Environmental
Rachman proposed three pathways for the development of phobias: direct or classical conditioning (exposure to phobic stimulus), vicarious acquisition (seeing others experience phobic stimulus), and informational/instructional acquisition (learning about phobic stimulus from others). Classical conditioning
Much of the progress in understanding the acquisition of fear responses in phobias can be attributed to classical conditioning (Pavlovian model). When an aversive stimulus and a neutral one are paired together, for instance, when an electric shock is given in a specific room, the subject can start to fear not only the shock but the room as well. In behavioral terms, the room is a conditioned stimulus (CS). When paired with an aversive unconditioned stimulus (UCS) (the shock), it creates a conditioned response (CR) (fear for the room) (CS+UCS=CR). For example, in case of the fear of heights (acrophobia), the CS is heights. Such as a balcony on the top floors of a high rise building. The UCS can originate from an aversive or traumatizing event in the persons life, such as almost falling from a great height. The original fear of nearly falling is associated with being high, leading to a fear of heights. In other words, the CS (heights) associated with the aversive UCS (almost falling) leads to the CR (fear). Though historically influential in the theory of fear acquisition, this direct conditioning model is not the only proposed way to acquire a phobia. This theory in fact has limitations as not everyone that has experienced a traumatic event develops a phobia and vice versa.
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 receptors in the hippocampus monitor the amount of cortisol in the system and through negative feedback can tell the hypothalamus to stop releasing CRH.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 receptors or even serotonin (5-HT). 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 one of these regions is damaged. Damage to the cortical areas involved in the limbic system, such as the cingulate cortex or frontal lobes, has resulted in extreme emotion changes. 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.