In a nutshell: The identification of a new connection in the brain involved in reducing the fear response upends the current model of fear extinction.

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When we feel fear in response to a threat, networks of brain cells work together to evaluate the threat, helping us to learn from experience and to react appropriately to dangerous situations. Dysfunction of these circuits – which involve several different parts of the brain – can lead to anxiety-related disorders such as post-traumatic stress disorder.

In certain circumstances, the brain can be trained to reduce the fear response – a process known as fear extinction. Behavioural studies suggested that fear learning and extinction both begin in the amygdala but are then regulated by distinct parts of the medial prefrontal cortex: the prelimbic (PL) for learning and the infralimbic (IL) for extinction. However, anatomical and electrophysiological studies have shown that the PL and IL are significantly connected.

To see if the PL is involved in fear extinction as well as fear learning, Brain Function CoE postdoctoral research fellow Roger Marek, chief investigator Pankaj Sah and colleagues from the Queensland Brain Institute mapped these connections in rats. They found not only that brain cells in the PL can send signals to cells in the IL, but also that activating this connection enhances fear extinction.

This discovery redefines the role of the PL and means that the current brain circuitry model of fear learning and extinction needs to be revised. The finding will also help us to better understand the brain circuits involved in anxiety disorders.

Next steps:
The researchers are trying to identify the precise patterns of activity between brain cells that are involved in the opposing but related behaviours of fear learning and fear extinction.

Marek, R., Xu, L., Sullivan, R. K. P., & Sah, P. (2018). Excitatory connections between the prelimbic and infralimbic medial prefrontal cortex show a role for the prelimbic cortex in fear extinction. Nature Neuroscience, 21(5), 654-658. doi:10.1038/s41593-018-0137-x

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