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Vol. LXV, No. 12
June 7, 2013
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Digest

Scientists Discover Molecule That Triggers Sensation of Itch

NIH scientists have discovered in mouse studies that a small molecule released in the spinal cord triggers a process that is later experienced in the brain as the sensation of itch.
NIH scientists have discovered in mouse studies that a small molecule released in the spinal cord triggers a process that is later experienced in the brain as the sensation of itch.

NIH scientists discovered in mouse studies that a small molecule released in the spinal cord triggers a process that is later experienced in the brain as the sensation of itch.

The small molecule, called natriuretic polypeptide b (Nppb), streams ahead and selectively plugs into a specific nerve cell in the spinal cord, which sends the signal onward through the central nervous system. When Nppb or its nerve cell was removed, mice stopped scratching at a broad array of itch-inducing substances. The signal wasn’t going through.

Because the nervous systems of mice and humans are similar, the scientists say a comparable biocircuit for itch likely is present in people. If correct, this start switch would provide a natural place to look for unique molecules that can be targeted with drugs to turn off the sensation more efficiently in the millions of people with chronic itch conditions such as eczema and psoriasis.

The paper, published online in Science, also helps to solve a lingering scientific issue. “Our work shows that itch, once thought to be a low-level form of pain, is a distinct sensation that is uniquely hardwired into the nervous system with the biochemical equivalent of its own dedicated land line to the brain,” said senior author Dr. Mark Hoon of the National Institute of Dental and Craniofacial Research.

Molecular Explanation for Age-Related Fertility Decline in Women

Scientists supported by NIH have a new theory as to why a woman’s fertility declines after her mid-30s. They also suggest an approach that might help slow the process, enhancing and prolonging fertility.

They found that, as women age, their egg cells become riddled with DNA damage and die off because their DNA repair systems wear out. Defects in one of the DNA repair genes—BRCA1—have long been linked with breast cancer, and now also appear to cause early menopause.

“We all know that a woman’s fertility declines in her 40s. This study provides a molecular explanation for why that happens,” said Dr. Susan Taymans of the Fertility and Infertility Branch of the National Institute of Child Health and Human Development, which funded the study. “Eventually, such insights might help us find ways to improve and extend a woman’s reproductive life.”

The findings appeared in Science Translational Medicine.

Taming Suspect Gene Reverses Schizophrenia-Like Abnormalities in Mice

Scientists have reversed behavioral and brain abnormalities in adult mice that resemble some features of schizophrenia by restoring normal expression to a suspect gene that is over-expressed in humans with the illness. Targeting expression of the gene Neuregulin 1, which makes a protein important for brain development, may hold promise for treating at least some patients with the brain disorder, say researchers funded by the National Institute of Mental Health.

Like patients with schizophrenia, adult mice biogenetically engineered to have higher Neuregulin 1 levels showed reduced activity of the brain messenger chemicals glutamate and GABA. The mice also showed behaviors related to aspects of the human illness. For example, they interacted less with other animals and faltered on thinking tasks.

“The deficits reversed when we normalized Neuregulin 1 expression in animals that had been symptomatic, suggesting that damage which occurred during development is recoverable in adulthood,” explained NIMH grantee Dr. Lin Mei of the Medical College of Georgia at Georgia Regents University. Mei, Dr. Dong-Min Yin, Dr. Yong-Jun Chen and colleagues reported their findings May 22 in the journal Neuron.

“While mouse models can’t really do full justice to a complex brain disorder that impairs our most uniquely human characteristics, this study demonstrates the potential of dissecting the workings of intermediate components of disorders in animals to discover underlying mechanisms and new treatment targets,” said NIMH director Dr. Thomas Insel. “Hopeful news about how an illness process that originates early in development might be reversible in adulthood illustrates the promise of such translational research.”—compiled by Jeff Kopp


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