Fear - Fear in The Amygdala

Fear in The Amygdala

The brain structure that is the center of most neurobiological events associated with fear is the amygdala, located behind the pituitary gland. The role of the amygdala in fear is best understood as part of a circuitry of fear learning. It is essential for proper adaptation to stress and specific modulation of emotional learning and memory. In the presence of a threatening stimulus, the amygdala generates the secretion of hormones that influence fear and aggression. Once response to the stimulus in the form of fear or aggression commences, the amygdala may elicit the release of hormones into the body to put the person into a state of alertness, in which they are ready to move, run, fight, etc. This defensive response is generally referred to in physiology as the fight-or-flight response regulated by the hypothalamus.

Some of the hormones involved during the state of fight-or-flight include epinephrine and norepinephrine and cortisol. Epinephrine regulates heart rate and metabolism as well as dilating blood vessels and air passages. Norepinephrine increases heart rate, blood flow to skeletal muscles and the release of glucose from energy stores. Cortisol increases blood sugar and helps with metabolism.

After a situation which incites fear occurs, the amygdala and hippocampus record the event through synaptic plasticity. Plasticity and memory formation in the amygdala are generated by activation of the neurons in the region. Experimental data supports the notion that synaptic plasiticity of the neurons leading to the lateral amygdala occurs with fear conditioning. In some cases, this forms permanent fear responses such as post-traumatic stress disorder (PTSD) or a phobia. MRI and fMRI scans have shown that the amygdala in individuals diagnosed with such disorders including bipolar or panic disorder is larger and wired for a higher level of fear.

A treatment for fear conditioning and phobias via the amygdala is the use of glucocorticoids. In one study, glucocorticoid receptors in the central nucleus of the amygdala were disrupted in order to better understand the mechanisms of fear and fear conditioning. The glucocorticoid receptors were inhibited using lentiviral vectors containing Cre-recombinase injected into mice. Results of this study showed that disruption of the glucocorticoid receptors prevented conditioned fear behavior. The mice were subjected to auditory cues which caused them to freeze normally. However, a reduction of freezing was observed in the mice that had inhibited glucocorticoid receptors.

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