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.
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.
After setting a control and a valid experimental design, Fischer rats were exposed daily to different stressors in a complex environment.
[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.
Experimental data has been shown to support the idea that the plasticity and fear memory formation in the lateral amygdala are triggered by unconditioned stimulus-induced activation of the region's neurons.
[7] It is believed that monoamine transmitters such as norepinephrine and dopamine that are released in emotional situations function in regulating glutamatergic transmission and Hebbian plasticity.
In a variety of model systems, it has been shown that monoamines modulate plasticity underlying memory formation such as a heightened percept of fear.
Recent studies have demonstrated that the blockade of norepinephrine β-adrenergic receptors (β-ARs) in the lateral nucleus of the amygdala interferes with the acquisition of fear learning when given pretraining stimuli but has no effect when applied posttraining or before memory retrieval.
One theory suggests that the mechanism of β-AR involvement in the acquisition of fear learning is that they act on GABAergic interneurons to suppress feed-forward inhibition and enhance Hebbian plasticity.
They may also act in a parallel fashion with Hebbian mechanisms to implement synapses in the lateral amygdala and promote plasticity and fear learning through their respective signaling pathways.
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.
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.
[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.
If so, this information is relayed to the amygdala and the muscle contraction, increased heart rate and blood pressure begins, thus activating the sympathetic neuronal pathway.
A presentation of a neutral visual stimuli has been shown to intensify the percept of fear or suspense induced by a different channel of information, such as audition.
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.