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FAU FeAtUres
Study Sheds Light On degree to which IL-1 acts directly on hippocampal neurons
Neuroinflammation And to influence cognitive and mood changes with stress. To
define the IL-1R-mediated neuronal response, they used
Psychological Disorders novel and comprehensive IL-1R transgenic/reporter lines
in which one can selectively delete IL-1R or restore
Anxiety and depression are significantly heightened IL-1R on specific cell types, including glutamatergic
during times of great stress such as the COVID-19 neurons. They also used modified viruses to manipulate
pandemic. Unfortunately, psychosocial stress is a major hippocampal neurons and investigate the role of IL-1R in
contributing factor to anxiety and depression. There eliciting behavioral responses to stress. Their data show
is evidence that stress is associated with increased that social defeat-induced IL-1R signaling in hippocampal
inflammation – increases in inflammatory cytokines, neurons perpetuated inflammation and promoted deficits
circulating monocytes, and microglial activation, which in social interaction and working memory.
are detected in patients with anxiety and mood disorders. The research team previously detailed how
Chronic stress has long been associated with the The image shows a reporter protein, tdTomato, in a coronal psychosocial stress results in peripheral immune
pathogenesis of psychological disorders such as section of the brain containing hippocampus. Researchers activation, increased levels of circulating monocytes,
depression and anxiety. Recent studies have found engineered the tdTomato in the IL-1R gene so the expression and robust neuroimmunological responses in the brain.
chronic stress can cause neuroinflammation: activation of IL-1R can be visualized. In addition to expression in These responses include increases in IL-1 and other
of the resident immune cells in the brain, microglia, to endothelial cells, which forms vasculature, the image shows inflammatory cytokines, activation of brain glial cells and
produce inflammatory cytokines. Numerous studies have IL-1R in the dentate gyrus (resembling teeth, hence dentate), movements of peripheral immune cells to the brain, along
implicated the inflammatory cytokine, interleukin-1 on both side of the brain. The dentate IL-1Rs are on neurons, with enhanced activity of specific neuronal pathways. The
(IL-1), a master regulator of immune cell recruitment allowing the inflammatory cytokine IL-1 to directly signal work makes it clear that inflammatory-related effects of
and activity in the brain, as the key mediator of these neurons. stress are not just global effects but are associated with
psychopathology. However, how IL-1 disrupts neural increased IL-1 signaling within specific brain circuits.
circuits to cause behavioral and emotional problems seen these types of disorders. Findings from the study augment According to the Anxiety and Depression Association
in psychological disorders has not been determined. the understanding of IL-1R signaling in physiological of America, nearly 40 million people in the United
A groundbreaking study by neuroscientists at Florida and behavioral responses to stress and also suggest that it States (18 percent) experience an anxiety disorder in
Atlantic University and The Ohio State University, may be possible to develop better medications to treat the any given year. Globally, the World Health Organization
published in the journal Molecular Psychiatry is the first consequences of chronic stress by limiting inflammatory (WHO) notes that one in 13 people suffers from anxiety.
to identify a role of the neuronal receptor for IL-1 (nIL-1R) signaling not just generally, which may not be beneficial Anxiety disorders are the most common mental disorders
in psychological disorders. Researchers demonstrate that in the long run, but to specific brain circuits. worldwide with specific phobia, major depressive
nIL-1R straddles the intersection between social stress, “We created and validated a unique genetic mouse disorder and social phobia being the most common
inflammation, and anxiety in rodent models of stress. model to restrict IL-1R1 expression to different cell anxiety disorders.
The study shows for the first time that neuronal IL-1Rs types to visualize and control IL-1Rs,” said Ning Quan, “We are experiencing unprecedented levels of stress
in the hippocampus, a brain structure connected to learning Ph.D., lead author, a professor of biomedical science in that will likely have long-lasting effects on millions of
and memory, is necessary and sufficient to mediate some of FAU’s Schmidt College of Medicine, and a member of people of all ages around the world. When psychosocial
the behavioral deficits caused by chronic stress, pointing the FAU Brain Institute (I-BRAIN). “We demonstrated stress becomes chronic, the effects are not just emotionally
to a critical neuroimmune mechanism for the etiology of that chronic social stress caused the mice to show social debilitating, they also are physically debilitating and can
withdrawal and working memory deficits. These changes lead to high blood pressure, heart disease and even addictive
could be prevented if the neuronal IL-1R1 was deleted
behavior,” said Randy Blakely, Ph.D., executive director of
Happy and restored if IL-1R1 was only allowed to be expressed FAU’s I-BRAIN. “Findings from this cutting-edge study
on hippocampal neurons.”
4th of July For the study, researchers wanted to determine the Study Sheds Light on page 17
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