Fear processing in the brain

Many experiments have been done to find out how the brain interprets stimuli and how animals develop fear responses. The emotion, fear, has been hard-wired into almost every individual, due to its vital role in the survival of the individual. Researchers have found that fear is established unconsciously and that the amygdala is involved with fear conditioning.

By understanding how fear is developed within individuals, it may be possible to treat human mental disorders such as

Neuronal fear pathways

In fear conditioning, the main circuits that are involved are the sensory areas that process the conditioned and unconditioned stimuli, certain regions of the amygdala that undergo

It has been observed that fear can contribute to behavioral changes.[2] One way this phenomenon has been studied is on the basis of the repeated stress model done by Camp RM et al.(among others). In this particular study, it was examined that the contribution fear conditioning may play a huge role in altering an animal's (Fischer rat's) behavior in a repeated stress paradigm. Behavioral changes that are commonly referred to as depressive-like behaviors resulted from this model of testing. After setting a control and a valid experimental design, Fischer rats were exposed daily to different stressors in a complex environment. After four days of stressor exposure, both exploratory behavior and social interaction were tested on day 5 in either the same environment or a new environment. The rats showed much decreased exploration and social interaction when tested in different contexts compared to control rats.^[3] To further make a correlation to the biochemistry (as mentioned below), chronic infusion of propranolol (beta-adrenergic receptor antagonist) prevented the behavioral changes following repeated stressor exposure thus halting long term potentiation. Some physiological changes also occurred including the decrease in body weight gain and adrenal hypertrophy observed in animals exposed to stress. Overall, the conditioned fear responses can contribute to behavioral changes in a repeated stress paradigm. This can be extended to correlate to other animals as well but with varying degrees of responses.^[3]

Molecular basis

Molecular mechanisms that have been linked directly to the behavioral expression of conditioning are easier to study in a clinical setting as opposed to mechanisms that underlie long-term potentiation (LTP), in which synaptic plasticity is induced by electrical or chemical stimulation of lateral amygdala circuits. LTP is important for fear processing because it strengthens the synapses in neural circuits.^[4] These strengthened synapses are how long-term memory is developed and how fear is developed.^[5]

Hebbian synaptic plasticity

Synaptic input can be strengthened when activity in the presynaptic neuron co-occurs with

Plasticity and learning can also be modulated by metabotropic glutamate receptors (mGluRs). The proteins mGluRs likely serve a modulatory function and do not participate directly in Hebbian processes. This is because due to the fact these receptors do not contribute to depolarization during synapses. They are also not activated by receptors that participate in Hebbian processes. Finally, they do not detect pre- and postsynaptic neural activity. However, the activation of group I mGluRs in the lateral amygdala and basal nucleus enhances the acquisition, reduction, and amplification of fear conditioning by providing an influx of calcium ions.

Fear circuitry

Fear recognition

Research studies have shown that damage to the bilateral amygdala^[15] affects mostly the recognition of fear. In a specific study conducted by Andrew J. Calder and Andrew W. Young, they had subjects classify morphed images of facial expressions ranging from happiness to surprise to fear to sadness to disgust to anger. While control subjects classified these images to the nearest expression, subjects who had damage to the bilateral amygdala had problems with this task, especially with the recognition of facial expressions that show fear. The subjects with the damaged bilateral amygdala had no problems differentiating happiness from sadness, but they could not differentiate the expression of anger from fear.^[16]

However, in an experiment conducted by Ralph Adolphs, it elucidated the mechanism of the impaired fear recognition. Adolphs found that his main subject, who had a rare bilateral amygdala damage, could not discern fear expressions because of her inability to look at the eye region of the face. When the subject was instructed to look directly at the eye region of faces with expression, the subject could recognize fear expressions of faces.^[17] Although the amygdala does play an important part in the recognition of fear, further research shows that there are alternate pathways that are capable to support fear learning in the absence of a functional amygdala.^[18] A study by Kazama also shows that although the amygdala may be damaged, it is still possible for patients to distinguish the difference between safety cues and fear.^[19]

Conditioned stimuli

There has been a substantial amount of research done on

Exposure to different types of emotion and levels of arousal also appear to influence pain through an interaction known as the valence-by-arousal interaction. During this reaction, negative emotions experienced by an individual with low levels of arousal tend to cause enhanced pain while negative valenced emotions with higher levels of arousal have been observed to decrease the perception of pain. Low levels of arousal would include reactive emotions such as anxiety while higher levels of arousal include emotions such as fear.^[24]

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