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Category: genetics – Page 259

Neuroscientists removed fear from rats by inactivating amygdala — brain region mediating fear.

#Neuroscience #Brain #YuriNeuro #Neurobiology #Amygdala.

Timecodes:
0:00-Introduction.
0:17-Amygdala role in fear regulation.
0:45-Difficulties in exploring prey-predator interaction.
1:02-Lego robot to simulate a predator. Robogator (LEGO Mindstorms robot)
1:53-Fear response before the amygdala inactivation.
2:33-Fear response aftert the amygdala inactivation.
3:59-Amygdala is one of the key regions of the fear regulation.
4:50 — Human-based experiments on the electrical stimulation of amygdala.
6:01-Future prospects. Optogenetics.
6:34-Share your ideas and emotions in the comments.

In this video I review a scientific neuroscience publication :“Amygdala regulates risk of predation in rats foraging in a dynamic fear environment” from University of Washington and Korea University, Seoul. The scientific paper addresses the mechanism of fear regulation in rats. Neuroscientists inactivated neurons of the brain region regulating fear — amygdala. In order to inactivate amygdala neurons neurobiologists applied GABAA receptor agonist muscimol. In this way neuroscientists made the rat fearless. Neurobiologists simulated fear enviroment by using lego robot — Robogator (LEGO Mindstorms robot) programmed to surge toward the animal as it emerges from the nesting area in search of food.

Continue reading “Scientists made this rat fearless” | >

An aging/longevity/junk dna link.

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The human body is essentially made up of trillions of living cells. It ages as its cells age, which happens when those cells eventually stop replicating and dividing. Scientists have long known that genes influence how cells age and how long humans live, but how that works exactly remains unclear. Findings from a new study led by researchers at Washington State University have solved a small piece of that puzzle, bringing scientists one step closer to solving the mystery of aging.

A research team headed by Jiyue Zhu, a professor in the College of Pharmacy and Pharmaceutical Sciences, recently identified a DNA region known as VNTR2-1 that appears to drive the activity of the telomerase gene, which has been shown to prevent aging in certain types of . The study was published in the journal Proceedings of the National Academy of Sciences (PNAS).

Continue reading “The potential role of ‘junk DNA’ sequence in aging, cancer” | >

Scientists at Cambridge and Leeds have successfully reversed age-related memory loss in mice and say their discovery could lead to the development of treatments to prevent memory loss in people as they age.

In a study published today in Molecular Psychiatry, the team show that changes in the extracellular matrix of the brain — ‘scaffolding’ around nerve cells—lead to loss of with aging, but that it is possible to reverse these using genetic treatments.

Recent evidence has emerged of the role of perineuronal nets (PNNs) in neuroplasticity—the ability of the brain to learn and adapt—and to make memories. PNNs are cartilage-like structures that mostly surround inhibitory neurons in the brain. Their main function is to control the level of plasticity in the brain. They appear at around five years old in humans, and turn off the period of enhanced plasticity during which the connections in the brain are optimized. Then, plasticity is partially turned off, making the brain more efficient but less plastic.

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In March 2017, Read and his Penn State colleague David Kennedy published a paper in the Proceedings of the Royal Society B in which they outlined several strategies that vaccine developers could use to ensure that future vaccines don’t get punked by evolutionary forces. One overarching recommendation is that vaccines should induce immune responses against multiple targets. A number of successful, seemingly evolution-proof vaccines already work this way: After people get inoculated with a tetanus shot, for example, their blood contains 100 types of unique antibodies, all of which fight the bacteria in different ways. In such a situation, it becomes much harder for a pathogen to accumulate all the changes needed to survive. It also helps if vaccines target all the known subpopulations of a particular pathogen, not just the most common or dangerous ones. Richard Malley and other researchers at Boston Children’s Hospital are, for instance, trying to develop a universal pneumococcal vaccine that is not serotype-specific.

Vaccines should also bar pathogens from replicating and transmitting inside inoculated hosts. One of the reasons that vaccine resistance is less of a problem than antibiotic resistance, Read and Kennedy posit, is that antibiotics tend to be given after an infection has already taken hold — when the pathogen population inside the host is already large and genetically diverse and might include mutants that can resist the drug’s effects. Most vaccines, on the other hand, are administered before infection and limit replication, which minimizes evolutionary opportunities.

But the most crucial need right now is for vaccine scientists to recognize the relevance of evolutionary biology to their field. Last month, when more than 1000 vaccine scientists gathered in Washington, D.C., at the World Vaccine Congress, the issue of vaccine-induced evolution was not the focus of any scientific sessions. Part of the problem, Read says, is that researchers are afraid: They’re nervous to talk about and call attention to potential evolutionary effects because they fear that doing so might fuel more fear and distrust of vaccines by the public — even though the goal is, of course, to ensure long-term vaccine success. Still, he and Kennedy feel researchers are starting to recognize the need to include evolution in the conversation. “I think the scientific community is becoming increasingly aware that vaccine resistance is a real risk,” Kennedy said.

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Nature always finds a way…so they say! But it looks like it may actually be true in the case of our global plastic waste dilemma. Genetic mutations have been discovered in specific natural bacteria that enable them to break the polymer chains of certain plastics. Where have we found these bacteria? Well…in plastic recycling dumps of course. So, gloves and masks on everyone. We’re going in!

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Continue reading “Nature has learnt how to eat our plastic!” | >

To quickly express learning and memory genes, brain cells snap both strands of DNA in many more places and cell types than previously realized, a new study shows.

The urgency to remember a dangerous experience requires the brain to make a series of potentially dangerous moves: Neurons and other brain cells snap open their DNA in numerous locations — more than previously realized, according to a new study — to provide quick access to genetic instructions for the mechanisms of memory storage.

The extent of these DNA double-strand breaks (DSBs) in multiple key brain regions is surprising and concerning, says study senior author Li-Huei Tsai, Picower Professor of Neuroscience at MIT and director of The Picower Institute for Learning and Memory, because while the breaks are routinely repaired, that process may become more flawed and fragile with age. Tsai’s lab has shown that lingering DSBs are associated with neurodegeneration and cognitive decline and that repair mechanisms can falter.

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One of the scientists prodding and poking the Kelly brothers is Prof Christopher E Mason, the lead geneticist on the Twins Study. Mason’s lab at Cornell University is nothing if not ambitious. Its work centres on a “500-year plan for the survival of the human species on Earth, in space, and on other planets.”

As well as studying what happens to astronauts, it involves laying the genetic groundwork for humans to live among the stars. Mason envisions a future in which the human genome can be bioengineered to adapt to almost any environment, augmented with genes from other species that allow us to explore and settle the farthest corners of the Universe.

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We probably at this point should make all animals immortal: 3.

The advance promises to unlock new insights into human biology and disease, aiding in the study of everything from the developing immune system to tissue regeneration to skin cancer.

“Studying biodiversity is not just about exploring the biology of a bunch of interesting organisms, but ultimately for a better understanding of human biology,” developmental biologist and lead study author Hiroshi Kiyonari said via email.

Five years ago, his team began to systematically work out the problem that had so long plagued the opossum field. The first barrier was to collect zygotes (fertilized eggs) at the right time. Ideally, that would be before they began dividing, when they are still a single cell. If you inject CRISPR at this stage, you can be sure all the resulting animals’ cells will carry whatever DNA changes you make. Doing it later can mean some cells but not others will be edited — a less ideal outcome known as mosaicism. Another benefit of collecting fertilized eggs as early as possible is that the shell coat hasn’t had time to thicken.

Continue reading “Scientists produce first genetically engineered marsupials” | >

The findings, published in Nature Communications, could have important implications for human health: minis have been found at every type of synapse studied so far, and defects in miniature neurotransmission have been linked to range of neurodevelopmental disorders in children. Figuring out how a reduction in miniature neurotransmission changes the structure of synapses, and how that in turn affects behavior, could help to better understand neurodegenerative disorders and other brain conditions.

Summary: Study reveals how miniature release events help to keep neurons intact and preserve motor neuron function in aging insects.

Source: EPFL

Neurons communicate through rapid electrical signals that regulate the release of neurotransmitters, the brain’s chemical messengers. Once transmitted across a neuron, electrical signals cause the juncture with another neuron, known as a synapse, to release droplets filled with neurotransmitters that pass the information on to the next neuron. This type of neuron-to-neuron communication is known as evoked neurotransmission.

Continue reading “Brain ‘Noise’ Keeps Nerve Connections Young” | >