Joseph LeDoux, in a new interview in Nautilus magazine, explains why it’s wrong to call the amygdala the brain’s fear circuit:
“The amygdala is a small region in the temporal lobe. We say “the amygdala,” but there are two amygdalas. Amygdalae. Traditionally it’s thought of as the fear center, an idea for which I’m partly responsible, maybe largely responsible, through my book The Emotional Brain. But I was a little sloppy with the language, even though back then I was saying the amygdala is an implicit fear circuit, and the explicit fear, the conscious fear, is a cortical process. Still, over time, the amygdala has been become a term for a fear center, not an implicit fear center, and that’s what I’ve been trying to correct.”
He prefers to use the term ‘survival circuit’. But does the amygdala produce fear emotions?
“The amygdala is not where you consciously experience fear. It’s just a way station in the flow of information from the sensory systems into the motor systems. You can have a person with amygdala damage who can still feel fear. Given that fact, the amygdala can’t be making fear. It’s making behavioral responses, but not the experience of fear. Let’s say there’s a snake at your feet. That’s probably enough to activate a fear schema in your circuits and begin to pattern-complete a concept of the situation you’re in. That concept is then the foundation of the conscious experience.”
LeDoux, whose book Anxiety I read last year, and who has a new book “The Deep History of Ourselves: The Four-Billion-Year Story of How We Got Our Conscious Brains”, believes that emotions (such as fear) are cognitive-assembled states exclusive to humans.
A new study of fear in mice published this week weighs in with some new evidence. Nadine Gogolla and her team at the Max Planck Institute of Neurobiology were able to show how the insular cortex of mice processes such strong “feelings” as fear or bodily discomfort, and how this affects their behavior.
“For example, if a mouse smells a fox, the feeling of fear causes it to hesitate from exploring its surroundings, and also stops it from eating,”
Gogolla says. In LeDoux’s view, that fear wouldn’t be an emotion, but rather a negative body state.
Negative bodily states such as nausea have a similar inhibitory influence. Gogolla and her team have now shown that these very different negative feelings and behavioral adjustments are linked via the posterior insular cortex.
First author Daniel Gehrlach and his colleagues in Gogolla’s group discovered that nerve cells of the posterior insular cortex respond to a large number of different sensory information, emotions and bodily states. All of the information that is processed here has a direct negative effect or acts as an aversive signal for the animal.
Interestingly, individual nerve cells can react to many different negative stimuli such as bitter taste, fear, pain, thirst, or bodily discomfort.
As soon as the cells detect these negative states, they forward the information to the amygdala or nucleus accumbens via two different pathways. These two brain regions are known to directly regulate an animal’s behavior.
“For the first time, we could now demonstrate the influence of the insular cortex on behavior via these two connections,”
Activation of the neuronal pathway from the insular cortex to the amygdala primarily causes behavioral adjustments to fear: The mouse reduces its food intake, social contacts and exploration of its surroundings.
When the researchers suppressed this pathway’s activity, the animals become less afraid (or at least behaved as if they were less afraid. We can’t know what, if anything they were feeling).
“It is possible that the insular cortex learns from previous experiences, so that the cells react stronger or faster to the next negative impression. Once we have learned to understand such relationships, we may be able to find a way to reverse or at least contain them,”
Gogolla says. I wonder what LeDoux would say about that.
Footnote: Daniel A. Gehrlach et al. Aversive state processing in the posterior insular cortex, Nature Neuroscience (2019). DOI: 10.1038/s41593-019-0469-1