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Signal coupling between neuron-glia super-network may lead to improved memory formation -- ScienceDaily
"Glial cells appear to have the capacity of coding information," says professor Ko Matsui of the Super-network Brain Physiology lab at Tohoku University, who led the research. "However, the role of the added layer of signals encoded in the glial circuit has always been an enigma."
Using patch clamp electrophysiology techniques in acute brain slices from mice, Dr. Kaoru Beppu, Matsui, and their team show that glial cells in the cerebellum react to excitatory transmitter glutamate released from synapses of neurons. The glial cells then release additional glutamate in return. Therefore, these glial cells effectively function as excitatory signal amplifiers.
Flickering light mobilizes brain chemistry that may fight Alzheimer's -- ScienceDaily
n 2016, researchers discovered that light flickering at 40 Hz mobilized microglia in mice afflicted with Alzheimer's to clean up that junk. The new study looked for brain chemistry that connects the flicker with microglial and other immune activation in mice and exposed a surge of 20 cytokines -- small proteins secreted externally by cells and which signal to other cells. Accompanying the cytokine release, internal cell chemistry -- the activation of proteins by phosphate groups -- left behind a strong calling card.
"The phosphoproteins showed up first. It looked as though they were leading, and our hypothesis is that they triggered the release of the cytokines," said Singer, who co-led the new study and is an assistant professor in the Wallace H. Coulter Department of Biomedical Engineering at Georgia Tech and Emory.
Immune cells destroy healthy brain connections, diminish cognitive function in obese mice: Obesity may drive microglia into a synapse-eating frenzy that leads to cognitive impairment -- ScienceDaily
Nearly two billion adults worldwide are overweight, more than 600 million of whom are obese. In addition to increasing risk of conditions such as diabetes and heart disease, obesity is also a known risk factor for cognitive disorders including Alzheimer's disease. The cellular mechanisms that contribute to cognitive decline in obesity, however, are not well understood.
Elise Cope and colleagues replicated previous research by demonstrating diet-induced obesity in mice impairs performance on cognitive tasks dependent on the hippocampus and results in loss of dendritic spines -- the neuronal protrusions that receive signals from other cells -- and activates microglia. Using genetic and pharmacological approaches to block microglial activity, the researchers established microglia are causally linked to obesity-induced dendritic spine loss and cognitive decline. The results suggest obesity may drive microglia into a synapse-eating frenzy that contributes to the cognitive deficits observed in this condition.
Often overlooked glial cell is key to learning and memory: Biomedical scientists offer simple advice: Keep the brain active -- ScienceDaily
In the lab, the researchers artificially increased levels of ephrin-B1 in mice and then tested them for memory retention. They found that the mice could not remember a behavior they had just learned. In cell culture studies, they added neurons to astrocytes that overexpressed ephrin-B1 and were able to see synapse removal, with the astrocytes "eating up" the synapses.
"Excessive loss of synapses is a problem," Ethell said. "The hippocampus, the region of the brain associated primarily with memory, is plastic. Here, new neuronal connections are formed when we learn something new. But the hippocampus has a limited capacity; some connections need to go to 'make space' for new connections -- new memories. To learn, we must first forget."
In contrast to an ephrin-B1 increase, when this protein decreases (or is down-regulated) it results in more synapses -- and better learning. The astrocytes, in this case, are not able to attach to the synapses.
"But you don't want to remember everything," said Amanda Q Nguyen, a Neuroscience Graduate Program student working in Ethell's lab, and a co-first author of the research paper. "It's all about maintaining a balance: being able to learn but also to forget."
Advice the researchers have for the public is simple: keep the brain -- that is, the neurons -- active.
"Reading and solving puzzles is a good start," Ethell said.
Early source of irritable bowel syndrome discovered -- ScienceDaily
"The gut has its own brain and that has more neurons in the intestines than in the spinal cord. Within your intestines lies a 'second brain' called the enteric nervous system," said Brian Gulbransen, MSU neuroscientist and the study's senior author. "The enteric nervous system is an exceedingly complex network of neural circuits that programs a diverse array of gut patterns and is responsible for controlling most gastrointestinal functions."
Accompanying the neurons in this second brain are enteric glia, which are responsible for regulating inflammation. The disruption of neural circuits in the gut by inflammation is considered an important factor in the development of irritable bowel syndrome and inflammatory bowel disease.
