Syndicate content

Archive - Mar 8, 2010

Date

Two Dopamine Receptors Are Key to Ritalin Activity

Research reported by scientists from the University of California-San Francisco (UCSF) has shown that, in a rat model, Ritalin (methylphenidate) boosts both the ability to focus on tasks and the speed of learning by increasing the activity of the neurotransmitter dopamine through mechanisms involving two distinct dopamine receptors in the amygdala region of the brain. "We found that a dopamine receptor, known as the D2 receptor, controls the ability to stay focused on a task--the well-known benefit of Ritalin," said Dr. Patricia Janak, co-senior author of the paper. "But we also discovered that another dopamine receptor, D1, underlies learning efficiency." "Since we now know that Ritalin improves behavior through two specific types of neurotransmitter receptors, the finding could help in the development of better targeted drugs, with fewer side effects, to increase focus and learning," said Dr. Antonello Bonci, the other co-senior author of the article. The research assessed the ability of rats to learn that they could get a sugar water reward when they received a signal--a flash of light and a sound. The scientists compared the behavior of animals receiving Ritalin with those that did not receive it, and found those receiving Ritalin learned much better. However, they also found that if they blocked the dopamine D1 receptors with drugs, Ritalin was unable to enhance learning. And if they blocked D2 receptors, Ritalin failed to improve focus. The experiments established the distinct role of each of the dopamine receptors in enabling Ritalin to enhance cognitive performance.

Vaccine Protects Monkeys Against Chicamanguya Virus

Chicamanguya virus (CHIKV) is an insect-borne infectious agent that can cause severe disease in humans and against which there is presently no vaccine. This alphavirus has infected millions of people in Africa, Europe, and Asia since it reemerged in Kenya in 2004. The severity of the disease and the epidemic spread of the virus present a serious public health threat in the absence of vaccines or antiviral therapies. Although seldom fatal, infection with the virus causes highly painful arthritis-like symptoms that can linger for months or even years. CHIKV is capable of adapting to spread through a mosquito species common in much of North America. The virus has been the focus of intense scientific interest ever since a 2006 outbreak on the island of La Reunion in the Indian Ocean infected approximately 266,000 people, killing 260 of them. The name “chicamanguya” comes from an East African tribal word describing the contorted postures of the virus’s pain-wracked victims. Now, scientists at the National Institute of Allergy and Infectious Diseases (NIAID) and collaborators have reported development of a virus-like particle (VLP) vaccine that protects rhesus macaques against infection by CHIKV. "This vaccine did an excellent job of protecting the macaques from chikungunya," said Dr. Stephen Higgs, one of the paper's authors.

MicroRNA Binds Protein to Help Prevent Leukemia Progression

In an international study, researchers have discovered that loss of a particular microRNA (miR-328) appears to be a key factor in causing the progression of the more treatable chronic phase of chronic myelogenous leukemia (CML) to its life-threatening phase known as the “blast crisis” stage. The study indicates that CML progresses when immature white blood cells lose miR-328, trapping the cells in their rapidly growing, immature state. The cells soon fill the bone marrow and spill into the bloodstream, a tell-tale sign that the disease has advanced to the blast crisis stage. "These findings indicate that the loss of miR-328 is probably essential for progression from the chronic phase of the disease to the blast crisis stage," said principal investigator and senior author Dr. Danilo Perrotti of Ohio State University. "Our findings also suggest that maintaining the level of this microRNA might represent a new therapeutic strategy for CML blast crisis patients who do not benefit from targeted agents such as imatinib (Gleevec) and dasatinib (Sprycel)," Dr. Perrotti continued. The study also revealed a new function for microRNAs. Researchers have known for some time that microRNAs help regulate the kinds of proteins that cells produce by base-pairing with mRNA targets. But this study shows, reportedly for the first time, that microRNAs can also attach directly to proteins and alter their function. In this case, miR-328 binds to a protein (hnRNP E2) that normally prevents immature blood cells from maturing. "We believe that it [miR-328] normally acts as a decoy molecule, tying up the protein [hnRNP E2] and enabling the white blood cells to mature as they should," Dr. Perrotti said "These findings may help unravel novel pathways responsible for the initiation and progression of leukemia generally," Dr. Perrotti asserted.