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New Research: Fearlessness can be learned

New Research: Fearlessness can be learned

#Research #Fearlessness #learned Welcome to Alaska Green Light Blog, here is the new story we have for you today:

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No sign of fear

Researchers looked at how the lack of a specific receptor affects the ability to unlearn fear.

The lack of a specific serotonin receptor has been linked to a reduction in previously acquired anxiety responses.

Serotonin, a neurotransmitter, plays a crucial role in both causing and eliminating anxiety and restlessness. A research team from the Chair of General Zoology and Neurobiology at the Ruhr University Bochum, led by Dr. Catherine Spoida and Dr. Sandra Süss has investigated the underlying mechanisms of this process.

In their experiments, the researchers found that mice lacking a specific serotonin receptor were able to unlearn fear faster than wild-type mice. These findings could help explain how drugs commonly used to treat post-traumatic stress disorder (PTSD) affect brain activity. PTSD sufferers often struggle with an inability to unlearn fear, which can prevent them from seeking therapies. The study was recently published in the journal Translational Psychiatry.

Everyday sensory stimuli can trigger fear reactions.

People who have been affected by a traumatic experience sometimes suffer from a long-lasting exaggerated fear response. In such cases, the fear response is triggered by certain sensations that occur in our everyday environment and can then become overwhelming. Experts refer to this condition as post-traumatic stress disorder (PTSD). With this disorder, it is difficult or impossible for those affected to unlearn the connection between a neutral environmental stimulus and the fear reaction they have learned, which impairs the success of the therapy.

Knowing that the neurotransmitter serotonin plays an important role in the development of fear, the research team investigated its role in extinction learning, i.e. unlearning fear, in more detail. To do this, they examined so-called knock-out mice, which lack a certain serotonin receptor – the 5-HT2C receptor – due to genetic changes. In one day, these mice learned to associate a specific sound with a mild but unpleasant electrical stimulus. “As a result of this learning process, the next day they showed an anxiety response characterized by a motionless pause as soon as the sound was played, which we refer to as ‘freezing’,” explains Katharina Spoida.

The absence of the receptor is an advantage

In the next step, the researchers played the sound repeatedly to the mice without applying the electrical stimulus. “Interestingly, we found that knock-out mice learned that the sound does not predict the fear stimulus much faster than mice that lacked this specific genetic change,” says Katharina Spoida. “Consequently, it appears that the absence of the serotonin receptor provides an advantage for extinction learning.”

The researchers examined this phenomenon in more detail and found that the knock-out mice showed changes in their neuronal activity in two different brain areas. One is a specific sub-region of the dorsal raphe nucleus (DRN), which is typically the main site of serotonin production in our brain. In addition, the researchers discovered aberrant neuronal activity in the so-called bed nucleus of the stria terminalis (BNST), which is part of the so-called extended amygdala. “In the knock-out mice, we first found increased basal activity in certain serotonin-producing cells of the dorsal raphe nucleus. In a further step, we showed that the absence of the receptor also changes neuronal activity in two subnuclei of the BNST, which ultimately supports extinction learning,” describes first author Sandra Suess. The research also suggests a connection between the two brain regions, leading the scientists to speculate that an interaction is important for enhanced extinction learning.

A possible effect of drugs revealed

The results of the study may show how medications typically used in the treatment of PTSD affect the brain regions analyzed in this study. “There are already drugs in clinical use that regulate the amount of available serotonin, so-called selective serotonin reuptake inhibitors, or SSRIs for short,” emphasizes Katharina Spoida.

“Taking these drugs over a longer period of time causes the corresponding receptor to become less responsive to serotonin, similar to what we did in our knock-out model. We therefore assume that the changes described could be essential for the positive effect of SSRIs,” adds Sandra Suess. The researchers hope their findings will help develop more targeted treatment strategies for PTSD patients in the future.

Reference: “Constitutive 5-HT2C receptor knockout facilitates anxiety quenching through altered activity of a dorsal raphe bed nucleus of the stria-terminalis pathway” by Sandra T. Suess, Linda M. Olbricht, Stefan Herlitze, and Katharina Spoida, November 19, 2022 , Translation Psychiatry.
DOI: 10.1038/s41398-022-02252-x

The study was funded by the German Research Foundation.

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