Faculty Mentor
Dr. Matthew A. Cooper, J. Alex Grizzell
Department (e.g. History, Chemistry, Finance, etc.)
Psychology
College (e.g. College of Engineering, College of Arts & Sciences, Haslam College of Business, etc.)
Colege of Arts & Sciences
Year
2018
Abstract
Research suggests a causal relationship between neuroinflammation and stress-related psychopathologies. Exposure to moderate psychological stress in rodent models leads to elevated markers of immune activity in the brain, for example, microglia. Research has shown that tail shock stress can prime the subsequent, immune-challenged activation of microglia, which can lead to a degradative, proinflammatory response. Although social defeat is an ethologically relevant model of acute stress, there has been little research investigating the effects of acute social defeat stress on immune activity. Here, we used an acute social defeat paradigm in Syrian hamsters consisting of three, 5-minute aggressive encounters in the home cage of a three, novel resident aggressors. Then, 24-hours following social defeat, the effects of stress-induced priming of microglial activation was assessed by exposure to an endotoxin immune challenge via intraperitoneal injection of lipopolysaccharide (LPS). Four hours after injection, hamsters were euthanized and the activation of microglia was determined via immunolabeling of the ionized calcium-binding adaptor protein-1 (Iba-1), a marker that is expressed in activated microglia. Preliminary data suggest that LPS injection leads to increased Iba-1 immunoreactivity both in the presence and absence of social defeat stress in the ventral medial prefrontal cortex and dorsal raphe nucleus. Interestingly, acute social defeat also led to the activation of microglia in these regions in the absence of an LPS injection. Furthermore, it appears that all defeated animals, regardless of LPS treatment, maintain microglia activation as much as 9 days following defeat. Taken together, these results demonstrate that acute stress can activate innate immune mechanisms in key brain areas for stress processing, which extends our understanding of cellular mechanisms controlling responses to trauma.
Included in
Acute social defeat stress induces microglial activation in key limbic regions
Research suggests a causal relationship between neuroinflammation and stress-related psychopathologies. Exposure to moderate psychological stress in rodent models leads to elevated markers of immune activity in the brain, for example, microglia. Research has shown that tail shock stress can prime the subsequent, immune-challenged activation of microglia, which can lead to a degradative, proinflammatory response. Although social defeat is an ethologically relevant model of acute stress, there has been little research investigating the effects of acute social defeat stress on immune activity. Here, we used an acute social defeat paradigm in Syrian hamsters consisting of three, 5-minute aggressive encounters in the home cage of a three, novel resident aggressors. Then, 24-hours following social defeat, the effects of stress-induced priming of microglial activation was assessed by exposure to an endotoxin immune challenge via intraperitoneal injection of lipopolysaccharide (LPS). Four hours after injection, hamsters were euthanized and the activation of microglia was determined via immunolabeling of the ionized calcium-binding adaptor protein-1 (Iba-1), a marker that is expressed in activated microglia. Preliminary data suggest that LPS injection leads to increased Iba-1 immunoreactivity both in the presence and absence of social defeat stress in the ventral medial prefrontal cortex and dorsal raphe nucleus. Interestingly, acute social defeat also led to the activation of microglia in these regions in the absence of an LPS injection. Furthermore, it appears that all defeated animals, regardless of LPS treatment, maintain microglia activation as much as 9 days following defeat. Taken together, these results demonstrate that acute stress can activate innate immune mechanisms in key brain areas for stress processing, which extends our understanding of cellular mechanisms controlling responses to trauma.