
Let me talk about loneliness from a neuroscientific point of view.
Imagine these three scenarios:
· A child who has just arrived at a new high school eats lunch in a box alone with the laughter of his classmates;
Divorced men sitting alone on the sofa, counting down the years;
· A disturbed prisoner locked in a single cell.
These different scenes in different places and times have one thing in common -- they all feel "lonely".
As social animals, humans have an innate desire to build and strengthen social networks. This intrinsically driven behavior is hardwired to make us feel more secure around tissue, which, in turn, takes less time and energy to find food, leads to healthier offspring and a better chance of survival. It is not difficult to understand that feelings of loneliness and rejection brought about by social isolation and rejection can trigger strong negative emotions and, in extreme cases, even lead to physical and mental illness.
In neuroscience, research over the years has shown how the neural circuits behind rewards, especially warm human interactions, motivate us. That "yuck, yuck" feeling you get when you're with your favorite person is triggered by dopaminergic neurons (nerve cells that release dopamine neurotransmitters). These cells cluster in the reward center of our brain, the ventral tegmental area (VTA).
But have you ever wondered what's going on inside our brains when we're isolated? Did the VTA fail? What neural mechanisms allow us to bounce back and feel attached again when we're feeling lonely and cold?
A 2016 study published in the journal Cell delved deeper into these questions with the help of another social animal that is equally dependent on its friends: rats.
To investigate the neural mechanisms behind loneliness, Matthews, Nieh and colleagues at THE Massachusetts Institute of Technology and Imperial College London tagged dopamergic neurons in some mice with green fluorescent protein. The treated mice were then divided into two groups, one that spent 24 hours alone and the other with other mice.
They recorded the activity of dopamine neurons labeled with green fluorescent protein in two brain regions using electrophysiological equipment:
1. One brain region is the PREVIOUSLY mentioned VTA, where most of the dopaminergic neurons gather to Party;
2. Another brain region is the dorsal raphe nucleus (DRN), which has only a small number of dopaminergic neurons.
Experimental findings:
1. In VTA, there were almost no physiological differences between the solitary and social groups.
2. However, dopamine cells in the DRN brain region showed a strong intergroup difference: compared with the social group, the solitary group showed a significant increase in synaptic strength in this region. In other words, the synapses of the mice grew stronger in the face of intense loneliness.
In other words, social isolation enhances the synapses of dopamine neurons in the DRN brain region, leading us to feel what we call "loneliness."
We fear prolonged loneliness and isolation. In both rodents and humans, brief periods of social isolation are followed immediately by a desire to rejoin the social circle. The name for this phenomenon is "social rebound".
With that in mind, the researchers conducted a follow-up experiment to explore the neurological underpinnings of social rebound. Neurons located in the DRN brain region are tagged with a calcium fluorescent indicator, and the more active the neuron, the brighter the indicator, making it easy to see directly.
The researchers put the mice that had been left alone back in an environment where they could hook up with other mice, mimicking a "social rebound". Social activity significantly increased the activity of dopaminergic neurons in the DRN brain in the alone group compared to the animals that were kept in a social environment.
The results suggest that neurons in the DRN brain region not only help us experience loneliness when we are socially isolated, but also help us experience positive emotions when we return to social situations.
So far, studies have shown that social states (isolation and social rebound) in mice modulate dopamine neuron activity in the DRN brain region. If these DRN neurons are the driving force behind loneliness and socializing, perhaps simply increasing their activity can make mice more socially engaged?
To test this hypothesis, the researchers used optogenetics to artificially tweak the DRN's dopaminergic neurons. They added a protein called light-sensitive channelins to the neurons in the DRN and lit them up with blue light.
When the DRN neurons were stimulated, the mice seemed more sociable. By contrast, if the DRN neurons were suppressed, the mice showed no social rebound even after experiencing periods of social isolation and loneliness. Instead of fitting in, they stay alone.
The researchers speculate that dopaminergic neurons in the DRN brain are one of the sources of our social motivation.
How, many must ask, can this research be applied to explain human behavior? We're obviously a lot more complicated than mice. Some define "socializing" as "making lots of friends," while others follow the principle of "making less, making more." In society, our perceived position in society (such as feeling superior or inferior) also affects sensitivity to social isolation.
So loneliness in humans is much more subjective and internal than the behavior of a lab rodent. But this study sheds new light on a fascinating and important partner, the DRN brain region, and the important role it plays in social behavior.




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