The contextual brain: implications for fear conditioning, extinction and psychopathology

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Abstract

Contexts surround and imbue meaning to events; they are essential for recollecting the past, interpreting the present and anticipating the future. Indeed, the brain’s capacity to contextualize information permits enormous cognitive and behavioural flexibility. Studies of Pavlovian fear conditioning and extinction in rodents and humans suggest that a neural circuit including the hippocampus, amygdala and medial prefrontal cortex is involved in the learning and memory processes that enable context-dependent behaviour. Dysfunction in this network may be involved in several forms of psychopathology, including post-traumatic stress disorder, schizophrenia and substance abuse disorders.

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Neural mechanisms of extinction learning and retrieval.

Gregory J. Quirk, Devin Mueller (2008)

Emotional learning is necessary for individuals to survive and prosper. Once acquired, however, emotional associations are not always expressed. Indeed, the regulation of emotional expression under varying environmental conditions is essential for mental health. The simplest form of emotional regulation is extinction, in which conditioned responding to a stimulus decreases when the reinforcer is omitted. Two decades of research on the neural mechanisms of fear conditioning have laid the groundwork for understanding extinction. In this review, we summarize recent work on the neural mechanisms of extinction learning. Like other forms of learning, extinction occurs in three phases: acquisition, consolidation, and retrieval, each of which depends on specific structures (amygdala, prefrontal cortex, hippocampus) and molecular mechanisms (receptors and signaling pathways). Pharmacological methods to facilitate consolidation and retrieval of extinction, for both aversive and appetitive conditioning, are setting the stage for novel treatments for anxiety disorders and addictions.

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Neurobiological basis of failure to recall extinction memory in posttraumatic stress disorder.

Mohammed Milad, Roger K. Pitman, Cameron B. Ellis … (2009)

A clinical characteristic of posttraumatic stress disorder (PTSD) is persistently elevated fear responses to stimuli associated with the traumatic event. The objective herein is to determine whether extinction of fear responses is impaired in PTSD and whether such impairment is related to dysfunctional activation of brain regions known to be involved in fear extinction, viz., amygdala, hippocampus, ventromedial prefrontal cortex (vmPFC), and dorsal anterior cingulate cortex (dACC). Sixteen individuals diagnosed with PTSD and 15 trauma-exposed non-PTSD control subjects underwent a 2-day fear conditioning and extinction protocol in a 3-T functional magnetic resonance imaging scanner. Conditioning and extinction training were conducted on day 1. Extinction recall (or extinction memory) test was conducted on day 2 (extinguished conditioned stimuli presented in the absence of shock). Skin conductance response (SCR) was scored throughout the experiment as an index of the conditioned response. The SCR data revealed no significant differences between groups during acquisition and extinction of conditioned fear on day 1. On day 2, however, PTSD subjects showed impaired recall of extinction memory. Analysis of functional magnetic resonance imaging data showed greater amygdala activation in the PTSD group during day 1 extinction learning. During extinction recall, lesser activation in hippocampus and vmPFC and greater activation in dACC were observed in the PTSD group. The magnitude of extinction memory across all subjects was correlated with activation of hippocampus and vmPFC during extinction recall testing. These findings support the hypothesis that fear extinction is impaired in PTSD. They further suggest that dysfunctional activation in brain structures that mediate fear extinction learning, and especially its recall, underlie this impairment.

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

Scott L Rauch, Lisa Shin, Elizabeth A Phelps (2006)

The prevailing neurocircuitry models of anxiety disorders have been amygdalocentric in form. The bases for such models have progressed from theoretical considerations, extrapolated from research in animals, to in vivo human imaging data. For example, one current model of posttraumatic stress disorder (PTSD) has been highly influenced by knowledge from rodent fear conditioning research. Given the phenomenological parallels between fear conditioning and the pathogenesis of PTSD, we have proposed that PTSD is characterized by exaggerated amygdala responses (subserving exaggerated acquisition of fear associations and expression of fear responses) and deficient frontal cortical function (mediating deficits in extinction and the capacity to suppress attention/response to trauma-related stimuli), as well as deficient hippocampal function (mediating deficits in appreciation of safe contexts and explicit learning/memory). Neuroimaging studies have yielded convergent findings in support of this model. However, to date, neuroimaging investigations of PTSD have not principally employed conditioning and extinction paradigms per se. The recent development of such imaging probes now sets the stage for directly testing hypotheses regarding the neural substrates of fear conditioning and extinction abnormalities in PTSD.

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Author and article information

Journal

Journal ID (nlm-journal-id): 100962781

Journal ID (pubmed-jr-id): 22270

Journal ID (nlm-ta): Nat Rev Neurosci

Journal ID (iso-abbrev): Nat. Rev. Neurosci.

Title: Nature reviews. Neuroscience

ISSN (Print): 1471-003X

ISSN (Electronic): 1471-0048

Publication date Nihms-submitted: 13 October 2016

Publication date (Electronic): 02 May 2013

Publication date (Print): June 2013

Publication date PMC-release: 20 October 2016

Volume: 14

Issue: 6

Pages: 417-428

Affiliations

[1 ]Department of Psychology and Institute for Neuroscience, Texas A&M University, College Station, Texas 77843–3474, USA

[2 ]Department of Psychiatry, University of Illinois at Chicago and Mental Health Service Line, Jesse Brown VA Medical Center, Chicago, Illinois 60608, USA

[3 ]VA Ann Arbor Healthcare System and Departments of Psychology, Psychiatry and Neuroscience Program, University of Michigan, Ann Arbor, Michigan 48109, USA

Author notes

Correspondence to S.M. maren@ 123456tamu.edu

Article

Accession ID: PMC5072129 Pmcid ID: PMC5072129 Pmc-uid ID: 5072129 Manuscript ID: nihpa822461

DOI: 10.1038/nrn3492

PMC ID: 5072129

PubMed ID: 23635870

SO-VID: 798bc488-8a39-4a53-8b61-601ff8475d75

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The contextual brain: implications for fear conditioning, extinction and psychopathology

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cGMP: Generators, Effectors and Therapeutic Implications Conference

Most cited references 95

Neural mechanisms of extinction learning and retrieval.

Neurobiological basis of failure to recall extinction memory in posttraumatic stress disorder.

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

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