Neurocircuitry models of posttraumatic stress disorder and extinction: human neuroimaging research--past, present, and future.

By Scott L. Rauch, Lisa M. Shin, Elizabeth A. Phelps. Biological Psychiatry, 2006

1,377 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Cognitive Neuroscience, Developmental Neuroscience

View Paper: https://www.semanticscholar.org/paper/5596c18ccc41817d4412635de81d1dc5f765e727

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Citations in the corpus

Social bonds and posttraumatic stress disorder. (2008, background): “…has focused on individuallevel factors, such as neural circuits responsible for fear processing, modulation, and extinction (Phelps & LeDoux 2005, Rauch et al. 2006); alterations in the HPA axis (Marmar et al. 2006, Pitman et al. 2006, Yehuda 2006); or the nature of emotional memory (Cahill et…”
Functional neuroimaging of anxiety: a meta-analysis of emotional processing in PTSD, social anxiety disorder, and specific phobia. (2007, methodology): “Finally, we performed novel tests of coactivation across regions to test whether, across individual studies, limbic dysregulation is reliably associated with medial prefrontal dysfunction (41, 42).”
Optogenetic investigation of neural circuits underlying brain disease in animal models (2012, background): “PTSD is a class of pervasive anxiety disorder that can occur following a traumatic experience under specific conditions (for example, involving subjective helplessness) and is remarkably debilitating owing to its chronic influence on many aspects of social and occupational functioning and its resist”
Psychobiology and molecular genetics of resilience (2009, positive): “Current models of the pathophysiology of PTSD, an example of conditions that are characterized by diminished resilience on exposure to a traumatic stressor, involve abnormal fear learning and an underlying dysfunction in the neural circuitry of fear, comprising the amygdala, the hippocampus and the ”
Neurobiological Basis of Failure to Recall Extinction Memory in Posttraumatic Stress Disorder (2009, background): “fear is deficient in PTSD (3,39) is supported by de novo fear”
Recall of fear extinction in humans activates the ventromedial prefrontal cortex and hippocampus in concert. (2007, background): “…Milad and Quirk 2002). ndeed, on the basis of data in rodents and in patients with nxiety disorders, several investigators have hypothesized that he human vmPFC plays a specific role in extinction recall Maren and Quirk 2004; Milad et al. 2006; Rauch et al. 1998, 2006; otres-Bayon et al. 2004).”
A validated network of effective amygdala connectivity (2007, background): “, 2006; Maren and Quirk, 2004) as well as in humans where data suggest that the mPFC is an inhibitory input to the amygdala (Rauch et al., 2006).”
Sensitive periods of amygdala development: The role of maltreatment in preadolescence (2014, background): “025 function have been reported in psychiatric disorders marked by affective dysregulation (Rauch et al., 2006; Saleh et al., 2012; Lange and Irle, 2004; Schmahl et al., 2003a).”
Posttraumatic Stress Disorder (2015, background): “Increased amygdala activation resulting from faulty modulatory input from the left ventromedial prefrontal cortex and, to a lesser extent, thehippocampus, underlies fear responses in PTSD.(42,43) The amygdala encodes the salience of aversive cues and integrates a reflex response mediated by effector”
How Does Mindfulness Meditation Work? Proposing Mechanisms of Action From a Conceptual and Neural Perspective (2011, neutral): “Wie wirkt”
Neural Mechanisms of Extinction Learning and Retrieval (2008, background): “Understanding retrieval of extinction is clinically important, because anxiety disorders and relapse of drug abuse are thought to be caused by a failure to retrieve an extinction memory generated in extinction-based treatment (Rauch et al, 2006; Kalivas et al, 2006).”