Our understanding of how the brain processes fear has taken a surprising turn. Scientists have long believed that fast-acting neurotransmitters, like glutamate, are responsible for relaying fear signals. But a new study published in the journal *Cell* challenges this notion.
Researchers at the Salk Institute, led by Sung Han, discovered that slower-acting molecules called neuropeptides play a primary role in the fear response circuit. Neuropeptides are released in larger packages than neurotransmitters, and they trigger a cascade of enzyme activity and gene expression rather than simply opening ion channels.
To investigate the role of neuropeptides in fear, Han and his team developed innovative tools to monitor and manipulate neuropeptide release in live mice. They found that inhibiting the release of specific neuropeptides, not glutamate, significantly reduced the mice’s fear response. This finding indicates that neuropeptides are the key players in conveying threat signals to the amygdala, the brain’s fear center.
The researchers also discovered that multiple neuropeptides can be packaged together within a single vesicle. Inhibiting the release of this entire group of neuropeptides led to a more substantial reduction in fear response compared to inhibiting a single neuropeptide.
This groundbreaking research opens new avenues for developing more effective treatments for anxiety, PTSD, and other fear-related disorders. Current therapies often target single neurotransmitters, but the study suggests that targeting multiple neuropeptides simultaneously could be a more effective approach.
Han believes that this research could lead to the development of novel drugs that target neuropeptide receptors, potentially providing a new wave of treatments for debilitating fear-related disorders. This discovery is a significant step forward in understanding the complexities of the brain’s fear circuitry and its implications for mental health.
