Maslow

Newly discovered windows of brain plasticity may help with treatment of stress-related disorders

Chronic stress can lead to changes in neural circuitry that leave the brain trapped in states of anxiety and depression. But even under repeated stress, brief opportunities for recovery can open up, according to new research at The Rockefeller University.

(Image caption: Routine versus disruptive: A familiar stressor (left) did not increase NMDA receptors (dark spots), a booster of potentially harmful glutamate signaling, in the brains of mice. However, when subjected to an unfamiliar stress (right), mice expressed more NMDA receptors)

“Even after a long period of chronic stress, the brain retains the ability to change and adapt. In experiments with mice, we discovered the mechanism that alters expression of key glutamate-controlling genes to make windows of stress-related neuroplasticity—and potential recovery—possible,” says senior author Bruce McEwen, Alfred E. Mirsky Professor, and head of the Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology. Glutamate is a chemical signal implicated in stress-related disorders, including depression.

“This sensitive window could provide an opportunity for treatment, when the brain is most responsive to efforts to restore neural circuitry in the affected areas,” he adds.

The team, including McEwen and first author Carla Nasca, wanted to know how a history of stress could alter the brain’s response to further stress. To find out, they accustomed mice to a daily experience they dislike, confinement in a small space for a short period. On the 22nd day, they introduced some of those mice to a new stressor; others received the now-familiar confinement.

Then, the researchers tested both groups for anxiety- or depression-like behaviors. A telling split emerged: Mice tested shortly after the receiving the familiar stressor showed fewer of those behaviors; meanwhile those given the unfamiliar stressor, displayed more. The difference was transitory, however; by 24 hours after the final stressor, the behavioral improvements seen in half of the mice had disappeared.

Molecular analyses revealed a parallel fluctuation in a part of the hippocampus, a brain region involved in the stress response. A key molecule, mGlu2, which tamps down the release of the neurotransmitter glutamate, increased temporarily in mice subjected to the familiar confinement stress. Meanwhile, a molecular glutamate booster, NMDA, increased in other mice that experienced the unfamiliar stressor. In stress-related disorders, excessive glutamate causes harmful structural changes in the brain.

The researchers also identified the molecule regulating the regulator, an enzyme called P300. By adding chemical groups to proteins known as histones, which give support and structure to DNA, P300 increases expression of mGlu2, they found.

In other experiments, they looked at mice genetically engineered to carry a genetic variant associated with development of depression and other stress-related disorders in humans, and present in 33 percent of the population.

“Here again, in experiments relevant to humans, we saw the same window of plasticity, with the same up-then-down fluctuations in mGlu2 and P300 in the hippocampus,” Nasca says. “This result suggests we can take advantage of these windows of plasticity through treatments, including the next generation of drugs, such as acetyl carnitine, that target mGlu2—not to ‘roll back the clock’ but rather to change the trajectory of such brain plasticity toward more positive directions.”

On Oct 31, 2015 scientists used radar imaging to photograph a little dead comet. Much to their surprise, it looked quite a lot like a skull! Due to that and the timing, they nicknamed it Death Comet.

Death Comet will swing by us again this year (albeit a little later than last time). 

You can read more about the Death Comet here: https://www.universetoday.com/140108/the-death-comet-will-pass-by-earth-just-after-halloween/

Happy Halloween, all!!! 💀🎃

Have you ever seen a Lybia crab? Often called boxer crabs, or pom-pom crabs, these tiny crustaceans are easily identified by a unique behavior: they hold anemones on their claws to defend themselves from predators, keeping the anemones small enough to wield by limiting their food intake. But how do they get the anemones in the first place? Researchers think they have an answer: by stealing one from another crab, and then splitting it in half to create two identical clones—one for each claw.

Two graduate students, Yisrael Schnytzer and Yaniv Giman, set out to discover how the Lybia crabs acquire their anemones. They spent years observing and collecting crabs (Lybia leptochelis, specifically) from the Red Sea. Given that Lybia crabs are exceptionally well-camouflaged and only a few centimeters across, this was no easy task, but they managed to observe or collect more than 100 individuals.

Every specimen Schnytzer and Giman found was in possession of a pair of anemones, and each anemone belonged to the genus Alicia. Interestingly, the anemones themselves were not found living by themselves; they were only found already living on the claws of Lybia crabs. The researchers decided to study some of the crabs in a laboratory, to see if more observation would solve the mystery of how they acquired their anemones to begin with.

In the lab, the researchers conducted several experiments, the first of which was to take one anemone away from a crab. When left with just one anemone, the crab solved the problem by splitting the remaining anemone into two. The two halves of the anemone would then regenerate into two identical clones, one for each claw, over the course of several days.

The second experiment involved removing both anemones from one crab and placing it in a tank with a crab that still had both its anemones. The result: the two crabs would fight, with the anemone-less crab usually succeeding in stealing one anemone from the other crab. These fights did not tend to result in injuries to the crabs themselves, and once each crab was in possession of one anemone, both crabs would split their anemone into halves to create a pair of clones.

In addition to these experiments, Schnytzer and Giman examined the genes of the anemones found on the wild crabs. Every crab collected from the wild was holding a pair of identical clones. This might mean that anemone theft is rampant among Lybia crabs in the Red Sea, and that it might be the main way that these crabs acquire their anemones.

At any rate, it is clear that the crabs are frequently splitting anemones in two, inducing asexual reproduction in another species and potentially limiting that species’ genetic diversity in the process—a rarity outside the human world.

Based on materials provided by PeerJ and ScienceDaily

Journal reference: Yisrael Schnytzer, Yaniv Giman, Ilan Karplus, Yair Achituv. Boxer crabs induce asexual reproduction of their associated sea anemones by splitting and intraspecific theft. PeerJ, 2017; 5: e2954 DOI: 10.7717/peerj.2954

Image credit: Yisrael Schnytzer

Submitted by volk-morya

THE 👏🏾 ALIENS 👏🏾 ARE 👏🏾 COMING 👏🏾 BINCH

New theory explains how beta waves arise in the brain

Beta rhythms, or waves of brain activity with an approximately 20 Hz frequency, accompany vital fundamental behaviors such as attention, sensation and motion and are associated with some disorders such as Parkinson’s disease. Scientists have debated how the spontaneous waves emerge, and they have not yet determined whether the waves are just a byproduct of activity, or play a causal role in brain functions. Now in a new paper led by Brown University neuroscientists, they have a specific new mechanistic explanation of beta waves to consider.

The new theory, presented in the Proceedings of the National Academy of Sciences, is the product of several lines of evidence: external brainwave readings from human subjects, sophisticated computational simulations and detailed electrical recordings from two mammalian model organisms.

“A first step to understanding beta’s causal role in behavior or pathology, and how to manipulate it for optimal function, is to understand where it comes from at the cellular and circuit level,” said corresponding author Stephanie Jones, research associate professor of neuroscience at Brown University. “Our study combined several techniques to address this question and proposed a novel mechanism for spontaneous neocortical beta. This discovery suggests several possible mechanisms through which beta may impact function.”

Making waves

The team started by using external magnetoencephalography (MEG) sensors to observe beta waves in the human somatosensory cortex, which processes sense of touch, and the inferior frontal cortex, which is associated with higher cognition.

They closely analyzed the beta waves, finding they lasted at most a mere 150 milliseconds and had a characteristic wave shape, featuring a large, steep valley in the middle of the wave.

The question from there was what neural activity in the cortex could produce such waves. The team attempted to recreate the waves using a computer model of a cortical circuitry, made up of a multilayered cortical column that contained multiple cell types across different layers. Importantly, the model was designed to include a cell type called pyramidal neurons, whose activity is thought to dominate the human MEG recordings.

They found that they could closely replicate the shape of the beta waves in the model by delivering two kinds of excitatory synaptic stimulation to distinct layers in the cortical columns of cells: one that was weak and broad in duration to the lower layers, contacting spiny dendrites on the pyramidal neurons close to the cell body; and another that was stronger and briefer, lasting 50 milliseconds (i.e., one beta period), to the upper layers, contacting dendrites farther away from the cell body. The strong distal drive created the valley in the waveform that determined the beta frequency.

Meanwhile they tried to model other hypotheses about how beta waves emerge, but found those unsuccessful.

With a model of what to look for, the team then tested it by looking for a real biological correlate of it in two animal models. The team analyzed measurements in the cortex of mice and rhesus macaques and found direct confirmation that this kind of stimulation and response occurred across the cortical layers in the animal models.

“The ultimate test of the model predictions is to record the electrical signals inside the brain,” Jones said. “These recordings supported our model predictions.”

Beta in the brain

Neither the computer models nor the measurements traced the source of the excitatory synaptic stimulations that drive the pyramidal neurons to produce the beta waves, but Jones and her co-authors posit that they likely come from the thalamus, deeper in the brain. Projections from the thalamus happen to be in exactly the right places needed to deliver signals to the right positions on the dendrites of pyramidal neurons in the cortex. The thalamus is also known to send out bursts of activity that last 50 milliseconds, as predicted by their theory.

With a new biophysical theory of how the waves emerge, the researchers hope the field can now investigate whether beta rhythms affect or merely reflect behavior and disease. Jones’s team in collaboration with Professor of Neuroscience Christopher Moore at Brown is now testing predictions from the theory that beta may decrease sensory or motor information processing functions in the brain. New hypotheses are that the inputs that create beta may also stimulate inhibitory neurons in the top layers of the cortex, or that they may may saturate the activity of the pyramidal neurons, thereby reducing their ability to process information; or that the thalamic bursts that give rise to beta occupy the thalamus to the point where it doesn’t pass information along to the cortex.

Figuring this out could lead to new therapies based on manipulating beta, Jones said.

“An active and growing field of neuroscience research is trying to manipulate brain rhythms for optimal function with stimulation techniques,” she said. “We hope that our novel finding on the neural origin of beta will help guide research to manipulate beta, and possibly other rhythms, for improved function in sensorimotor pathologies.”

A fascinating new science experiment proves that we can grow babies outside of their mother’s womb

Keep reading

Israeli scientists see breakthrough in AIDS cure

Drug now being tested causes HIV-infected cells to self-destruct without harming the rest of the body

Israeli scientists see breakthrough in AIDS cure

Drug now being tested causes HIV-infected cells to self-destruct without harming the rest of the body

BY

TIMES OF ISRAEL STAFF

November 1, 2016, 3:26 am

HIV and AIDS patients may find new hope in a drug developed at Hebrew University in Jerusalem which is currently being tested at the Kaplan Medical Center in Rehovot.

The drug was inserted into test tubes containing the blood of ten AIDS patients currently being treated at the hospital, and was found to decrease the HIV virus count in the blood samples by as much as 97 percent in just eight days, Channel 2 reported Monday.

The active ingredient in the drug is a peptide, or smaller version of a protein, that was developed by Abraham Loyter and Assaf Friedler at Hebrew University. The peptide causes several copies of the virus’s DNA to enter the infected cell, instead of just one copy, causing the cell to self-destruct.

HIV is currently treated with a cocktail of drugs that slow the progression of the infection in the body but never rid the patient of the virus entirely. These drugs have allowed doctors to treat AIDS as a chronic illness as opposed to a fatal one.

Loyter explained that the new approach is superior to previous efforts.

“With our approach,” Loyter told Channel 2, “we are destroying the cells, so there is no chance that the virus will awaken one day, because there are no cells, there will be no cells that contain the virus.”

Loyter explained that “the drug enhances certain processes in the body during the spreading of the virus and that enhancement kills certain cells.”

In a separate but related development, the Health Ministry announced last week it would begin distributing prophylactic drugs for the first time to populations at higher risk of contracting HIV. The drugs, when taken regularly, have been found to be effective in preventing the spread of HIV during contact.

Photographs taken of Saturn by NASA. Yes, these are real pictures; they are not illustrations. 

(Source)

Just Made a Bad Decision?

Most people experience anxiety in their lives. For some, it is just a bad, passing feeling, but, for many, anxiety rules their day-to-day lives, even to the point of taking over the decisions they make.

Scientists at the University of Pittsburgh have discovered a mechanism for how anxiety may disrupt decision making. In a study published in The Journal of Neuroscience, they report that anxiety disengages a region of the brain called the prefrontal cortex (PFC), which is critical for flexible decision making. By monitoring the activity of neurons in the PFC while anxious rats had to make decisions about how to get a reward, the scientists made two observations. First, anxiety leads to bad decisions when there are conflicting distractors present. Second, bad decisions under anxiety involve numbing of PFC neurons.

The data indicates that anxiety has an exquisitely selective effect on neuronal activity that supports decision making, says Bita Moghaddam, the lead author of the study and a professor in the Department of Neuroscience within the Kenneth P. Dietrich School of Arts and Sciences. Up to now, scientists have mostly studied anxiety in animal models in the context of fear and measured how brain cells react to a threatening situation. But human anxiety is devastating, not merely because of how the person feels, but also because it can interfere with nearly all aspects of daily life including decision making, Moghaddam says.

Pitt researchers studied this aspect of anxiety by monitoring the activity of a large number of neurons as rats made decisions about which choice was most optimal for receiving a reward. They compared behavior and neuronal activity in two groups: one group that had a placebo injection and another that got a low dose of an anxiety-inducing drug.

As with many people who suffer from anxiety but go through day-to-day life and make decisions, the anxious rats completed the decision-making task and, actually, did not do too badly. But they made far more mistakes when the correct choice involved ignoring distracting information. “A brain locus of vulnerability for these anxiety-induced mistakes was a group of cells in the PFC that specifically coded for choice. Anxiety weakened the coding power of these neurons.

“We have had a simplistic approach to studying and treating anxiety. We have equated it with fear and have mostly assumed that it over-engages entire brain circuits. But this study shows that anxiety disengages brain cells in a highly specialized manner.”

Perhaps, down the line, this better understanding of the brain mechanics behind anxiety and decision making, she says, could lead to better treatment of anxiety in people and, subsequently, better outcomes in the treatment of psychiatric disorders.