Ivan Pavlov is a name familiar to most, whether scientific expert or budding psychology student. Pavlov founded the basis of classical, or Pavlovian, conditioning, in which an animal or person learns to associate an initially meaningless stimulus in their environment with a stimulus that produces an automatic response, therefore eliciting the response when the newly meaningful stimulus is presented. Most famously, you might recognize Pavlov’s experiment where he conditioned dogs to associate sounds with the arrival of food, eventually producing a salivary response from the dogs with just the sound alone.
Following Pavlov, in 1919 a scientist named John B Watson became one of the first people to demonstrate fear conditioning: using Pavlovian conditioning to induce a fear response or a phobia. You may have heard of his notorious and ethically questionable “Little Albert” experiment, in which he induced phobias of rabbits and other normally pleasing objects in an infant through an association with loud, unpleasant noises.
Fear conditioning can be used for more than just questionable experiments on infants, though. In recent years, scientists have been using what we know about fear conditioning to study disorders like PTSD (Post Traumatic Stress Disorder), in hopes of finding new treatments.
PTSD, or post traumatic stress disorder, is a disorder where fear learned in a traumatic situation is triggered by seemingly neutral stimuli in ordinary, safe situations, producing detrimental physiological and behavioral responses. Studies have shown that the brain areas affected in PTSD – mainly the amygdala, hippocampus, and prefrontal cortex – are similar to the brain areas affected in rodents who have been fear conditioned. Evidence suggests that flawed synaptic plasticity, the ability for the brain to rewire itself, could be part of the cause of PTSD.
During fear conditioning, rodent’s brains rewire themselves to make a connection between a certain stimulus and a fear response. During extinction, the process in which a conditioned response to a stimulus goes away, the synaptic connections rewire themselves, no longer associating the certain stimulus to a fear response. In patients with PTSD, it is possible that the flawed synaptic ability hinders the fear response from being overwritten effectively. This results in the production of an otherwise unwarranted fear response in patients, when exposed to neutral stimuli.
By attempting to understand the synaptic basis for PTSD using animal models of fear conditioning, scientists can work toward developing new medications that effect chemical action at the synapses. Hopefully, these medications will be able to lessen the symptoms of PTSD in patients and eventually work toward more accessible treatment for flawed synaptic plasticity, and fear and anxiety disorders in general.
Heatherton, Todd, and Diane Halpern. “Chapter 6, Learning.” Psychological Science. By Michael Gazzaniga. 5th ed. New York: W W Norton, 2013. 222-37. Print.
Mahan, Amy L., and Kerry J. Ressler. “Fear Conditioning, Synaptic Plasticity and the Amygdala: Implications for Post Traumatic Stress Disorder.” Cell Press 35 (2012): 24-35. Web. 13 Oct. 2015.