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Neuroscientists at the University of Bristol have discovered fear mechanisms rooted in the cerebellum that could lead to new anti-anxiety medications and treatments for post-traumatic stress disorder a.k.a PTSD (Paci et al., 2022 )
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"These findings show that the cerebellum is a part of the brain's survival network which regulates fear-memory processes. [This study] raises the possibility that disruption of the cerebellum might underlie anxiety and other fear-related disorders, thereby providing a new target for future therapies."
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In animal experiments using fear-conditioned rats, Paci et al. (2022) found that the cerebellum modulates how another brain area called the periaqueductal gray (PAG) triggers automatic defensive behaviors such as freezing in place during times of perceived danger.
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This research increases our understanding of how survival networks rooted in subcortical brain areas cause the body to automatically freeze in response to fear. When the cerebellum is functioning well, a momentary freeze response promotes survival. However, Paci et al. (2022) found that when cerebellar functions were disrupted , the animals used in this study were paralyzed by fear.
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The cerebellum coordinates fluid motor movements in sports and daily life. It also coordinates our thoughts, as well as coordinating our movements. As part of a survival network, it facilitates gracefully taking flight, fighting it out with well-coordinated muscle movements, or freezing in place for just long enough to plot your next move.
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For their recent study, Paci et al. (2022) encoded a fear memory by pairing a mild electric foot shock with an audible tone. Once their lab rats were conditioned to fear the auditory tone by itself, they implanted electrodes to monitor neuronal activity within the PAG. When the rats heard the fear-conditioned tone, it triggered a momentary freeze response, and specific neurons in the PAG simultaneously "lit up."
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Notably, when a rat's cerebellum was functioning properly, the freeze response was brief and didn't stop an animal in its tracks for too long.
However, Paci et al. (2022) found that when the cerebellum's ability to communicate with the PAG was blocked, freeze responses went into overdrive and became exaggerated. Instead of freezing momentarily, hearing the fear-conditioned tone immobilized the animals for an extended period of time.
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The findings suggest that the cerebellum plays a crucial role in coordinating perfectly-timed behavioral responses to threatening stimuli. But cerebellar dysfunctions can cause havoc with perfectly-timed freeze responses. Without a well-functioning cerebellum, the freeze response lasts too long.
Paci et al. (2022)'s research sheds light on why crippling anxiety is so immobilizing and may provide a new target for anxiolytic medications.
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"Until now, little was understood about how the cerebellum modulates neuronal activity in other brain regions, especially those related to fear and anxiety"
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"Importantly, our results show that the cerebellum is part of the brain's survival network that regulates fear memory processes at multiple timescales and in multiple ways; raising the possibility that dysfunctional interactions in the brain's cerebellar-survival network may underlie fear-related disorders and comorbidities"
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New research on fear-induced "freeze" responses
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