Researchers track neurons that make humans social

Representational image of neurons
File photo

A team of researchers from the University of Geneva studied the neurobiological mechanisms to find that the motivation to indulge in social interactions is the activation of dopaminergic neurons.

The study has been published in the ‘Nature Neuroscience Journal’.

These results will make it possible to study physiologically the possible dysfunctions of these neurons in diseases affecting social interactions, such as autism, schizophrenia or depression.

Social interaction is an integral part of our daily lives, although the intention to interact with others requires an effort to act. So why do we do it? What is the mechanism behind the motivation we feel to engage with others?

To identify which neurobiological circuit is the basis of social interaction, a team from the UNIGE and a member of the National Centre of Competence in Research (NCCR) Synapsy, observed what happened in the brains of mice seeking contact with their conspecific.

“In order to observe which neurons are activated during social interaction, we taught mice to perform a simple task that allows them to enter in contact with their fellow mouse,” explained Camilla Bellone, professor in the Department of Basic Neuroscience at the UNIGE Faculty of Medicine and director of the NCCR Synapsy.

Similarly, if the mouse presses the lever but the door does not open in the end, there is a sudden drop in the activity of the dopaminergic neurons, indicating great disappointment in the mouse
Camille Bellone

Two mice were placed in two different compartments and separated by a door. When the first mouse pressed a lever, the door opened temporarily, allowing social contact to be established with the second mouse through a grid.

“As the experiment progressed, the mouse understood that it had to press the lever to join its fellow mouse. With this task, we can measure the effort the mice are willing to put to engage in interaction with conspecifics,” continued Clement Solie, a researcher in Camilla Bellone’s team.

Using electrodes, the scientists measured the activation of neurons.

“We found that the interaction between two mice, similarly to other natural rewards, led to the activation of dopaminergic neurons, which are located within the reward system,” said Camille Bellone.

These neurons release dopamine -- the so-called pleasure molecule -- which is crucial for several motivated behaviours.

“What is even more interesting is that while during the first sessions, the dopaminergic neurons are activated when the mice interact with the conspecific, as soon as the mouse learn the association between the lever press and the interaction, the activity of dopaminergic neurons precedes the reward,” continued Benoit Girard, a researcher in the Department of Basic Neuroscience.

“Similarly, if the mouse presses the lever but the door does not open in the end, there is a sudden drop in the activity of the dopaminergic neurons, indicating great disappointment in the mouse,” explained Camilla Bellone.

“This predicting signal is the neural substrate for learning and is crucial for social motivation,” Bellone added.

Several psychiatric diseases such as autism, schizophrenia or depression are characterised by social dysfunctions and social motivation deficits are described in some of these patients. Thanks to this study, scientists now know that these difficulties may result from dysfunctions within the reward system and more precisely at the level of dopaminergic neurons.

“We will now be able to use these neurons as targets to find treatments for these diseases,” said Benoit Girard.

“Furthermore, the reward system is at the basis of the occurrence of addictive behaviours. Whether the excessive use of social media networks could hijack the dopaminergic system and be at the basis of maladaptive behaviours toward social media is an interesting hypothesis that can be now tested,” noted Camilla Bellone.

The Geneva team will now focus its research on the study of these psychological illnesses via the functioning of these neurobiological mechanisms.