Editing Phobia (section)

==== Amygdala ====
The [[amygdala]] is an almond-shaped mass of nuclei located deep in the brain's medial temporal lobe. It processes the events associated with fear and is linked to [[Social anxiety disorder|social phobia]] and other anxiety disorders. The amygdala's ability to respond to fearful stimuli occurs through [[fear conditioning]]. Like [[classical conditioning]], the amygdala learns to associate a conditioned stimulus with a negative or avoidant stimulus, creating a conditioned fear response often seen in phobic individuals. The amygdala is responsible for recognizing certain stimuli or cues as dangerous and plays a role in the storage of threatening stimuli to memory. The basolateral nuclei (or [[basolateral amygdala]]) and the hippocampus interact with the amygdala in-memory storage. This connection suggests why memories are often remembered more vividly if they have emotional significance.<ref name=Whalen>{{Cite book |title=The Human Amygdala |year=2009 |publisher=The Guilford Press |location=New York | veditors = Whalen PJ, Phelps EA }}</ref>

In addition to memory, the amygdala also triggers the secretion of [[hormone]]s that affect [[fear]] and [[aggression]]. When the fear or aggression response is initiated, the amygdala releases hormones into the body to put the human body into an "alert" state, which prepares the individual to move, run, fight, etc.<ref name=winerman>{{cite web | vauthors = Winerman L | url = http://www.apa.org/monitor/julaug05/figuring.html | title = Figuring Out Phobia | archive-url = https://web.archive.org/web/20071005171325/http://www.apa.org/monitor/julaug05/figuring.html | archive-date=2007-10-05 | publisher = [[American Psychological Association]] | work = Monitor on Psychology | date = August 2007 }}</ref> This defensive "alert" state and response are known as the [[fight-or-flight response]].<ref>{{cite web | vauthors = Rogers K |title=Fight-or-flight response |url=https://www.britannica.com/science/fight-or-flight-response |website=Britannica.com |access-date=19 February 2019}}</ref>

However, inside the brain, this stress response can be observed in the [[hypothalamic-pituitary-adrenal axis]] (HPA). This circuit incorporates the process of receiving stimuli, interpreting them, and releasing certain hormones into the bloodstream. The parvocellular neurosecretory neurons of the hypothalamus release [[corticotropin-releasing hormone]] (CRH), which is sent to the anterior pituitary. Here the pituitary releases [[adrenocorticotropic hormone]] (ACTH), which ultimately stimulates the release of [[cortisol]]. In relation to anxiety, the amygdala activates this circuit, while the hippocampus is responsible for suppressing it. [[Glucocorticoid receptor|Glucocorticoid]] receptors in the hippocampus monitor the amount of cortisol in the system and through negative feedback can tell the hypothalamus to stop releasing CRH.<ref name="Bear" />

Studies on mice engineered to have high concentrations of CRH showed higher levels of anxiety, while those engineered to have no or low amounts of CRH receptors were less anxious. In people with phobias, therefore, high amounts of cortisol may be present, or there may be low levels of [[glucocorticoid receptor]]s or even [[serotonin]] (5-HT).<ref name="Bear" />

===== Disruption by damage =====
For the areas in the brain involved in emotion – most specifically, fear – the processing and response to emotional stimuli can be altered when there are damage to any of these regions. Damage to the cortical areas involved in the limbic system, such as the cingulate cortex or frontal lobes, has resulted in extreme emotion changes.<ref name="Bear" /> Other types of damage include [[Klüver–Bucy syndrome]] and [[Urbach–Wiethe disease]]. In Klüver–Bucy syndrome, a temporal lobectomy, or removal of the temporal lobes, results in changes involving fear and aggression. Specifically, the removal of these lobes results in decreased fear, confirming its role in fear recognition and response. Damage to both side (Bilateral damage) of the medial temporal lobes is known as Urbach–Wiethe disease. It presents with similar symptoms of decreased fear and aggression but with the addition of the inability to recognize emotional expressions, especially angry or fearful faces.<ref name="Bear" />

The amygdala's role in learned fear includes interactions with other brain regions in the neural circuit of fear. While damage in the amygdala can inhibit its ability to recognize fearful stimuli, other areas such as the ventromedial prefrontal cortex and the basolateral nuclei of the amygdala can affect the region's ability to not only become conditioned to fearful stimuli but to extinguish them eventually. Through receiving stimulus info, the basolateral nuclei undergo synaptic changes that allow the amygdala to develop a conditioned response to fearful stimuli. Damage to this area, therefore, have been shown to disrupt the acquisition of learned responses to fear.<ref name="Bear" /> Likewise, damage in the ventromedial prefrontal cortex (the area responsible for monitoring the amygdala) has been shown to slow down the speed of extinguishing a learned fear response and how effective the extinction is. This suggests there is a pathway or circuit among the amygdala and nearby cortical areas that process emotional stimuli and influence emotional expression, all of which can be disrupted when damage occurs.<ref name="Tillfors" />