Emotional memories can be nearly indelible and directly influence our identities. One of the strongest emotions we have is fear. Fear can be a helpful survival mechanism that prevents us from jumping recklessly into dangerous situations, but it can also be a debilitating emotion that makes it impossible for some people to live without constant anxiety. It is a major component of many psychiatric illnesses, including post-traumatic stress disorder.

Once fear takes hold, it is extremely difficult to erase. Psychiatrists and psychologists have found ways to help patients control their responses to fear, but the root fear memory appears to be immune to treatment, making relapses common. Recently, a new therapeutic possibility has emerged: neuroscientists discovered a drug (propranolol) that lessened indications of fear in rats on a long-term basis. This naturally led scientists to determine how propranolol will affect fear memory in humans.

University of Amsterdam scientists Merel Kindt, Marieke Soeter, and Bram Vervliet tested propranolol on volunteers in three phases. In the first phase, they conditioned volunteers to fear pictures of spiders by associating them with an uncomfortable electric shock to the wrist. In phase two, which took place 24 hours later, the researchers gave participants either propranolol or a placebo. They then reinforced what the participants had learned on the first day by showing the fear stimulus again.

After another 24 hours, they commenced the final phase of the experiment, which included what are called fear extinction and reinstatement. In fear extinction, the participants were shown the pictures of spiders without any shock 10 times in a row. Then, the scientists reinstated the fear by accompanying the pictures again with electric shock. Throughout this process, they measured the participants’ fear responses using electromyography of the right orbicularis oculi muscle, the muscle that closes the right eyelid.

Fear responses were dramatically different between the participants who took propranolol and those who took the placebo. Even before the fear extinction procedure, the propranolol group showed almost no observable responses to the spider pictures, while the placebo group continued to display elevated fear. The fear extinction procedure was also less effective on the placebo group, who still showed higher levels of fear responses than the propranolol group. In addition, the placebo group was significantly more susceptible to the fear reinstatement process, while the propranolol treated participants experienced almost no relapse in fear.

Propranolol seems to be effective both in lowering fear responses and preventing their reoccurrence. Since propranolol prevented the reinstatement of fear, the authors suggest that "the fear memory may either be erased or may be unavailable as a result of retrieval failure.” However, there is no way to tell which of these two types of amnesia is produced by propranolol with current neuroscience technology.

What they do know is that propranolol selectively targets receptors in the amygdala that are involved in emotional information processing. The authors hypothesize that propranolol may interfere with protein synthesis in neurons, which is important for memory consolidation. Further research is necessary to pin down propranolol's exact mechanism of action and to determine how permanent its effects are. Kindt, Soeter, and Verliet hope that their current and future studies will lead to better treatments for the “millions of people who suffer from emotional disorders and the relapse of fear, even after successful treatment.”

Nature Neuroscience, 2009. DOI: 10.1038/nn.2271

Listing image by Merel Kindt