Dysfunction of Ca2+/CaM kinase IIα cascades in the amygdala in post-traumatic stress disorder

Xiao, Bing; Han, Fang; Shi, Yonghui

doi:10.3892/ijmm_00000294

Int J Mol Med

2009

DOI: 10.3892/ijmm_00000294

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Dysfunction of Ca2+/CaM kinase IIα cascades in the amygdala in post-traumatic stress disorder

Bing Xiao

Fang Han²,

Yonghui Shi³

Abstract: Abstract. Single-prolonged stress (SPS) is an established animal model for post-traumatic stress disorder (PTSD). The calcium (Ca 2+ )-calmodulin (CaM)-CaM kinase (K)II· signal passage plays an important role in the plasticity of central nervous, learning and memory, mind and behavior and other types of cognitive activities. The amygdala is known to play an important role in fear, rage and emotional memory. In this study, we investigated changes in Ca 2+ -CaM-CaMKII· in the basolateral amygdala of rats after S… Show more

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Cited by 3 publications

References 25 publications

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Stress-related cellular pathophysiology as a crosstalk risk factor for neurocognitive and psychiatric disorders

Palamarchuk,

Slavich,

Vaillancourt

et al. 2023

BMC Neurosci

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In this narrative review, we examine biological processes linking psychological stress and cognition, with a focus on how psychological stress can activate multiple neurobiological mechanisms that drive cognitive decline and behavioral change. First, we describe the general neurobiology of the stress response to define neurocognitive stress reactivity. Second, we review aspects of epigenetic regulation, synaptic transmission, sex hormones, photoperiodic plasticity, and psychoneuroimmunological processes that can contribute to cognitive decline and neuropsychiatric conditions. Third, we explain mechanistic processes linking the stress response and neuropathology. Fourth, we discuss molecular nuances such as an interplay between kinases and proteins, as well as differential role of sex hormones, that can increase vulnerability to cognitive and emotional dysregulation following stress. Finally, we explicate several testable hypotheses for stress, neurocognitive, and neuropsychiatric research. Together, this work highlights how stress processes alter neurophysiology on multiple levels to increase individuals’ risk for neurocognitive and psychiatric disorders, and points toward novel therapeutic targets for mitigating these effects. The resulting models can thus advance dementia and mental health research, and translational neuroscience, with an eye toward clinical application in cognitive and behavioral neurology, and psychiatry.

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Stress-related cellular pathophysiology as a crosstalk risk factor for neurocognitive and psychiatric disorders

Palamarchuk,

Slavich,

Vaillancourt

et al. 2023

BMC Neurosci

View full text Add to dashboard Cite

show abstract

Traumatic Stress Produces Distinct Activations of GABAergic and Glutamatergic Neurons in Amygdala

Fang

Huang

et al. 2018

Front. Neurosci.

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Posttraumatic stress disorder (PTSD) is an anxiety disorder characterized by intrusive recollections of a severe traumatic event and hyperarousal following exposure to the event. Human and animal studies have shown that the change of amygdala activity after traumatic stress may contribute to occurrences of some symptoms or behaviors of the patients or animals with PTSD. However, it is still unknown how the neuronal activation of different sub-regions in amygdala changes during the development of PTSD. In the present study, we used single prolonged stress (SPS) procedure to obtain the animal model of PTSD, and found that 1 day after SPS, there were normal anxiety behavior and extinction of fear memory in rats which were accompanied by a reduced proportion of activated glutamatergic neurons and increased proportion of activated GABAergic neurons in basolateral amygdala (BLA). About 10 days after SPS, we observed enhanced anxiety and impaired extinction of fear memory with increased activated both glutamatergic and GABAergic neurons in BLA and increased activated GABAergic neurons in central amygdala (CeA). These results indicate that during early and late phase after traumatic stress, distinct patterns of activation of glutamatergic neurons and GABAergic neurons are displayed in amygdala, which may be implicated in the development of PTSD.

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Using the Single Prolonged Stress Model to Examine the Pathophysiology of PTSD

2017

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The endurance of memories of emotionally arousing events serves the adaptive role of minimizing future exposure to danger and reinforcing rewarding behaviors. However, following a traumatic event, a subset of individuals suffers from persistent pathological symptoms such as those seen in posttraumatic stress disorder (PTSD). Despite the availability of pharmacological treatments and evidence-based cognitive behavioral therapy, a considerable number of PTSD patients do not respond to the treatment, or show partial remission and relapse of the symptoms. In controlled laboratory studies, PTSD patients show deficient ability to extinguish conditioned fear. Failure to extinguish learned fear could be responsible for the persistence of PTSD symptoms such as elevated anxiety, arousal, and avoidance. It may also explain the high non-response and dropout rates seen during treatment. Animal models are useful for understanding the pathophysiology of the disorder and the development of new treatments. This review examines studies in a rodent model of PTSD with the goal of identifying behavioral and physiological factors that predispose individuals to PTSD symptoms. Single prolonged stress (SPS) is a frequently used rat model of PTSD that involves exposure to several successive stressors. SPS rats show PTSD-like symptoms, including impaired extinction of conditioned fear. Since its development by the Liberzon lab in 1997, the SPS model has been referred to by more than 200 published papers. Here we consider the findings of these studies and unresolved questions that may be investigated using the model.

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Dysfunction of Ca2+/CaM kinase IIα cascades in the amygdala in post-traumatic stress disorder

Cited by 3 publications

References 25 publications

Stress-related cellular pathophysiology as a crosstalk risk factor for neurocognitive and psychiatric disorders

Stress-related cellular pathophysiology as a crosstalk risk factor for neurocognitive and psychiatric disorders

Traumatic Stress Produces Distinct Activations of GABAergic and Glutamatergic Neurons in Amygdala

Using the Single Prolonged Stress Model to Examine the Pathophysiology of PTSD

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