Researchers Uncover Cellular Mechanisms for Attention in the Brain

The ability to pay attention to relevant information while ignoring distractions is a core brain function. Without the ability to focus and filter out “noise,” we could not effectively interact with our environment. Despite much study of attention in the brain, the cellular mechanisms responsible for the effects of attention have remained a mystery… until now.

In a study appearing in the journal Nature, researchers from Dartmouth’s Geisel School of Medicine and the University of California Davis studied communications between synaptically connected neurons under conditions where subjects shifted their attention toward or away from visual stimuli that activated the recorded neurons. Using this highly sensitive measure of attention’s influence on neuron-to-neuron communication, they were able to demonstrate that attention operates at the level of the synapse to improve sensitivity to incoming signals, sharpen the precision of these signals, and selectively boost the transmission of attention-grabbing information while reducing the level of noisy or attention-disrupting information.

The results point to a novel mechanism by which attention shapes perception by selectively altering presynaptic weights to highlight sensory features among all the noisy sensory input.

"While our findings are consistent with other reported changes in neuronal firing rates with attention, they go far beyond such descriptions, revealing never-before tested mechanisms at the synaptic level," said study co-author Farran Briggs, PhD, assistant professor of Physiology and Neurobiology at the Geisel School of Medicine.

In addition to expanding our understanding of brain, this study could help people with attention deficits resulting from brain injury or disease, possibly leading to improved screening and new treatments.

Molecule key to sustaining brain communication

Scientists have discovered the powerful role the molecule Myosin VI plays in communication between nerve cells in the brain.

Researchers at the University of Queensland’s (UQ) Queensland Brain Institute (QBI) have found that Myosin VI is integral to maintaining the neurotransmitter release that allows neurons to pass on information to other neurons.

The discovery made by Vanesa Tomatis, a PhD student in Associate Professor Frederic Meunier’s laboratory, demonstrates how Myosin VI has the impressive ability to anchor secretory vesicles that are at least 5,000 times greater in size, near their release site.

"By tethering and anchoring secretory granules, Myosin VI helps to maintain an active pool of vesicles near the plasma membrane, which is key to sustaining communication between neuronal cells," Associate Professor Meunier said.

Associate Professor Meunier and his team are now looking to better understand how the Myosin VI manages to grab and hold vesicles through the use of super resolution microscopy.

They hope the discovery will lead to new ways to reinstate or regulate neuronal communication in various brain disorders.

The paper was published in The Journal of Cell Biology on February 4 2013

(Image credit: Wikipedia)

Rapid fragmentation of neuronal networks at the onset of propofol-induced unconsciousness

General anesthesia involves rapidly inducing a reversible coma by administering a large dose of a fast-acting drug, such as propofol. Previous research has demonstrated that propofol enhances inhibitory input to neurons throughout the spinal cord, brainstem, thalamus, and cortex. However, how these effects in single cells translate to larger-scale neural circuits and cause unconsciousness is not well understood. We recorded spiking activity from ensembles of single neurons and intracranial electrical activity during the induction of propofol general anesthesia in human subjects undergoing surgery. We found that loss of consciousness (LOC) corresponds to the abrupt onset of a slow cortical oscillation that marks a fragmentation of neuronal networks. These results identify the slow oscillation as a dramatic neural correlate of LOC and demonstrate that slow oscillation marks the transition into a brain state in which local neuronal networks are isolated, impairing both temporal and spatial communication throughout the cortex.

Read more