By mopping up excess neurotrophic factor from neuronal synapses, astrocytes may finely tune synaptic transmission to affect processes such as learning and memory, say Bergami et al.

The major cellular events of learning and memory are long-term potentiation (LTP) and long-term depression (LTD), both of which affect neurons' ability to communicate with one another. Neurons that have undergone LTP display a stronger electrical response to the same level of a stimulus, whereas neurons that have gone through LTD display a weaker response. These changes are thought to result from modifications of the neuronal synapses, such as alterations in the density of postsynaptic receptors, or downstream signaling events.

Secretion of the neurotrophic factor BDNF (brain-derived neurotrophic factor) has been implicated in long-term synaptic modification, and the function of BDNF on synaptic strength depends on its particular form: in its pro-BDNF form it is believed to promote LTD, and in its mature form it prompts LTP.

Researchers at Georgetown University Medical Center have discovered a new way to limit inflammation caused by the activation of microglia - key immune cells in the brain. Although the role of such cells is to "clean up damage" after injury, they often worsen the damage by releasing toxic inflammatory factors.

In the October issue of the journal Glia, now published online, the scientists say that the type of chemical they used to deactivate these cells could possibly be developed as a drug to treat a variety of acute and chronic disorders marked by brain cell damage - including stroke, head and spinal cord injury, and possibly Alzheimer's disease and Parkinson's disease.

"Inflammation associated with the activation of microglial cells is an important factor that appears to contribute to tissue damage and disability in many of the important neurodegenerative disorders. By decreasing this inflammatory response, tissue loss after injury can be reduced. Thus, what we found in this study has important potential therapeutic implications for the treatment of a number of important neurological disorders," says the study's senior investigator, Alan I. Faden, M.D., a professor of neuroscience and director of the Laboratory for the Study of Central Nervous System Injury.

Again and again, experiments confirmed it. Without glia, neurons die. So scientists who wanted to study in living animals what glia - the most abundant brain cells - do for neurons besides keep them alive were out of luck. But now, a breakthrough.

A system unveiled and described by Rockefeller University scientists shows that in the Caenorhabditis elegans worm, neurons live on despite the absence of glia, a landmark discovery that paves the way for scientists to explore the dialogue between these team players in their natural environment.

"As far as we know, this is the first system where removing glia does not affect neuronal survival," says Shai Shaham, head of the Laboratory of Developmental Genetics, who made the discovery along with graduate student Satoshi Yoshimura. "So now we can study glia and the contributions they make in the developing brain in this in vivo context."

To allow nerve cells to transmit information efficiently over long distances, advanced life forms have developed a mechanism known as saltatory conduction. This is made possible by an insulating sheath of myelin that forms at certain intervals around the axonal extensions of nerve cells that specialise in the transmission of stimuli. In disorders such as multiple sclerosis or leukodystrophy, the formation or function of the myelin is disturbed.

Previously, the molecular mechanisms of myelin formation were not well understood. Two projects undertaken by the Department of Molecular Cell Biology of the Faculty of Biology at the Johannes Gutenberg University in Mainz have now made a significant contribution towards understanding these complex cellular processes.

In simple terms, signals transmitted during saltatory conduction jump from one non-myelinated area (the nodes of Ranvier) to another, which enormously increases the speed of transmission. Myelin is formed in the central nervous system when oligodendrocytes - a specific type of brain cell - wrap their cellular extensions around the axons of the nerve cells several times, thus forming a compact stack of cellular membranes.

The team of scientists under Professor Jacqueline Trotter from the Mainz Department of Molecular Cell Biology have now been able to show which mechanisms contribute towards the formation of an intact myelin sheath and how the nerve cells control the place and time of myelin production.

Brain cells known as neurons process information by joining into complex networks, transmitting signals to each other across junctions called synapses. But "neurons don't just connect to other neurons," emphasizes Z. Josh Huang, Ph.D., "in a lot of cases, they connect to very specific partners, at particular spots." Dr. Huang, a professor at Cold Spring Harbor Laboratory (CSHL), leads a team that has identified molecules guiding this highly specific neuronal targeting in the developing brains of mice.

The researchers report in PLoS Biology that in some cases, these molecular guides -- non-signaling brain cells known as glia -- form a kind of scaffold. This scaffold, in turn, directs the growth of nerve fibers and their connections between specific types of neurons.

As they learn through research like this how the brain develops its complex wiring, the scientists hope they can clarify what goes wrong in disorders like autism.

Although scientists have long regarded the brain's white matter as passive infrastructure, new work shows that it actively affects learning and mental illness

Imagine if we could peek through the skull to see what makes one brain smarter than another. Or to discover whether hidden traits might be driving a person's schizophrenia or dyslexia. A new kind of imaging technique is helping scientists observe such evidence, and it is revealing a surprise: intelligence, and a variety of mental syndromes, may be influenced by tracts within the brain made exclusively of white matter.

Gray matter, the stuff between your ears your teachers chided you about, is where mental computation takes place and memories are stored. This cortex is the "topsoil" of the brain; it is composed of densely packed neuronal cell bodies - the decision-making parts of nerve cells, or neurons.

Underneath it, however, is a bedrock of "white matter" that fills nearly half of the human brain - a far larger percentage than found in the brains of other animals.

Since our ancestors first harnessed fire, we've used heat to cook burgers, forge steel and power rockets. Now, Rockefeller University researchers are using heat for another purpose: turning genes on and off at will.

By exploiting the heat shock response, an ancient mechanism that protects cells from dangerously high temperatures, researchers have developed a new method to introduce foreign genes, called transgenes, into an organism and control when and where these transgenes are expressed. Unlike other techniques, which are labor intensive and inefficient, this new method makes controlling transgene expression as easy as turning the dial on an oven.

During heat shock, a protein called heat shock factor-1 travels from a cell's cytoplasm to the nucleus, where it binds to a specific sequence of DNA. This interaction initiates the transcription of heat shock protein, a shield that deflects excess heat from cells and protects them from damage. Since these two proteins are expressed at a specific time - when organisms experience heat shock at a specific temperature - scientists had long designed transgenes to be expressed the moment heat shock factor-1 binds to this sequence of DNA.

However, while scientists could know when this transgene was expressed, they couldn't limit its expression in specific cell types and study a particular protein's effect on them. To do so, they would have to target a single cell with a laser beam until the heat shock response kicked in for the transgene to be expressed. In Caenorhabditis elegans, that's 34 degrees Celsius.

Glial cells of the nervous system, once thought to function strictly as support cells for neurons, are now thought to actively modulate them. Providing further evidence in support of this theory, researchers at the Department of Neuroscience and the Center for Neuroscience Research (CNR) at Tufts University School of Medicine (TUSM) recently identified a specific population of glial cells that is required for the control of circadian behavior in Drosophila (the fruit fly). Their findings, which confirm and extend their earlier work, are published in the August 2, 2007, issue of Neuron.

"Our results suggest that an autonomous glial mechanism may drive circadian rhythms in the activity of a Drosophila protein known as Ebony," says F. Rob Jackson, PhD, director of the CNR and professor of neuroscience at TUSM. "Ebony activity and the glia containing that activity" explains Jackson, "function independently of, or in concert with, other brain cells (neurons) to control circadian behavior."

"Most organisms," says Jackson, "from Drosophila to humans, have the ability to adapt the timing of behavior or other processes to environmental cycles using an intrinsic time-keeping device called a circadian clock."

The insulating myelin sheath enwrapping the cable-like axons of nerve cells is the major target of attack of the immune system in multiple sclerosis. Such attack causes neural short-circuits that give rise to the muscle weakness, loss of coordination, and speech and visual loss in the disease.

Now, Douglas Fields of the National Institute of Child Health and Human Development and his colleagues have reported in Neuron that supporting cells called astrocytes in the central nervous system (CNS) promote myelination by releasing an immune system molecule that triggers myelin-forming cells to action. The finding, they say, "may offer new approaches to treating demyelinating diseases."

Astrocytes, so named because of their star-like shape, are the most prominent supporting cells in the nervous system. They provide critical regulatory molecules that enable nerve cells to develop and connect properly.

The key to understanding our brains may lie within a one-millimeter long worm, new research from Rockefeller University indicates. Reporting in the June issue of Developmental Cell, Shai Shaham, Ph.D., and graduate student Elliot Perens use the roundworm, C. elegans, to investigate the mysterious glial cell, which makes up 90 percent of the human brain and, when it malfunctions, can contribute to diseases like Parkinson's disease and schizophrenia.

Studying glial cells is technically difficult as they are essential for neuronal cell survival: disturbing them in any way puts the organism's life in jeopardy. Shaham and Perens show that worms are the perfect model system to study the function of these cells in the nervous system, because the glial cells can be manipulated and the neurons still form and function, though not entirely as normal.

"Glial cells have been traditionally hard to study in vertebrates because it is difficult to ask how they influence neurons beyond how they affect a neuron's survival," says Shaham, head of the Strang Laboratory of Developmental Genetics. "This is the first paper to take a serious crack at glial cells in C. elegans. It shows that the worm really is a great system in which to study glial cells, because we are able to get the kind of answers that could help us understand how they are functioning in the human brain."