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Theodore Berger and his team at the USC Viterbi School of Engineering's Department of Biomedical Engineering have developed a neural prosthesis for rats that is able to restore their ability to form long-term memories after they had been pharmacologically blocked. In a dramatic demonstration, Berger blocked the ability to rats to form long-term memories by using pharmacological agents to disrupt the neural circuitry that communicates between two subregions of the hippocampus, CA1 and CA3, which interact to create long-term memory, prior research has shown. The rats were unable to remember which lever to pull to gain a reward, or could only remember for 5-10 seconds, when previously they could remember for a long period of time. The researchers then developed an artificial hippocampal system that could duplicate the pattern of interaction between CA3-CA1 interactions. Long-term memory capability returned to the pharmacologically blocked rats when the team activated the electronic device programmed to duplicate the memory-encoding function. The researchers went on to show that if a prosthetic device and its associated electrodes were implanted in animals with a normal, functioning hippocampus, the device could actually strengthen the memory being generated internally in the brain and enhance the memory capability of normal rats. "These integrated experimental modeling studies show for the first time that with sufficient information about the neural coding of memories, a neural prosthesis capable of real-time identification and manipulation of the encoding process can restore and even enhance cognitive mnemonic processes," says the paper. Next steps, according to Berger and Deadwyler, will be attempts to duplicate the rat results in primates (monkeys), with the aim of eventually creating prostheses that might help human victims of Alzheimer's disease, stroke, or injury recover function. Ref.: "A Cortical Neural Prosthesis for Restoring and Enhancing

Creative Bioarray provides various human and animal cell lines that are invaluable for medical, scientific and pharmaceutical institutions. Creative Bioarray offers Rat Embryonic Stem Cells for your research.

A study by USC scientists of the brain connections in a small area of the rat brain showed them as patterns of circular loops, suggesting that at least in this part of the rat brain, the wiring diagram looks like a distributed network, rather than a hierarchy, the traditional view.

"We provide novel evidence for the effects of metabolic dysfunctions on brain function using the rat model of metabolic syndrome induced by high fructose intake. * We describe that the deleterious consequences of unhealthy dietary habits can be partially counteracted by dietary supplementation of n-3 fatty acid. * High sugar consumption impaired cognitive abilities and disrupted insulin signalling by engaging molecules associated with energy metabolism and synaptic plasticity; in turn, the presence of docosahexaenoic acid, an n-3 fatty acid, restored metabolic homeostasis. * These findings expand the concept of metabolic syndrome affecting the brain and provide the mechanistic evidence of how dietary habits can interact to regulate brain functions, which can further alter lifelong susceptibility to the metabolic disorders. "

"Mice have a jungle of bacteria, viruses and fungi in their stomachs-and so do we. These microorganisms help both mice and us break down dinner. As we are finding, these bugs also help to regulate the immune system. But we are just starting to learn how these tiny organisms influence us and how changing their composition changes us... Interestingly, though, the mice with these microbes did not: their immune systems remained underdeveloped. Even when researchers gave rat microbiota to mice, the mice's immune systems failed to mature"

Has a cheap and effective treatment for chronic pain been lying under clinicians' noses for decades? Researchers have found that a very high dose of an opiate drug that uses the same painkilling pathways as morphine can reset the nerve signals associated with continuous pain - at least in rats. If confirmed in humans, the procedure could reduce or eliminate the months or years that millions of patients spend on pain-managing prescription drugs. The results of the study are described today in Science1.

Harald Ott: Scientists at the Massachusetts General Hospital in Boston have created a bioengineered kidney that can be transplanted back into a rat, where it begins making urine"

Fats in foods like potato chips and french fries make them nearly irresistible because they trigger natural marijuana-like chemicals in the body called endocannabinoids, researchers at the University of California, Irvine, have found. The researchers discovered that when rats tasted something fatty, cells in their upper gut started producing endocannabinoids, while sugars and proteins did not have this effect. How fats create, like, a buzz It starts on the tongue, where fats in food generate a signal that travels first to your brain, and then through a nerve bundle called the vagus to your intestines. There, the signal stimulates the production of endocannabinoids, which initiates a surge in cell signaling that prompts you to totally pig out - probably by initiating the release of digestive chemicals linked to hunger and satiety that compel us to eat more. And that leads to obesity, diabetes and cancer, the researchers said. But they suggest it might be possible to curb this process by obstructing endocannabinoid activity: for example, by using drugs that "clog" cannabinoid receptors. The trick: bypassing the brain to avoid creating anxiety and depression (which happens when endocannabinoid signaling is blocked in the brain). I'm guessing McDonald's won't be adding that drug to their fries. Ref.: Daniele Piomelli, et al., An endocannabinoid signal in the gut controls dietary fat intake, PNAS, 2011; in press

"We have sensitive body parts wired to the same area of the brain as rodents' fine-tuned whiskers. In people, "stimulating the fingers, lips or face in general could all have a similar effect," says UCI doctoral student Melissa Davis, co-author of the study, which appears in the June issue of PLoS ONE. "It's gender-neutral," adds co-author Ron Frostig, professor of neurobiology & behavior. He cautions that the research, funded by the National Institutes of Health, is a first step, albeit an important one.... "with the potential for maybe doing things before a victim even reaches the emergency room.""