Fear is an instinctive reaction essential for survival, but it can also become a hindrance in daily life, particularly in cases of phobias, anxiety disorders, or post-traumatic stress.
Researchers from the Sainsbury Wellcome Centre (SWC) at University College London have recently identified the brain mechanisms that allow mammals to overcome their instinctive fear. Their work, published in the journal
Science, paves the way for new therapeutic strategies to treat these disorders.
An experiment based on animal models
To understand how the brain learns to inhibit fear responses, the researchers conducted an experiment on mice exposed to an overhead shadow, simulating a predator attack. Initially, the rodents instinctively fled to a shelter. However, after 30 to 50 exposures without negative consequences, they gradually learned to ignore the threat and continue their normal activities.
The researchers inserted silicon probes into the mice's brains to analyze neuronal activity during this learning process. They thus highlighted the predominant role of a brain region previously little explored in this context: the ventral lateral geniculate nucleus (vLGN), located near the thalamus.
Two key brain regions in fear suppression
The study revealed that learning to suppress fear relies on the interaction between two main brain regions:
- The visual cortex: This region, responsible for processing visual information, plays a fundamental role in learning to suppress fear. The researchers observed that when this area was deactivated, the mice could not unlearn their fear response.
- The ventral lateral geniculate nucleus (vLGN): Contrary to conventional wisdom that placed the visual cortex as the main memory center, the results show that it is actually this subcortical structure that stores the memory of fear suppression. It acts as a bridge between the neocortex and the brainstem, thus modulating instinctive reactions.
The researchers also identified an essential biochemical mechanism involved in this process. They discovered that molecules called
endocannabinoids are released in the vLGN during learning. These neurotransmitters act by increasing neuronal activity in this region, thereby promoting the suppression of fear responses.
Towards new therapeutic approaches
These findings could have significant implications for the treatment of anxiety disorders and phobias in humans. Since the neural circuits involved are similar between mice and humans, it is conceivable to develop treatments targeting the vLGN or the endocannabinoid system directly.
The researchers now plan to explore the clinical applications of these discoveries, particularly through deep brain stimulation, neurotransmitter modulation, or adapted behavioral therapies. These advances could thus improve the management of patients suffering from disorders related to excessive and maladaptive fear.
To go further: Why does the vLGN influence fear learning?
The ventral lateral geniculate nucleus (vLGN) modulates the transmission of visual information to the amygdala, a key region in the fear response. Its role is not limited to a simple sensory relay; it actively participates in regulating threatening signals.
Studies have revealed that deactivating the vLGN prevents the extinction of conditioned fear. This suggests that it adjusts the perception of frightening stimuli by gradually reducing their impact, thereby facilitating behavioral adaptation.
By modulating communication between the thalamus and the amygdala, the vLGN influences the distinction between real danger and perceived threat. This process is essential to avoid excessive fear responses and promote an appropriate reaction to past experiences.
Article author: Cédric DEPOND