Fruit flies’ eyes shrink a little to see

I spy, with my mechanical eye. It seems a simple mechanical change plays a role in sensory perception in fruit flies, and possibly in many other animals, including humans.

The eyes of the common fruit fly (Drosophila melanogaster) contain clusters of light-sensitive cells organised into rods. When light strikes one of these cells, it triggers a series of chemical reactions. These cause a protein called a transient receptor potential (TRP) ion channel to open. When it’s open, the TRP allows charged particles to flow into the cell, causing the cell to send a signal to the fly’s brain.

TRP channels play a part in sensory perception in many animals, from nematodes to humans. But nobody knew how the chemical signals make the TRP channel open.

Ray Kurzweil, the bold futurist and author of The New York Times bestseller "The Singularity Is Near", is arguably today’s most influential technological visionary. A pioneering inventor and theorist, he has explored for decades how artificial intelligence can enrich and expand human capabilities.

Now, in his much-anticipated How to Create a Mind, he takes this exploration to the next step:  reverse-engineering the brain to understand precisely how it works, then applying that knowledge to create vastly intelligent machines.

Drawing on the most recent neuroscience research, his own research and inventions in artificial intelligence, and compelling thought experiments, he describes his new theory of how the neocortex (the thinking part of the brain) works: as a self-organizing hierarchical system of pattern recognizers. Kurzweil shows how these insights will enable us to greatly extend the powers of our own mind and provides a roadmap for the creation of superintelligence—humankind’s most exciting next venture. We are now at the dawn of an era of radical possibilities in which merging with our technology will enable us to effectively address the world’s grand challenges.

How to Create a Mind is certain to be one of the most widely discussed and debated science books in many years—a touchstone for any consideration of the path of human progress.

Futurist Ray Kurzweil believes that the cloud will help expand the capacity of the human brain beyond its current limitations.

Futurist and author Ray Kurzweil predicts the cloud will eventually do more than store our emails or feed us streaming movies on demand: it’s going to help expand our brain capacity beyond its current limits.

In a question-and-answer session following a speech to the DEMO technology conference in Santa Clara, California last week, Kurzweil described the human brain as impressive but limited in its capacity to hold information. “By the time we’re even 20, we’ve filled it up,” he said, adding that the only way to add information after that point is to “repurpose our neocortex to learn something new.” (Computerworld has posted up the full video of the talk.)

The solution to overcoming the brain’s limitations, he added, involves “basically expanding our brains into the cloud.”

Kurzweil is one of the more prominent advocates of the technological Singularity, or the idea that computers will become super-intelligent and self-replicating, essentially reducing human progress to a sideshow. He is an optimist in this scenario, arguing in talks and books that the Singularity will effectively make humanity immortal by allowing us to transfer our consciousness into non-organic systems.

Mechanisms Underlying Childhood Neuromuscular Disease Found

A study by scientists from the Motor Neuron Center at Columbia University Medical Center (CUMC) suggests that spinal muscular atrophy (SMA), a genetic neuromuscular disease in infants and children, results primarily from motor circuit dysfunction, not motor neuron or muscle cell dysfunction, as is commonly thought. In a second study, the researchers identified the molecular pathway in SMA that leads to problems with motor function. Findings from the studies, conducted in fruit fly, zebrafish and mouse models of SMA, could lead to therapies for this debilitating and often fatal neuromuscular disease. Both studies were published today in the online edition of the journal Cell (1, 2).

“Scientists call SMA a motor neuron disease, and there is post-mortem evidence that it does cause motor neurons to die,” said Brian McCabe, PhD, assistant professor of pathology and cell biology and of neuroscience in the Motor Neuron Center, who led the first study. “However, it was not clear whether the death of motor neurons is a cause of the disease or an effect. Our findings in the fruit fly SMA model show that the disease originates in other motor circuit neurons, which then causes motor neurons to malfunction.”

In motor circuits, which coordinate muscle movement, specialized sensory neurons called proprioceptive neurons pick up and relay information to the spinal cord and brain about the body’s position in space. The central nervous system then processes and relays the signals, including via interneurons, to motor neurons, which in turn stimulate muscle movement.

“To our knowledge, this is the first clear demonstration in a model organism that defects in the function of a neuronal circuit are the cause of a neurological disease,” added Dr. McCabe.

The Marshmallow Study Revisited

For the past four decades, the “marshmallow test” has served as a classic experimental measure of children’s self-control: will a preschooler eat one of the fluffy white confections now or hold out for two later?

Now a new study demonstrates that being able to delay gratification is influenced as much by the environment as by innate ability. Children who experienced reliable interactions immediately before the marshmallow task waited on average four times longer—12 versus three minutes—than youngsters in similar but unreliable situations [Video]

"Our results definitely temper the popular perception that marshmallow-like tasks are very powerful diagnostics for self-control capacity," says Celeste Kidd, a doctoral candidate in brain and cognitive sciences at the University of Rochester and lead author on the study to be published online October 11 in the journal Cognition.

Target for obesity drugs comes into focus

Researchers at the University of Michigan have determined how the hormone leptin, an important regulator of metabolism and body weight, interacts with a key receptor in the brain.

Leptin is a hormone secreted by fat tissue that has been of interest for researchers in obesity and Type 2 diabetes since it was discovered in 1995. Like insulin, leptin is part of a regulatory network that controls intake and expenditure of energy in the body, and a lack of leptin or resistance to it has been linked to obesity in people.

Although there can be several complex reasons behind leptin resistance, in some cases the underlying cause is malfunction of the leptin receptor in the brain. An understanding of how leptin and its receptor interact could lead to new treatments for obesity and metabolic disorders, but the structure of this signaling complex has evaded researchers for years.

Georgios Skiniotis, a faculty member at the Life Sciences Institute and assistant professor in biological chemistry at the U-M Medical School, employed electron microscopy to obtain the first picture of the interaction between leptin and its receptor.

Skiniotis also traced similarities between the leptin receptor and other receptors of the same family, which may provide insight into new targets for treatment of other hormone-related diseases.