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]

Contents
[hide]

1Neurobiology

o 1.1Amygdala

o 1.2Hippocampus

o 1.3Glutamate
 o 1.4Epigenetics

2Across development

3See also

4References

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][10]

See also[edit]
 Amygdala

Classical conditioning

Extinction (psychology)

Eyeblink conditioning

Fear processing in the brain

Infralimbic cortex

Intercalated cells of the amygdala

Measures of conditioned emotional response

Ventromedial prefrontal cortex

References[edit]
1. Jump up^ 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. Jump up^ 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. Jump up^ 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: 318. |
doi=10.1016/j.nlm.2013.11.014 | PMID 24321650

4. Jump up^ LeDoux, Joseph (1996). The Emotional Brain: The

Mysterious Underpinnings of Emotional Life. New York: Simon &
Schuster.[page needed]

5. Jump up^ 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. Jump up^ 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 246
74862.
 7. Jump up^ Dias, B. G.; Ressler, K. J. (2013). "Parental olfactory
experience influences behavior and neural structure in subsequent
generations". Nature Neuroscience. 17: 89
96. doi:10.1038/nn.3594. PMC 3923835 . PMID 24292232.

8. Jump up^ 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. PMID 26190765.

9. Jump up^ 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 4209932
. PMID 24527726.

10. Jump up^ Kim, Jee Hyun; Perry, Christina J.; Ganella, Despina E.;
Madsen, Heather B. "Postnatal development of neurotransmitter
systems and their relevance to extinction of conditioned
fear". Neurobiology of Learning and
Memory. doi:10.1016/j.nlm.2016.10.018.
Categories:
Behavioral concepts
Fear
Behaviorism

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