The role of β-arrestin-2 on Fear/anxious-related memory in a rat model of Post-traumatic stress disorder

Ding, Jinlan; Han, Fang; Wen, Lei; Xiao, Bing; Shi, Yonghui

doi:10.1016/j.jad.2016.12.043

Cited by 9 publications

(8 citation statements)

References 39 publications

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“…Furthermore, amygdala’s response to fear stimuli could be used to evaluate the treatment effect (Bryant et al, 2008). A series of molecular substrates in amygdala have been implicated in the PTSD-associated behaviors, such as glucocorticoid receptor (Kohda et al, 2007; Cohen et al, 2012), betaarrestin-2 (Ding et al, 2017), β-adrenoreceptor (Ronzoni et al, 2016), and mTOR signaling pathway (Oh et al, 2018). We also recently found different activating patterns of glutamatergic and GABAergic neurons in amygdala, specifically delayed enhancement of glutamatergic pyramidal neuron activation in BLA (Fang et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Traumatic Stress Produces Delayed Alterations of Synaptic Plasticity in Basolateral Amygdala

et al. 2019

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Acute traumatic event exposure is a direct cause of post-traumatic stress disorder (PTSD). Amygdala is suggested to be associated with the development of PTSD. In our previous findings, different activation patterns of GABAergic neurons and glutamatergic neurons in early or late stages after stress were found. However, the neural plastic mechanism underlying the role of basolateral amygdala (BLA) in post-traumatic stress disorder remains unclear. Therefore, this study mainly aimed at investigating time-dependent morphologic and electrophysiological changes in BLA during the development of PTSD. We used single prolonged stress (SPS) procedure to establish PTSD model of rats. The rats showed no alterations in anxiety behavior as well as in dendritic spine density or synaptic transmission in BLA 1 day after SPS. However, 10 days after SPS, rats showed enhancement of anxiety behavior, and spine density and frequency of miniature excitatory and inhibitory postsynaptic currents in BLA. Our results suggested that after traumatic stress, BLA displayed delayed increase in both spinogenesis and synaptic transmission, which seemed to facilitate the development of PTSD.

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Section: Introductionmentioning

confidence: 99%

Traumatic Stress Produces Delayed Alterations of Synaptic Plasticity in Basolateral Amygdala

et al. 2019

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“…Strongly involved in forming emotional memories, especially fear-related memories, the amygdala is thus regarded as the central brain region and attracts many scientists’ special attention. Using animal model of PTSD, previous studies have found that glucocorticoid receptor ( Kohda et al, 2007 ), 5-HT 2 C ( Harada et al, 2008 ), Rin1 and Stathmin ( Han et al, 2017 ), beta-adrenoreceptors ( Ronzoni et al, 2016 ), and beta-arrestin-2 ( Ding et al, 2017 ) are involved in the PTSD-associated behaviors. Besides, the amygdala is composed of several functionally distinct nuclei that interact during stress responses.…”

Section: Discussionmentioning

confidence: 99%

“…Exaggerated of the amygdala activity has been observed in response to trauma-related stimuli ( Shin et al, 1997 ; Liberzon et al, 1999 ; Pissiota et al, 2002 ; Hendler et al, 2003 ), and also during acquisition of conditioned fear ( Bremner et al, 2005 ). Using animal model of PTSD, a few studies found that 5-HT2C ( Harada et al, 2008 ), Rin1 and Stathmin ( Han et al, 2017 ), beta-adrenoreceptors ( Ronzoni et al, 2016 ), Neuropeptide S ( Cohen et al, 2018 ), and beta-arrestin-2 ( Ding et al, 2017 ) may be implicated in PTSD associated behaviors. Recently, through using c-Fos or other markers of neuronal activity, increased activation of the amygdala was found to be associated with traumatic stress-induced behavioral changes, such as anxiety-like behaviors and deficit in fear extinction ( Muigg et al, 2008 ; Hoffman et al, 2014 ; Ritov et al, 2014 ; Yu et al, 2015 ; Knox et al, 2018 ).…”

Section: Introductionmentioning

confidence: 99%

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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“…Our study presents and assesses different models for understanding depressive symptoms using the triad of fear, anxiety, and stress. Our model applies a solid framework on the influence of this triad on mental health and applies it in the presence of depressive symptoms [6][7][8][9]. Another strong point of the study is the use of statistical methods that consider all these variables within their analysis.…”

Section: Strengths and Limitationsmentioning

confidence: 99%

“…Fear is one of the most influential factors in the presence of emotional problems, such as anxiety and stress. Evidence from animal models of fear and human studies indicates that exposure to constant fear increases anxiety, which in turn can trigger traumatic stress [6][7][8][9]. One possible explanation is that the endocannabinoid system links the perception of external and internal stimuli with different neurophysiological and behavioral outcomes, such as the reaction to fear, anxiety, and stress.…”

Section: Introductionmentioning

confidence: 99%

Depression, post-traumatic stress, anxiety, and fear of COVID-19 in the general population and health-care workers: prevalence, relationship, and explicative model in Peru

et al. 2021

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Background This study has two aims. First, determine the fit of the fear model to COVID-19, anxiety, and post-traumatic stress in the general population and health-care workers. Second, determine which model best explains the relationship between depression and the triad of fear, anxiety, and post-traumatic stress in both groups. Method A cross-sectional study was conducted using self-reported questionnaires for anxiety, fear of COVID-19, depression, and post-traumatic stress. Information was collected from adults living in Lima, the capital and the most populous city in Peru. The explanatory models were evaluated using a structural equation model. Results A total of 830 participants were included, including general population (n = 640) and health-care workers (n = 190). A high overall prevalence of depressive symptoms (16%), anxiety (11.7%), and post-traumatic stress (14.9%) were identified. A higher prevalence of depressive, anxious, or stress symptoms was identified in the general population (28.6%) compared to health-care workers (17.9%). The triad model of fear of COVID-19, anxiety, and stress presented adequate goodness-of-fit indices for both groups. A model was identified that manages to explain depressive symptoms in more than 70% of the general population and health-care workers, based on the variables of the triad (CFI = 0.94; TLI = 0.94; RMSEA = 0.06; SRMR = 0.06). In the general population post-traumatic stress mediated the relationship between anxiety and depression (β = 0.12; 95%CI = 0.06 to 0.18) which was significant, but the indirect effect of post-traumatic stress was not significant in health care workers (β = 0.03; 95%CI = − 0.11 to 0.19). Limitations The prevalence estimates relied on self-reported information. Other variables of interest, such as intolerance to uncertainty or income level, could not be evaluated. Conclusions Our study proposes and tests one model that explains more than 70% of depressive symptoms. This explanatory model can be used in health contexts and populations to determine how emotional factors can affect depressive symptoms.

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The role of β-arrestin-2 on Fear/anxious-related memory in a rat model of Post-traumatic stress disorder

Cited by 9 publications

References 39 publications

Traumatic Stress Produces Delayed Alterations of Synaptic Plasticity in Basolateral Amygdala

Traumatic Stress Produces Delayed Alterations of Synaptic Plasticity in Basolateral Amygdala

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

Depression, post-traumatic stress, anxiety, and fear of COVID-19 in the general population and health-care workers: prevalence, relationship, and explicative model in Peru

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