March 31 (UPI) — Researchers at Stanford University report in a new study that they have uncovered the mechanism behind why taking deep, slow breaths can illicit a sense of calm in a person.
The team from Stanford University School of Medicine identified a small group of neurons that communicate in the brain’s respiratory control center with the structure responsible for the overall feeling of well being — essentially, connecting breathing to states of mind.
It has long been known that controlled breathing can induce a sense of calm in a person. Healthcare providers often prescribe breathing-control exercises for individuals with stress disorders, and the practice of controlling breathing in order to shift a person’s consciousness from a frantic state to a more meditative one, known as pranayama, is a core element in yoga and meditation.
In a mouse study in 1991, researchers discovered a tiny cluster of neurons linking respiration to relaxation, attention, excitement and anxiety located deep in the brainstem in an area called they refer to as the pacemaker for breathing. The same structure was later found in humans.
“The respiratory pacemaker has, in some respects, a tougher job than its counterpart in the heart,” Dr. Mark Krasnow, professor of biochemistry at Stanford, said in a news release.
“Unlike the heart’s one-dimensional, slow-to-fast continuum, there are many distinct types of breaths: regular, excited, sighing, yawning, gasping, sleeping, laughing, sobbing. We wondered if different subtypes of neurons within the respiratory control center might be in charge of generating these different types of breath.”
Krasnow and colleague Dr. Kevin Yackle, former graduate student at Stanford and faculty fellow at the University of California San Francisco, searched through public databases to create a list of genes that are preferentially activated in the part of the mouse brainstem where the breathing-control center is located, known as the pre-Botzinger complex or preBotC.
The team identified more than 60 separate neuronal subtypes that were physically differentiated from one another by their gene-activation signatures but comingling in the preBotC like well-stirred spaghetti strings.
They were able to use these genes and their protein products as markers to pinpoint the different neuronal subtypes and systematically assess the role of each neuronal subpopulation in lab mice.
Researchers could then selectively destroy any one of the neuronal subtypes and observe how the loss of a particular subtype affected the animal’s breathing.
They then studied the respiratory role of another subpopulation of 175 preBotC neurons distinguished by their shared expression of two genetic markers known as Cdh9 and Dbx1.
Their analysis of similar experiments suggested that the neurons did not regulate breathing, but rather spied on it and reported their findings to another structure in the brainstem known as the locus coeruleus, which sends projections to every part of the brain and drives arousal by waking from sleep, maintaining alertness and can trigger anxiety and distress.
“If something’s impairing or accelerating your breathing, you need to know right away,” Krasnow said. “These 175 neurons, which tell the rest of the brain what’s going on, are absolutely critical.”
