Stress Can Impact More Than Just Your Mood According To LSU Health New Orleans

 

NEW ORLEANS – In a recent press release from the LSU Health New Orleans School of Medicine, researchers are finding that stress – which is in abundant supply with the recent coronavirus pandemic plaguing the world – can ultimately change the structure of a person’s brain.

Si-Qiong June Liu, MD, PhD, Professor of Cell Biology and Anatomy at LSU Health New Orleans School of Medicine, led the research team in the discovery that was published in JNeurosci, the Journal of Neuroscience. 

“Stress alters brain function and produces lasting changes in human behavior and physiology,” said Liu in the press release. “The experience of traumatic events can lead to neuropsychiatric disorders including anxiety, depression and drug addiction. Investigation of the neurobiology of stress can reveal how stress affects neuronal connections and hence brain function. This knowledge is necessary for developing strategies to prevent or treat these common stress-related neurological disorders.”

Read the full press release below.

 


 

New Orleans, LA  — Research led by Si-Qiong June Liu, MD, PhD, Professor of Cell Biology and Anatomy at LSU Health New Orleans School of Medicine, has shown how stress changes the structure of the brain and reveals a potential therapeutic target to the prevent or reverse it. The findings are published in JNeurosci, the Journal of Neuroscience, available here.

            Working in a mouse model, Liu and her research team found that a single stressful event produced quick and long-lasting changes in astrocytes, the brain cells that clean up chemical messengers called neurotransmitters after they’ve communicated information between nerve cells. The stressful episode caused the branches of the astrocytes to shrink away from the synapses, the spaces across which information is transmitted from one cell to another.

            The team also discovered a mechanism resulting in communication disruption. They found that during a stressful event, the stress hormone norepinephrine suppresses a molecular pathway that normally produces a protein, GluA1, without which nerve cells and astrocytes cannot communicate with each other.

            “Stress affects the structure and function of both neurons and astrocytes,” notes Dr. Liu. “Because astrocytes can directly modulate synaptic transmission and are critically involved in stress-related behavior, preventing or reversing the stress-induced change in astrocytes is a potential way to treat stress-related neurological disorders. We identified a molecular pathway that controls GluA1 synthesis and thereby astrocyte remodeling during stress. This suggests new pharmacological targets for possible prevention or reversal of stress-induced changes.”

            She says that since many signaling pathways are conserved throughout evolution, the molecular pathways that lead to astrocyte structural remodeling and suppression of GluA1 production may also occur in humans who experience a stressful event.

            “Stress alters brain function and produces lasting changes in human behavior and physiology,” Liu adds. “The experience of traumatic events can lead to neuropsychiatric disorders including anxiety, depression and drug addiction. Investigation of the neurobiology of stress can reveal how stress affects neuronal connections and hence brain function. This knowledge is necessary for developing strategies to prevent or treat these common stress-related neurological disorders.”

            Besides Liu, members of the research team included Crhistian Bender; Xingxing Sun; Muhammad Farooq; Quan, Yang; Caroline Davison; Matthieu Maroteaux, Yi-shuian Huang and Yoshihiro Ishikawa from the LSU Health New Orleans School of Medicine Department of Cell Biology and Anatomy, Academia Sinica in Taipei, Taiwan, and Yokohama City University Graduate School of Medicine in Yokohama, Japan.

            The research was supported by grants from the National Institutes of Health and Department of Veterans Affairs.

 

 

 

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