebell
D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D001921:Brain / Q000473:pathology*; D001930:Brain Injuries / Q000473:pathology; D002135:Calcium-Binding Proteins / Q000378:metabolism; D005260:Female; D008297:Male; D008840:Microfilament Proteins / Q000378:metabolism; D017628:Microglia / Q000473:pathology*; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D017948:Retinal Rod Photoreceptor Cells / Q000473:pathology*; D013997:Time Factors
C100745:Aif1 protein, rat; D015415:Biomarkers; D002135:Calcium-Binding Proteins; D008840:Microfilament Proteins