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 anxiety, phobia, and posttraumatic stress disorder.

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 plasticity (or long-term potentiation) during learning, and the regions that bear an effect on the expression of specific conditioned responses. These pathways converge in the lateral amygdala. Long-term potentiation (LTP) and synaptic plasticity that enhances the response of lateral amygdala neurons to the conditioned stimulus occurs in the lateral amygdala. As a result, the conditioned stimulus is then able to flow from the lateral amygdala to the central nucleus of the amygdala. The basal and intercalated masses of the amygdala connect the lateral amygdala with the central nucleus of the amygdala directly and indirectly. Pathways from central nucleus of the amygdala to downstream areas then control defensive behavior (freezing) and autonomic and endocrine responses. Recent studies implicate the prelimbic cortex in fear expression as well, possibly by way of its connections to the basal and then to the central nucleus of the amygdala.^[1]

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 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]

The perception of fear is elicited by many different stimuli and involves the process described above in biochemical terms. Neural correlates of the interaction between language and visual information has been studied by Roel Willems et al.^[22] The study consisted of observing how visual and linguistic information interact in the perception of emotion. A common phenomenon from film theory was borrowed which states that the presentation of a neutral visual scene intensifies the percept of fear or suspense induced by a different channel of information, such as language. This principle has been applied in a way in which the percept of fear was present and amplified in the presence of a neutral visual stimuli. The main idea is that the visual stimuli intensify the fearful content of the stimuli (i.e. language) by subtly implying and concretizing what is described in the context (i.e. sentence). Activation levels in the right anterior temporal pole were selectively increased and is believed to serve as a binding function of emotional information across domains such as visual and linguistic information.^[23]

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]