Phenotypic characterization of frontal cortex microglia in a rat model of post‐traumatic stress disorder
| Autor: | Marcus A. Sanchez, Charina B. Hocog, Heather M. Sullivan, Joseph T. Ramsey, Angus G. Scrimgeour, Thomas S. Cotrone |
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| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
Male
medicine.medical_specialty Fear Extinction SPS 050105 experimental psychology lcsh:RC321-571 Extinction Psychological Rats Sprague-Dawley Stress Disorders Post-Traumatic 03 medical and health sciences Behavioral Neuroscience 0302 clinical medicine Internal medicine medicine Animals 0501 psychology and cognitive sciences Fear conditioning lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry Original Research Microglia business.industry 05 social sciences Traumatic stress Post‐traumatic Stress Disorder PTSD Extinction (psychology) Fear medicine.disease Phenotype Frontal Lobe Rats Arginase Freezing behavior Disease Models Animal Endocrinology medicine.anatomical_structure Rat Single Prolonged Stress business 030217 neurology & neurosurgery Anxiety disorder Stress Psychological |
| Zdroj: | Brain and Behavior Brain and Behavior, Vol 11, Iss 3, Pp n/a-n/a (2021) |
| ISSN: | 2162-3279 |
| Popis: | Introduction Post‐traumatic stress disorder (PTSD) is an anxiety disorder induced by psychologically traumatic events. Using a rat model, this study aimed to determine whether psychological trauma alters relative expression between pro‐inflammatory and anti‐inflammatory markers in microglia. To meet this goal, expression of genes encoding i‐NOS, arginase, TNF‐α, interleukin‐10, CD74, and Mannose Receptor C was analyzed on multiple days following trauma exposure. Methods Single‐prolonged stress (SPS) was used to model PTSD in male Sprague‐Dawley rats. Twenty‐four rats (12 Controls and 12 SPS‐exposed) were sacrificed on Days 1, 3, and 7 post‐SPS. Twenty‐four (12 Controls and 12 SPS‐exposed) additional rats were exposed to classical fear conditioning on Day 7, and fear extinction on Days 8, 9, 10, 15, 16, and 17. Freezing behavior was measured to assess fear resolution. Microglial isolates were collected from the frontal cortex, and RNA was extracted. Changes in relative expression of target genes were quantified via RT‐PCR. Results SPS rats showed significant decreases in IL‐10 and TNF‐α expression and increases in the i‐NOS:Arginase and TNF‐α:IL‐10 ratios compared to Controls on Day 1, but not on Day 3 or Day 7 for any of the dependent variables. Day 17 SPS rats showed a significant decrease in IL‐10 expression and an increase in the TNF‐α:IL‐10 ratio, further characterized by a significant inverse relationship between IL‐10 expression and fear persistence. Conclusion Psychological trauma impacts the immunological phenotype of microglia of the frontal cortex. Consequently, future studies should further evaluate the mechanistic role of microglia in PTSD pathology. This study tested the hypothesis that exposure to psychological trauma would result in increased expression of pro‐inflammatory markers relative to anti‐inflammatory markers by microglia of the frontal cortex. To do this, frontal cortices of rats were collected at various time points after exposure to a psychological trauma in the form of Single‐Prolonged Stress. A significant change in microglial gene expression was found that correlated with key behavioral changes, indicating a possible immunological basis for post‐traumatic stress disorder. |
| Databáze: | OpenAIRE |
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