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Fear conditioning

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Fear conditioning is a behavioral paradigm in which organisms learn to predict aversive events. 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 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. 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.

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.

Fear conditioning is thought to depend upon an area of the brain called the amygdala. Electrophysiological recordings from the amygdala have demonstrated that cells in the region undergo long-term potentiation (LTP), a form of synaptic plasticity believed to underlie learning. Additionally, inhibition of neurons in the amygdala disrupts fear conditioning, while stimulation of those neurons can drive fear-related behaviors, such as freezing behavior in rodents. This indicates that proper function of the amygdala is both necessary for fear conditioning and sufficient to drive fear behaviors.

Joseph E. LeDoux has been an instrumental scientist in elucidating the amygdala's role in fear conditioning. He was one of the first to show that the amygdala undergoes long-term potentiation during fear conditioning, and that ablation of amygdala cells disrupts both learning and expression of fear, among many other achievements.

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.

Glutamate[edit] Molecular Mechanisms

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. It has been suggested that NMDA receptors (NMDARs) in the amygdala are necessary for fear memory acquisition, because disruption of NMDAR function disrupts development of fear responses in rodents.

Epigenetics[edit]

A conditioned fear response may be inherited transgenerationally at behavioral, neuroanatomical and epigenetic levels. 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 activate an odorant receptor (Olfr151) in mice.

Conditioned fear may be inherited transgenerationally. In one experiment, mice were conditioned to fear an acetophenone odor and then set up to breed subsequent generations of mice. Those subsequent generations of mice also showed a behavioral sensitivity to acetophenone, which was accompanied by neuroanatomical and epigenetic changes that are believed to have been inherited from the parents' gametes.

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. Specifically, infant animals show an inability to develop fear associations, whereas their adult counterparts develop fear memories much more readily.