Neurons that serve as 'master controller' of habits identified

New York, Sep 7 : Researchers have identified a single type of neuron deep within the brain that serves as a "master controller" of habits.

The findings, published in the journal eLife, may point towards new treatment for addiction or compulsive behaviour in humans.

The research team found that habit formation boosts the activity of this influential cell, and that shutting it down with a drug is enough to break habits in sugar-seeking mice.

Though rare, this cell exerts its control through a web of connections to more populous cells that are known to drive habitual behaviour, according to a study published in the journal eLife.

"This cell is a relatively rare cell but one that is very heavily connected to the main neurons that relay the outgoing message for this brain region," said Nicole Calakos, Associate Professor at the Duke University Medical Center in North Carolina in the US.

"We find that this cell is a master controller of habitual behaviour, and it appears to do this by re-orchestrating the message sent by the outgoing neurons," Calakos said.

In experiments with mice, the researchers found that a single type of rare cell in the striatum called the fast-spiking interneuron (FSI) serves as the ky controller of habit.

The FSI belongs to a class neurons responsible for relaying messages locally between other types of neurons in a particular brain region.

Taking a closer look at the brain activity in mice, the researchers found that forming a habit appeared to make the FSIs more excitable.

When the mice were given a drug that decreases the firing of FSIs, their brains reverted to their "pre-habit" brain activity patterns, and the habit behaviour disappeared.

"Some harmful behaviours like compulsion and addiction in humans might involve corruption of the normally adaptive habit-learning mechanisms." Calakos said.

"Understanding the neurological mechanisms underlying our habits may inspire new ways to treat these conditions," Calakos added.