�Researchers at UT Southwestern Medical Center have discovered in mice that the brain must create new nerve cells for either exercise or antidepressants to reduce depression-like behavior.
In gain, the researchers found that antidepressants and exercise consumption the same biochemical footpath to exert their effects.
These results power help explain some unknown mechanisms of antidepressants and provide a new guidance for developing drugs to treat depression, said Dr. Luis Parada, chairman of developmental biology and aged author of a study in the Aug. 14 issue of the journal Neuron.
In animals, it was already known that long-term treatment with antidepressants causes new mettle cells to be generated in a part of the nous called the dentate gyrus. Exercise, which can likewise relieve the symptoms of depression, stimulates the generation of new nerve cells in the same area.
"We would never claim that what we study in mice directly relates to how antidepressants work in humans, but there are interesting features in parallel of latitude," Dr. Parada said. "The study unifies different observations that point to the brain's dentate gyrus region and to creation of nerve cells as existence important in depression."
Antidepressants dissemble very quickly to increase levels of natural compounds, called neurotransmitters, which face cells use to communicate. It takes several weeks to several months, still, for the patients wHO respond to such treatments to feel less down. Dr. Parada said this implies that some other long-term mechanism is likewise at work.
The current study was intentional to screen several phenomena that have long been observed in animal studies but have not been studied together to see if they are linked, Dr. Parada said.
The researchers focused on a speck called TrkB, or Track-B, which is found on the open of mettle cells and responds to several growth factors to cause new nerves to grow in the dentate gyrus.
They genetically engineered mice to deficiency TrkB specifically in the stem cells that give rise to new neurons, then gave them antidepressants for several weeks or allowed them to run on wheels. When the mice were tested for depressive demeanor, the tests revealed that neither the antidepressants nor the physical exertion had helped them, and the animals also had not full-grown new nerve cells in the dentate gyrus.
"At least in mice, this termination directly links antidepressants and voluntary employment with TrkB-mediated creation of nerve cells," Dr. Parada said.
The results also showed that antidepressants required TrkB to brace the ontogenesis of new nerve cells.
Matching the timeframe for medicated patients to feel less depressed, it takes several weeks for new mettle cells to grow, Dr. Parada aforementioned. This parallel of latitude effect, he said, may mean that antidepressants need to brace growth of new cells in the dentate convolution in order to reach their good effect.
"We can get biochemical, physiological, behavioural and anatomic results in animal models," Dr. Parada said. "These all resonate with the human condition, so possibly you have a physiologic relevancy.
"There could be a way to stimulate growth of nerve cells to fight depression, for example."
Other UT Southwestern researchers tortuous in the study were lead author Yun Li, graduate scholar in developmental biology; Bryan Luikart, old graduate pupil in developmental biology; Dr. Shari Birnbaum, assistant prof of psychiatry; Jian Chen, student research assistant in developmental biology; Dr. Chang-Hyuk Kwon, instructor of developmental biology; Dr. Steven Kernie, associate prof of pedology; and Dr. Rhonda Bassel-Duby, associate prof of molecular biology.
The work out was supported by the National Institute of Neurological Disorders and Stroke.
Visit hTTP://www.utsouthwestern.org/neurosciences to learn more about UT Southwestern's clinical services in neurosciences.
Dr. Luis Parada -- http://www.utsouthwestern.edu/findfac/professional/0,2356,15510,00.html
Source: Aline McKenzie
UT Southwestern Medical Center
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