Fear conditioning

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Fear conditioning is a behavioral paradigm in which organisms learn to predict aversive events.[1] It is a form of learning in which an aversive stimulus (e.g. an electrical shock) is associated with a particular neutral context (e.g., a room) or neutral stimulus (e.g., a tone), resulting in the expression of fear responses to the originally neutral stimulus or context. This can be done by pairing the neutral stimulus with an aversive stimulus (e.g., a shock, loud noise, or unpleasant odor[citation needed]). Eventually, the neutral stimulus alone can elicit the state of fear. In the vocabulary of classical conditioning, the neutral stimulus or context is the "conditional stimulus" (CS), the aversive stimulus is the "unconditional stimulus" (US), and the fear is the "conditional response" (CR).

Fear conditioning apparatus for mice equipped with a sound, a foot shock and an activity sensor with photobeams to measure freezing. Environment context can be changed. This apparatus is also used for PTSD studies.

Fear conditioning has been studied in numerous species, from snails to humans. In humans, conditioned fear is often measured with verbal report and galvanic skin response. In other animals, conditioned fear is often measured with freezing (a period of watchful immobility) or fear potentiated startle (the augmentation of the startle reflex by a fearful stimulus). Changes in heart rate, breathing, and muscle responses via electromyography can also be used to measure conditioned fear. A number of theorists have argued that conditioned fear coincides substantially with the mechanisms, both functional and neural, of clinical anxiety disorders.[2] Research into the acquisition, consolidation and extinction of conditioned fear promises to inform new drug based and psychotherapeutic treatments for an array of pathological conditions such as dissociation, phobias and post-traumatic stress disorder.[3]

Neurobiology[edit]

Amygdala[edit]

Fear conditioning is thought to depend upon an area of the brain called the amygdala. Ablation or deactivating of the amygdala can prevent both the learning and expression of fear. Joseph E. LeDoux finds two amygdala pathways in the brain of the laboratory mouse by the use of fear conditioning and lesion study. He names them the "high road" and "low road". The low road is a pathway which is able to transmit a signal from a stimulus to the thalamus, and then to the amygdala, which then activates a fear-response in the body. This sequence works without a conscious experience of what comprises the stimulus, and it is the fast way to a bodily response. The high road is activated simultaneously. This is a slower road which also includes the cortical parts of the brain, thus creating a conscious impression of what the stimulus is. The low road only involves the sub-cortical part of the brain and is therefore regarded as a more primitive mechanism of defense, only existing in its separate form in lesser developed animals who have not developed the more complex part of the brain. In more developed animals, the high road and the low road work simultaneously to provide both fear-response and perceptual feedback.[4]

Hippocampus[edit]

Some types of fear conditioning (e.g. contextual and trace) also involve the hippocampus, an area of the brain believed to receive affective impulses from the amygdala and to integrate those impulses with previously existing information to make it meaningful. Some theoretical accounts of traumatic experiences suggest that amygdala-based fear bypasses the hippocampus during intense stress and can be stored somatically or as images that can return as physical symptoms or flashbacks without cognitive meaning.[5]

Glutamate[edit]

One of the major neurotransmitters involved in conditioned fear learning is glutamate. Both the metabotropic glutamate 5 receptor and the NMDA receptor have been implicated in the control of conditioned fear.[6]

Epigenetics[edit]

A conditioned fear response may be inherited transgenerationally at behavioral, neuroanatomical and epigenetic levels.[7] This has been shown in experiments that use Acetophenone to examine the inheritance of parental traumatic exposure (odor fear conditioning). In these experiments, acetophenone's odor was shown to activates an odorant receptor (Olfr151) in mice.

Across development[edit]

The learning involved in conditioned fear, as well as the underlying neurobiology, changes dramatically from infancy, across childhood and adolescence, into adulthood and aging.[8][9]

See also[edit]

References[edit]

  1. ^ Maren, Stephen (2001). "Neurobiology of Pavlovian fear conditioning". Annual Review of Neuroscience. 24: 897–931. doi:10.1146/annurev.neuro.24.1.897. PMID 11520922. 
  2. ^ Rosen, Jeffrey B.; Schulkin, Jay (1998). "From normal fear to pathological anxiety". Psychological Review. 105 (2): 325–50. doi:10.1037/0033-295X.105.2.325. PMID 9577241. 
  3. ^ VanElzakker, M. B., Dahlgren, M. K., Davis, F. C., Dubois, S. & Shin, L. M. (2014). From Pavlov to PTSD: The extinction of conditioned fear in rodents, humans, and anxiety disorders. Neurobiology of Learning and Memory 113: 3–18. | doi=10.1016/j.nlm.2013.11.014 | PMID 24321650
  4. ^ LeDoux, Joseph (1996). The Emotional Brain: The Mysterious Underpinnings of Emotional Life. New York: Simon & Schuster. [page needed]
  5. ^ Bromberg, Philip M. (2003). "Something wicked this way comes: Trauma, dissociation, and conflict: The space where psychoanalysis, cognitive science, and neuroscience overlap". Psychoanalytic Psychology. 20 (3): 558–74. doi:10.1037/0736-9735.20.3.558. 
  6. ^ Handford, Charlotte E.; Tan, Shawn; Lawrence, Andrew J.; Kim, Jee Hyun (2014-09-01). "The effect of the mGlu5 negative allosteric modulator MTEP and NMDA receptor partial agonist D-cycloserine on Pavlovian conditioned fear". International Journal of Neuropsychopharmacology. 17 (9): 1521–1532. doi:10.1017/S1461145714000303. ISSN 1461-1457. PMID 24674862. 
  7. ^ Dias, B. G. & Ressler, K. J. (2013). Parental olfactory experience influences behavior and neural structure in subsequent generations. Nature Neuroscience, Dec 01, 2013. PMID 24292232 (Retrieved December 21, 2013)
  8. ^ Madsen, Heather Bronwyn; Kim, Jee Hyun (2016-02-01). "Ontogeny of memory: An update on 40 years of work on infantile amnesia". Behavioural Brain Research. Developmental Regulation of Memory in Anxiety and Addiction. 298, Part A: 4–14. doi:10.1016/j.bbr.2015.07.030. 
  9. ^ Ganella, Despina E; Kim, Jee Hyun (2014-10-01). "Developmental rodent models of fear and anxiety: from neurobiology to pharmacology". British Journal of Pharmacology. 171 (20): 4556–4574. doi:10.1111/bph.12643. ISSN 1476-5381. PMC 4209932Freely accessible. PMID 24527726.