martes, 16 de abril de 2013

Sensing Temperature - NIH Research Matters - National Institutes of Health (NIH)

Sensing Temperature - NIH Research Matters - National Institutes of Health (NIH)

April 15, 2013

Sensing Temperature

Researchers discovered that distinct sets of neurons respond to heat and cold. The findings provide an elegant explanation for how mammals sense temperature.
Photo of fire engulfing a stack of ice cubes.
Thermosensation—the ability to detect temperature—triggers our reflex to withdraw from painful heat or cold. But mammals are also able to detect more pleasant cool and warm temperatures. We sense temperature in our environment through specialized nerve cells that project into the outer layers of the skin.
Past research found that a type of ion channel called TRPV1 is activated by high temperature and capsaicin, the substance that makes chili peppers hot. Ion channels such as TRPV1 are essentially pores in the cell membrane that control the flow of electrically charged ions into and out of cells. This flow begins a signal that’s relayed to the brain. Another ion channel called TRPM8 was subsequently identified as a low-temperature sensor. Several other related TRP (transient receptor potential) channels were also found to be stimulated by heating or cooling. Figuring out how these channels work in concert over a wide range of temperatures, however, has been a difficult technical challenge.
A research team led by Dr. Mark A. Hoon of NIH’s National Institute of Dental and Craniofacial Research (NIDCR) devised a way to target different classes of neurons. Mice normally aren’t sensitive to diphtheria toxin. The scientists reasoned that if they put the human diphtheria toxin receptor under the control of genetic sequences that normally regulate different TRPs, they could selectively eliminate certain neurons with a simple toxin injection. Their study appeared on March 27, 2013, in the Journal of Neuroscience.
When the researchers put the human diphtheria toxin receptor under the control of TRPV1 regulatory sequences and injected diphtheria toxin into adult mice, TRPV1-expressing neurons were destroyed. Similarly, when the receptor was put under the control of the TRPM8 sequences, TRPM8 neurons were eliminated by a toxin injection.
The scientists found that mice without TRPV1 neurons didn’t avoid high temperatures but still avoided cold. These mice actually preferred higher temperatures than control mice. Mice without TRPM8 neurons, on the other hand, didn’t avoid cold temperatures but still avoided heat. These mice preferred lower temperatures than control mice. Mice without either TRPV1- or TRPM8-expressing cells were indifferent to temperatures between 0 and 50°C.
The scientists tested other suspected neurons and discovered that extreme heat and cold activate a separate class of neurons expressing a protein called Mrgprd. Mrgprd neurons were previously believed to be involved only in detecting painful mechanical stimuli.
Eliminating TRPV1 and TRPM8 neurons has a stronger effect than knocking out only these genes. This suggests that while these neurons may be responsible for detecting temperature, further study will be needed to identify all the receptors involved.
The sensation of moderate temperature, the researchers propose, depends on a balance of input from TRPV1 and TRPM8 neurons. “Even at temperatures that you would think that the ion channels are not doing anything, they’re actually sending out a small signal to the brain,” Hoon suggests. At hotter or colder temperatures, these neurons become more active. Extreme temperatures cause Mrgprd neurons to join in and signal an alarm.
—by Harrison Wein, Ph.D.

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Reference: J Neurosci. 2013 Mar 27;33(13):5533-41. doi: 10.1523/JNEUROSCI.5788-12.2013. PMID: 23536068.
Funding: NIH National Institute of Dental and Craniofacial Research (NIDCR).

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