Life threat during assaultive trauma: Critical posttraumatic stress disorder risk factors for injured patients

Timmer-Murillo, Sydney C; Schramm, Andrew T.; deRoon‐Cassini, Terri

doi:10.1097/ta.0000000000003543

Cited by 7 publications

(1 citation statement)

References 34 publications

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“…Due to rapid developments in the modern world, long-term, persistent mental and environmental stresses affect the physical and mental health of millions of people globally. Appropriate stress can increase the body's ability to adapt and cope with environmental changes [1]; however, excessive or persistent stress can cause acute or chronic organ dysfunction and metabolic disorders [2]. Many studies [3][4][5] have found that long-term persistent stress can lead to many neuropsychiatric disorders, such as anxiety, depression, epilepsy, schizophrenia, etc.…”

Section: Introductionmentioning

confidence: 99%

Norepinephrine-Activated p38 MAPK Pathway Mediates Stress-Induced Cytotoxic Edema of Basolateral Amygdala Astrocytes

Sun,

Zhang,

Dong

et al. 2024

Brain Sciences

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The amygdala is a core region in the limbic system that is highly sensitive to stress. Astrocytes are key players in stress disorders such as anxiety and depression. However, the effects of stress on the morphology and function of amygdala astrocytes and its potential mechanisms remain largely unknown. Hence, we performed in vivo and in vitro experiments using a restraint stress (RS) rat model and stress-induced astrocyte culture, respectively. Our data show that norepinephrine (NE) content increased, cytotoxic edema occurred, and aquaporin-4 (AQP4) expression was up-regulated in the basolateral amygdala (BLA) obtained from RS rats. Additionally, the p38 mitogen-activated protein kinase (MAPK) pathway was also observed to be significantly activated in the BLA of rats subjected to RS. The administration of NE to in vitro astrocytes increased the AQP4 level and induced cell edema. Furthermore, p38 MAPK signaling was activated. The NE inhibitor alpha-methyl-p-tyrosine (AMPT) alleviated cytotoxic edema in astrocytes, inhibited AQP4 expression, and inactivated the p38 MAPK pathway in RS rats. Meanwhile, in the in vitro experiment, the p38 MAPK signaling inhibitor SB203580 reversed NE-induced cytotoxic edema and down-regulated the expression of AQP4 in astrocytes. Briefly, NE-induced activation of the p38 MAPK pathway mediated cytotoxic edema in BLA astrocytes from RS rats. Thus, our data provide novel evidence that NE-induced p38 MAPK pathway activation may be one of the mechanisms leading to cytotoxic edema in BLA under stress conditions, which also could enable the development of an effective therapeutic strategy against cytotoxic edema in BLA under stress and provide new ideas for the treatment of neuropsychiatric diseases.

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