Smelling a Skunk After a Cold: Brain Changes After a Stuffed Nose Protect the Sense of Smell

ScienceDaily (Aug. 12, 2012) — Has a summer cold or mold allergy stuffed up your nose and dampened your sense of smell? We take it for granted that once our nostrils clear, our sniffers will dependably rebound and alert us to a lurking neighborhood skunk or a caramel corn shop ahead.

(Credit: http://www.sheridanent.com/)


 

That dependability is no accident. It turns out the brain is working overtime behind the scenes to make sure the sense of smell is just as sharp after the nose recovers.

A new Northwestern Medicine study shows that after the human nose is experimentally blocked for one week, brain activity rapidly changes in olfactory brain regions. This change suggests the brain is compensating for the interruption of this vital sense. The brain activity returns to a normal pattern shortly after free breathing has been restored.

Previous research in animals has suggested that the olfactory system is resistant to perceptual changes following odor deprivation. This new paper focuses on humans to show how that’s possible. The study is published in the journal Nature Neuroscience.

“You need ongoing sensory input in order for your brain to update smell information,” said Keng Nei Wu, the lead author of the paper and a graduate student in neuroscience at Northwestern University Feinberg School of Medicine. “When your nostrils are blocked up, your brain tries to adjust to the lack of information so the system doesn’t break down. The brain compensates for the lack of information so when you get your sense of smell back, it will be in good working order.”

For the study, Wu completely blocked the nostrils of 14 participants for a week while they lived in a special low-odor hospital room. At night, participants were allowed to breathe normally while they slept in the room.

After the smell deprivation, researchers found an increase in activity in the orbital frontal cortex and a decrease of activity in the piriform cortex, two regions related to the sense of smell.

“These changes in the brain are instrumental in maintaining the way we smell things even after seven days of no smell,” Wu said.

When unrestricted breathing was restored, people were immediately able to perceive odors. A week after the deprivation experience, the brain’s response to odors had returned to pre-experimental levels, indicating that deprivation-caused changes are rapidly reversed.

Such a rapid reversal is quite different from other sensory systems, such as sight, which typically have longer-lasting effects due to deprivation. The olfactory system is more agile, Wu suggested, because smell deprivation due to viral infection or allergies is common.

This study also has clinical significance relating to upper respiratory infection and sinusitis, especially when such problems become chronic, at which point ongoing deprivation could cause more profound and lasting changes, Wu noted.

“It also implies that deprivation has a significant impact on the brain, rather than on the nose itself,” Wu said. “More knowledge about how the system reacts to short-term deprivation may provide new insights into how to deal with this problem in a chronic context.”

Other Northwestern authors include Bruce K. Tan, James D. Howard, David B. Conley and Jay A. Gottfried, the senior author.

 

Story Source:

The above story is reprinted from materials provided byNorthwestern University, via EurekAlert!, a service of AAAS.


Journal Reference:

  1. Keng Nei Wu, Bruce K Tan, James D Howard, David B Conley, Jay A Gottfried. Olfactory input is critical for sustaining odor quality codes in human orbitofrontal cortexNature Neuroscience, 2012; DOI: 10.1038/nn.3186
Citation:

Northwestern University (2012, August 12). Smelling a skunk after a cold: Brain changes after a stuffed nose protect the sense of smell.ScienceDaily. Retrieved August 14, 2012, from http://www.sciencedaily.com/releases/2012/08/120812151714.htm

How Stress and Depression Can Shrink the Brain

ScienceDaily (Aug. 12, 2012) — Major depression or chronic stress can cause the loss of brain volume, a condition that contributes to both emotional and cognitive impairment. Now a team of researchers led by Yale scientists has discovered one reason why this occurs — a single genetic switch that triggers loss of brain connections in humans and depression in animal models.

Expression of a single gene dramatically decreases synaptic connections between brain cells. Yale scientists believe this may explain why people suffering from chronic stress and depression suffer loss of brain volume (Credit: Courtesy Yale University)

 

The findings, reported in the Aug. 12 issue of the journal Nature Medicine, show that the genetic switch known as a transcription factor represses the expression of several genes that are necessary for the formation of synaptic connections between brain cells, which in turn could contribute to loss of brain mass in the prefrontal cortex.

“We wanted to test the idea that stress causes a loss of brain synapses in humans,” said senior author Ronald Duman, the Elizabeth Mears and House Jameson Professor of Psychiatry and professor of neurobiology and of pharmacology. “We show that circuits normally involved in emotion, as well as cognition, are disrupted when this single transcription factor is activated.”

The research team analyzed tissue of depressed and non-depressed patients donated from a brain bank and looked for different patterns of gene activation. The brains of patients who had been depressed exhibited lower levels of expression in genes that are required for the function and structure of brain synapses. Lead author and postdoctoral researcher H.J. Kang discovered that at least five of these genes could be regulated by a single transcription factor called GATA1. When the transcription factor was activated, rodents exhibited depressive-like symptoms, suggesting GATA1 plays a role not only in the loss of connections between neurons but also in symptoms of depression.

Duman theorizes that genetic variations in GATA1 may one day help identify people at high risk for major depression or sensitivity to stress.

“We hope that by enhancing synaptic connections, either with novel medications or behavioral therapy, we can develop more effective antidepressant therapies,” Duman said.

The study was funded by the National Institutes of Health and the Connecticut Department of Mental Health and Addiction Services.

Other Yale authors of the paper are Bhavya Voleti, Pawel Licznerski, Ashley Lepack, and Mounira Banasr.

 


Story Source:

The above story is reprinted from materials provided byYale University.


Journal Reference:

  1. Hyo Jung Kang, Bhavya Voleti, Tibor Hajszan, Grazyna Rajkowska, Craig A Stockmeier, Pawel Licznerski, Ashley Lepack, Mahesh S Majik, Lak Shin Jeong, Mounira Banasr, Hyeon Son, Ronald S Duman. Decreased expression of synapse-related genes and loss of synapses in major depressive disorderNature Medicine, 2012; DOI:10.1038/nm.2886

 

Citation:

Yale University (2012, August 12). How stress and depression can shrink the brain.ScienceDaily. Retrieved August 14, 2012, from http://www.sciencedaily.com/releases/2012/08/120812151659.htm