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Vortex rings may look relatively calm, but they are concentrated regions of intensely spinning flow, as this poor jellyfish demonstrates. The rings form when a high-speed fluid gets pushed suddenly (and briefly) into a slower fluid. In the case of this bubble ring, a burst of air is pushed by a diver into relatively still water. The vorticity caused by the two areas of fluid trying to move past one another forms the ring. Like a spinning ice skater who pulls his arms inward, the narrow core of the vortex spins fast due to the conservation of angular momentum. Meanwhile, the bubble ring moves upward due to its buoyancy, pulling nearby water in as it goes. This catches the hapless jellyfish (who relies on vortex rings itself) and gives it quite a spin. But. don’t worry, the photographer confirmed that the jelly was okay after its ride. (Video credit: V. de Valles; via Ashlyn N.)

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Many chemical reactions, and the flows that accompany them, are invisible to the human eye. But in infrared wavelengths those same events are vibrant and energetic. In this video from the Beauty of Science group, various chemical reactions are shown in visible and IR wavelengths, revealing very different perspectives on the same thing. Many of the reactions are exothermic, meaning that they produce heat as they occur. Because of this the thermal imaging shows where the most intense reaction is occurring at a given time. Other areas gradually darken as diffusion and flow move and dilute the heat energy released. (Video and image credit: Beauty of Science, source)

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A Snapshot of Neural Activity

FLARE technique can reveal which cells respond during different tasks.

The research is in Nature Biotechnology. (full access paywall)

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(Image caption: Brain tissue from genetically engineered mice. Neurons that express CRFR1 appear in green and those that release the neurotransmitter CRF are in red. The image was obtained with fluorescence microscopy)

Keeping Up the Pressure

In addition to the classic stress response in our bodies – an acute reaction that gradually abates when the threat passes – our bodies appear to have a separate mechanism that deals only with chronic stress. These Weizmann Institute of Science findings, which recently appeared in Nature Neuroscience, may lead to better diagnosis of and treatment for anxiety and depression.

Dr. Assaf Ramot, a postdoctoral fellow in Prof. Alon Chen’s group in the Weizmann Institute’s Neurobiology Department, led the research pinpointing a small, previously unknown group of nerve cells in the paraventricular nucleus, or PVN, within the hypothalamus – a part of the brain involved in regulating many of the body’s reactions. These cells’ position in the PVN led the researchers to suppose that the nerve cells play a role in the stress response.

Chen explains that in the well-known stress response, the neurotransmitter CRF is released from the PVN and goes to the pituitary. The pituitary releases hormones that then cause the adrenal gland to flood the bloodstream with the “stress hormone” cortisol. Cortisol, along with the regular stress response, lowers the production of CRF, thus causing a negative feedback loop in which the mechanism slows down and stops.

A postive-feedback loop

The newly-discovered nerve cells express a receptor, CRFR1, on their outer walls, which enables them to take in the message of the CRF neurotransmitter. The experiments showed that in mice the cortisol actually increases the number of CRFR1 receptors on these nerve cells, suggesting a positive feedback loop that could be self-renewing, rather than abating.

Working with Prof. Nicholas Justice’s group at the University of Texas, Houston, Chen, Ramot and their group first characterized this special population of nerve cells, labeling them with fluorescent proteins in the brains of genetically engineered mice. When they removed the adrenal glands of these mice, and thus prevented the production of cortisol, the receptors did not appear on the PVN nerve cell walls, while injecting synthetic stress hormones caused them to appear and restart the chain reaction.

Next, the researchers asked when and how the CRFR1 cycle is initiated. They compared mice genetically engineered to lack the receptor with a control group and exposed them to different kinds of stress, testing the hormones in their blood afterward. When the mice experienced acute stress, both groups reacted in a similar manner, and their hormone levels were also similar. But chronic stressors told a different story: The genetically engineered mice stayed calmer and had lower levels of the cortisol-like hormone.

“In other words,” says Ramot, “the CRFR1 system is a separate one that evolved to deal with chronic stress.” Chen adds: “Some studies have shown that patients suffering from depression have more of this receptor than average, and this suggests further avenues of research and even ways to treat, in the future, disorders that arise from chronic stress.”

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What’s the difference between place cells and grid cells? http://buff.ly/2t80M4W http://ift.tt/2u2GvtX

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New discovery could be a major advance for understanding neurological diseases

The discovery of a new mechanism that controls the way nerve cells in the brain communicate with each other to regulate our learning and long-term memory could have major benefits to understanding how the brain works and what goes wrong in neurodegenerative disorders such as epilepsy and dementia. The breakthrough, published in Nature Neuroscience, was made by scientists at the University of Bristol and the University of Central Lancashire. The findings will have far-reaching implications in many aspects of neuroscience and understanding how the brain works.

The human brain contains around 100-billion nerve cells, each of which makes about 10,000 connections to other cells, called synapses. Synapses are constantly transmitting information to, and receiving information from other nerve cells. A process, called long-term potentiation (LTP), increases the strength of information flow across synapses. Lots of synapses communicating between different nerve cells form networks and LTP intensifies the connectivity of the cells in the network to make information transfer more efficient. This LTP mechanism is how the brain operates at the cellular level to allow us to learn and remember. However, when these processes go wrong they can lead to neurological and neurodegenerative disorders.

Precisely how LTP is initiated is a major question in neuroscience. Traditional LTP is regulated by the activation of special proteins at synapses called NMDA receptors. This study, by Professor Jeremy Henley and co-workers reports a new type of LTP that is controlled by kainate receptors.

This is an important advance as it highlights the flexibility in the way synapses are controlled and nerve cells communicate. This, in turn, raises the possibility of targeting this new pathway to develop therapeutic strategies for diseases like dementia, in which there is too little synaptic transmission and LTP, and epilepsy where there is too much inappropriate synaptic transmission and LTP.

Jeremy Henley, Professor of Molecular Neuroscience in the University’s School of Biochemistry in the Faculty of Biomedical Sciences, said: “These discoveries represent a significant advance and will have far-reaching implications for the understanding of memory, cognition, developmental plasticity and neuronal network formation and stabilisation. In summary, we believe that this is a groundbreaking study that opens new lines of inquiry which will increase understanding of the molecular details of synaptic function in health and disease.”

Dr Milos Petrovic, co-author of the study and Reader in Neuroscience at the University of Central Lancashire added: “Untangling the interactions between the signal receptors in the brain not only tells us more about the inner workings of a healthy brain, but also provides a practical insight into what happens when we form new memories. If we can preserve these signals it may help protect against brain diseases.

“This is certainly an extremely exciting discovery and something that could potentially impact the global population. We have discovered potential new drug targets that could help to cure the devastating consequences of dementias, such as Alzheimer’s disease. Collaborating with researchers across the world in order to identify new ways to fight disease like this is what world-class scientific research is all about, and we look forward to continuing our work in this area.”

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Thousands of neurons reflected by white, red and violet light

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It took an explosion and 13 pounds of iron to usher in the modern era of neuroscience.

In 1848, a 25-year-old railroad worker named Phineas Gage was blowing up rocks to clear the way for a new rail line in Cavendish, Vt. He would drill a hole, place an explosive charge, then pack in sand using a 13-pound metal bar known as a tamping iron.

But in this instance, the metal bar created a spark that touched off the charge. That, in turn, “drove this tamping iron up and out of the hole, through his left cheek, behind his eye socket, and out of the top of his head,” says Jack Van Horn, an associate professor of neurology at the Keck School of Medicine at the University of Southern California.

Gage didn’t die. But the tamping iron destroyed much of his brain’s left frontal lobe, and Gage’s once even-tempered personality changed dramatically.

“He is fitful, irreverent, indulging at times in the grossest profanity, which was not previously his custom,” wrote John Martyn Harlow, the physician who treated Gage after the accident.

This sudden personality transformation is why Gage shows up in so many medical textbooks, says Malcolm Macmillan, an honorary professor at the Melbourne School of Psychological Sciences and the author of An Odd Kind of Fame: Stories of Phineas Gage.

“He was the first case where you could say fairly definitely that injury to the brain produced some kind of change in personality,” Macmillan says.

Why Brain Scientists Are Still Obsessed With The Curious Case Of Phineas Gage

Photo via Wikimedia Commons