Science Writing, Jul 20 (EFE).- Memories are associated with positive or negative emotions and it depends on a molecule in the brain, which helps to carry out this distribution, according to a team of researchers from the Salk Institute (USA). ).
The discovery of the function of this neurotransmitter, published today by Nature, opens the way to a better understanding of why some people are more likely to retain negative emotions than positive, as can happen with anxiety, depression or post-traumatic stress disorder (PTSD).
Researcher Kay Tye, from the Salk Institute, pointed out that they’ve essentially succeeded in controlling the fundamental biological process of how you can remember if something is good or bad, which is “fundamental to our experience of life, and the notion that it can be reduced to a single molecule is incredibly exciting.”
For a human or animal to learn to avoid or seek out a certain experience in the future, their brain must associate a positive or negative feeling, or “valence,” with that stimulus. The brain’s ability to link these feelings to a memory is called valence assignment.
The team previously discovered in 2016 that a cluster of neurons in the basolateral amygdala (BLA) of the brain help assign valence when mice learn.
In an experiment on mice, the animals learned to associate a pitch with a sweet taste, which activated a pool of positive-valence BLA neurons.
Another set of neurons fired with negative valence as the animals learned to associate a different pitch with a bitter taste.
Tye explained that, like on the train, “these two lanes led to the positive and negative valence”, but they still did not know which signal acted “like the pointer operator to indicate which lane should be used at what time”. .
In the study published today, the team focused on the importance of neurotensin, a signaling molecule, for these BLA neurons.
They already knew that neurotensin is a neuropeptide produced by cells associated with valence processing, but so are other neurotransmitters.
The team used the CRISPR gene-editing technique to selectively knock out the neurotensin gene from the cells.
Without neurotensin signaling in the BLA, mice could no longer assign positive valence and did not learn to associate the first tone with a positive stimulus.
However, the absence of neurotensin did not block negative valence, but rather had a stronger association between the second tone and a negative stimulus.
The results suggest that the brain’s default state is to have a fear bias: neurons associated with the negative valence fire until neurotensin is released, which activates those associated with the positive valence.
From an evolutionary perspective, Tye said, it makes sense because it helps people avoid potentially dangerous situations.
In other experiments, researchers showed that high levels of neurotensin promoted reward learning and dampened negative valence, further supporting the idea that this neurotransmitter is responsible for positive valence.
Researchers have yet to investigate whether neurotensin levels can be modulated in people’s brains to treat anxiety or PTSD.
Additionally, they plan future studies to determine which other brain pathways and molecules are responsible for triggering neurotensin release. ECE
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