Anxiety Disorders and Posttraumatic Stress Disorder Update

Victor, Andrea M.; Bernstein, Gail A.

doi:10.1016/j.psc.2008.11.004

Cited by 8 publications

(3 citation statements)

References 59 publications

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“…Extreme variations or perturbations of these mechanisms can lead to prolonged (even irreversible) and disproportional states with respect to the triggering stimulus, persistence of anxiety following withdrawal of the stimulus, or omnipresent generalized anxiety. In their extreme or pathological forms, these states include panic disorders, phobias, and posttraumatic stress disorders (510, 523). These are common diseases with an estimated lifetime prevalence of up to 18% (8, 200), imposing a major challenge to health providers and burden on the economy.…”

Section: Introduction: the Case For An Animal Model Of Fear And Anmentioning

confidence: 99%

Plastic Synaptic Networks of the Amygdala for the Acquisition, Expression, and Extinction of Conditioned Fear

Pape¹,

Paré

2010

Physiological Reviews

900

870

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The last ten years have witnessed a surge of interest for the mechanisms underlying the acquisition and extinction of classically conditioned fear responses. In part, this results from the realization that abnormalities in fear learning mechanisms likely participate to the development and/or maintenance of human anxiety disorders. The simplicity and robustness of this learning paradigm, coupled to the fact that the underlying circuitry is evolutionarily well conserved makes it an ideal model to study the basic biology of memory and identify genetic factors and neuronal systems that regulate the normal and pathological expressions of learned fear. Critical advances have been made in determining how modified neuronal functions upon fear acquisition become stabilized during fear memory consolidation and how these processes are controlled in the course of fear memory extinction. With these advances, came the realization that activity in remote neuronal networks must be coordinated for these events to take place. In this paper, we review these mechanisms of coordinated network activity and the molecular cascades leading to enduring fear memory, and allowing for their extinction. We will focus on Pavlovian fear conditioning as a model and the amygdala as a key component for the acquisition and extinction of fear responses.

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Section: Introduction: the Case For An Animal Model Of Fear And Anmentioning

confidence: 99%

Plastic Synaptic Networks of the Amygdala for the Acquisition, Expression, and Extinction of Conditioned Fear

Pape¹,

Paré

2010

Physiological Reviews

900

870

View full text Add to dashboard Cite

show abstract

“…Intensively stressful and traumatic events often create aversive memories, which can be a predisposing factor of posttraumatic stress disorders (PTSDs) and other anxiety disorders (Heim and Nemeroff, 2009;Victor and Bernstein, 2009). These fear memories are readily retrieved by conditioned cues linked with the traumatic events, and weakening of this association might be helpful for removal of the aversive memories (see Ressler (2010) for review).…”

Section: Introductionmentioning

confidence: 99%

Prevention of Stress-Impaired Fear Extinction Through Neuropeptide S Action in the Lateral Amygdala

Chauveau

Lange

Jüngling

et al. 2012

Neuropsychopharmacol

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Stressful and traumatic events can create aversive memories, which are a predisposing factor for anxiety disorders. The amygdala is critical for transforming such stressful events into anxiety, and the recently discovered neuropeptide S transmitter system represents a promising candidate apt to control these interactions. Here we test the hypothesis that neuropeptide S can regulate stress-induced hyperexcitability in the amygdala, and thereby can interact with stress-induced alterations of fear memory. Mice underwent acute immobilization stress (IS), and neuropeptide S and a receptor antagonist were locally injected into the lateral amygdala (LA) during stress exposure. Ten days later, anxiety-like behavior, fear acquisition, fear memory retrieval, and extinction were tested. Furthermore, patch-clamp recordings were performed in amygdala slices prepared ex vivo to identify synaptic substrates of stress-induced alterations in fear responsiveness. (1) IS increased anxiety-like behavior, and enhanced conditioned fear responses during extinction 10 days after stress, (2) neuropeptide S in the amygdala prevented, while an antagonist aggravated, these stress-induced changes of aversive behaviors, (3) excitatory synaptic activity in LA projection neurons was increased on fear conditioning and returned to preconditioning values on fear extinction, and (4) stress resulted in sustained high levels of excitatory synaptic activity during fear extinction, whereas neuropeptide S supported the return of synaptic activity during fear extinction to levels typical of non-stressed animals. Together these results suggest that the neuropeptide S system is capable of interfering with mechanisms in the amygdala that transform stressful events into anxiety and impaired fear extinction.

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“…In this disorder, the patient is exposed to a traumatic event, which involves death or a threat of death, and the patient's responses to that event are very intense fear and distress. [1] The patient shows serious disturbed behaviors and clinical disorder in his/her individual, social, and occupational performance, which would not occur before the trauma because the patient repeatedly recalls the traumatic experience. [2] Recent neuro-imaging studies have shown the volume of hippocampus in patients with PTSD decreases.…”

Section: Introductionmentioning

confidence: 99%

Study of the variations in apoptotic factors in hippocampus of male rats with posttraumatic stress disorder

et al. 2013

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Background:Post-traumatic stress disorder (PTSD) is a stress-related psychosomatic disorder caused by occurrence of a traumatic event and the hippocampus volume of the patients with Post-traumatic stress disorder decreased. However, the mechanisms that cause such damage are not well-understood. The aim of this study is to detect the expression of apoptosis-related Bax, Bcl-2, Caspase-3 and Insulin-like growth Factor-I proteins in the hippocampus region in the Predatory stress rats.Materials and Methods:A total of 70 male wistar rats were divided into Predatory stress groups of 1d, 2d, 3d, 7d, 14d, 30d and a normal control group (N = 10). Rats were subjected to 5 min of predatory stress and then exposed to the elevated plus-maze (EPM). Serum corticosterone and Insulin-like growth factor-1 level of Hippocampus were measured by ELISA technique. The expression of Bax, Bcl-2, and Caspase-3 were detected by western blotting.Results:Rats spent significantly more time in closed arms of the elevated plus maze (EPM) than control group after exposure to stress. Serum levels of corticosterone significantly increased at 2d-3d. The expression of hippocampal IGF-1 was significantly up-regulated at 1d-2d after stress. Both Bax and the ratio of Bax/Bcl-2 significantly peaked at Predatory stress 2d-14d. Caspase3 was significantly active among 2d-30 compared to the normal control.Conclusion:The activation of caspase-3 in the stress groups indicates that apoptosis may be one of the reasons inducing hippocampus atrophy and play roles in the pathogenesis of PTSD. Increase in hippocampus levels of IGF-1 during early PTSD might be involved in the early molecular inhibitory mechanism of apoptosis in PTSD.

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Anxiety Disorders and Posttraumatic Stress Disorder Update

Cited by 8 publications

References 59 publications

Plastic Synaptic Networks of the Amygdala for the Acquisition, Expression, and Extinction of Conditioned Fear

Plastic Synaptic Networks of the Amygdala for the Acquisition, Expression, and Extinction of Conditioned Fear

Prevention of Stress-Impaired Fear Extinction Through Neuropeptide S Action in the Lateral Amygdala

Study of the variations in apoptotic factors in hippocampus of male rats with posttraumatic stress disorder

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