This form of learning, first described by Pavlov, involves pairing a neutral stimulus with an unconditioned stimulus to produce a conditioned response, and forms the basis of fear conditioning.
Classical Conditioning
ie. A child becomes anxious every time they hear a dentist’s drill after a painful filling; After being bitten by a dog, a person’s heart races and they feel panic whenever they see any dog;
This structure, particularly its basolateral and central nuclei, is considered the central hub of fear processing.
Amygdala
After witnessing a robbery, a person vividly recalls the event days later because the brain has stabilized the emotional memory; this process of stabilizing a memory after initial encoding is called this.
Memory Consolidation
Early-life stress can produce long-term changes through these modifications that alter gene expression without changing DNA sequence.
Epigenetic Changes
Administration of this steroid hormone during trauma memory reactivation can reduce PTSD symptoms by modulating HPA axis responses.
Hydrocortisone
B.F. Skinner applied this type of conditioning to fear, showing behaviors that reduce exposure to negative stimuli are reinforced.
Operant Conditioning
This brain region encodes contextual information in which a fear response occurs.
Hippocampus
After recalling a traumatic memory of a car accident during therapy, a person updates their fear response by pairing the memory with safety cues, weakening the original fear; this updating of a stored memory is called this.
Reconsolidation
During a sudden threat, the amygdala signals this structure which activates an endocrine axis leading to adrenaline and cortisol release and heightened physiological arousal.
Hypothalamus
This beta blocker has been studied for pre-retrieval therapy to reduce PTSD symptoms.
Propranolol
John B. Watson’s famous experiment that conditioned a child to fear a rat is known as this.
Little Albert Experience
This part of the brain helps regulate fear by modulating amygdala activity.
Prefrontal cortex
After repeated exposure to a loud thunderstorm, a person’s amygdala responds more strongly to thunder, enhancing the fear response; this strengthening of synaptic connections is called this.
Long term potentiation
A person freezes when startled by a loud noise because the amygdala projects to this brain region to coordinate autonomic and endocrine responses.
Brainstem
Psychedelic-assisted psychotherapy for fear disorders can involve agents such these.
MDMA
Psilocybin
Hull and Mowrer conceptualized fear as a learned state that motivates this kind of behavior.
Avoidance Behavior
Together with the amygdala and prefrontal cortex, this cortex is also involved in fear processing.
The anterior cingulate cortex.
The ventromedial prefrontal cortex inhibits amygdala activity to reduce fear when a person repeatedly encounters a previously frightening stimulus in a safe context; this neural process underlies what type of learning?
Extinction
(Reduced inhibition from this cortical region can impair extinction of fear responses in pathological conditions.)
In response to acute threat, this adrenal hormone is released to prepare the body for fight-or-flight.
Cortisol
This antibiotic-turned-drug is sometimes used to augment exposure therapy by enhancing extinction learning through NMDA receptor modulation.
D-cycloserine
A person who avoids walking down a dark alley after hearing about a recent mugging experiences less anxiety each time they avoid it; this increase in avoidance behavior illustrates this type of operant conditioning.
Negative reinforcement
This process strengthens synaptic connections in the lateral amygdala after repeated pairing of a conditioned stimulus with an unconditioned stimulus, enhancing the fear response.
Long term potentiation
Even after repeated safe exposures to elevators, a person sometimes still feels fear when recalling a past panic episode; this illustrates that extinction does not erase the original memory, which persists in this form.
Conditioned memory trace
In some individuals with PTSD, the HPA axis shows exaggerated suppression of cortisol in response to stress, reflecting increased this type of regulation that normally limits hormone release.
heightened negative feedback
Two agents that act on alpha adrenergic receptors, and thus modulate sympathetic tone and improve PTSD symptoms include these.
Prazosin