Gamma-aminobutyric acid (GABA) deficits have been implicated in schizophrenia and depression. In schizophrenia, deficits have been particularly well-described for a subtype of GABA neuron, the parvalbumin fast-spiking interneurons. The activity of these neurons is critical for proper cognitive and emotional functioning.
…Dr. Kim Do and collaborators, from the Center for Psychiatric Neurosciences of Lausanne University in Switzerland, have worked many years on the hypothesis that one of the causes of schizophrenia is related to vulnerability genes/factors leading to oxidative stress. These oxidative stresses can be due to infections, inflammations, traumas or psychosocial stress occurring during typical brain development, meaning that at-risk subjects are particularly exposed during childhood and adolescence, but not once they reach adulthood.
Their study was performed with mice deficient in glutathione, a molecule essential for cellular protection against oxidations, leaving their neurons more exposed to the deleterious effects of oxidative stress. Under those conditions, they found that the parvalbumin neurons were impaired in the brains of mice that were stressed when they were young. These impairments persisted through their life. Interestingly, the same stresses applied to adults had no effect on their parvalbumin neurons.
Most strikingly, mice treated with the antioxidant N-acetylcysteine, from before birth and onwards, were fully protected against these negative consequences on parvalbumin neurons….
(Source: Medical Xpress)
”Neuroscience over the next 50 years is going to introduce things that are mind-blowing.” - David Eagleman
Brainstorm: David Eagleman: 'We won't die – our consciousness will live forever on the internet'
Seeing God as a microbe is just one way the neuroscientist’s debut novel gets to grips with the afterlife.
In one of the stories in David Eagleman’s first work of fiction, Sum: Forty Tales from the Afterlives (Canongate), God consoles himself for the mess that is humankind by reading Mary Shelley’s Frankenstein. In another, people pay vast sums to ensure the glamorous afterlife they desire, only to find themselves marooned in the most cliched version of heaven, where they sit on white clouds, clad in ill-fitting white robes, strumming harps.
By day, Eagleman is a neuroscientist at Baylor College of Medicine in Houston, Texas, where he specialises in the study of time perception and synesthesia. He also directs the college’s Initiative on Neuroscience and Law….
Q: Somewhere in your belief system do you hope that our consciousness continues after we die physically?
A: I’m not certain. By the way, I don’t have a belief system, I only have a possibility system! But I do hope that consciousness will survive our bodies.
Q: Would you really want to live forever ?
A: For better or worse we probably have no choice. Option one is we might just die and shut off like going to sleep. Possibility number two is there might be something much bigger than us, in which case we don’t have a choice about it anyway – we’ll just find ourselves there.
Q: What do you do when you’re not writing fiction?
A: During the day, what I try to figure out is how the brain works and specifically this issue of how the brain constructs reality. How do you put together hundreds of billions of cells and get it to have a private subjective experience? Consciousness. In other words, if I gave you a hundred billion Tinkertoys and asked you to put them together in a complicated fashion, the question is at what point would you add one more Tinkertoy and suddenly it is having a private subjective experience. It can experience the colour red and the feeling of pain or the taste of feta cheese. Not only do we not have a theory of that but we don’t even know what a theory of that would look like. That’s the situation we’re in in modern neuroscience. What we are doing is seeking any sort of inroad and I recognise that with synesthesia, where people have a mixture of the senses. Your neighbour’s reality can be very different than your reality. The same stimuli in the world can be inducing very different experiences internally and it’s probably based on a single change in a gene. What I am doing is pulling the gene forward and imaging and doing behavioural tests to understand what that difference is and how reality can be constructed so differently….
(Source: Sean O’Hagan, The Guardian; Image: The New York Times)
Brainbeauty: Rat cortical neurons stained with Chicken antibody to NF-H and Rabbit antibody to GFAP
(Source: EnCor Biotechnology Inc.)
Brainstorm: Up All Night
The science of sleeplessness.
….New technologies have made the study of sleep cheaper, easier, and less intrusive. In 2003, one expert in the field announced the “dawn of the golden age of sleep research.” Since then, hundreds, perhaps thousands, of academic papers have been written on topics ranging from “sleep problems among Chinese school-aged children” to the “sleep behavior of the wild black rhinoceros.” Currently, in the United States alone, more than two thousand sleep clinics are in operation. All of which raises the question: If this is sleep research’s golden age, then why are we all so tired?
….Wolf-Meyer refers to the practice of going to bed at around eleven o’clock at night and staying there until about seven in the morning as sleeping “in a consolidated fashion.” Nowadays, adults are expected to sleep in this manner; anything else—sleeping during the day, sleeping in bursts, waking up in the middle of the night—is taken to be unsound, even deviant. This didn’t use to be the case. Until a century and a half or so ago, Wolf-Meyer observes, “Americans, like other people around the world, used to sleep in an unconsolidated fashion, that is, in two or more periods throughout the day.” They went to bed not long after the sun went down. Four or five hours later, they woke from their “first sleep” and rattled around—praying, chatting, smoking, or making love. (Benjamin Franklin reportedly liked to spend this time reading naked in a chair.) Eventually, they went back to bed for their “second sleep.”
….Each of us has an internal clock, or, to use Roenneberg’s term, a “chronotype.” Either we’re inclined to go to bed early and wake up at dawn, in which case we’re “larks,” or we like to stay up late and get up later, which makes us “owls.” (One’s chronotype seems to be largely inherited, although Roenneberg notes, not altogether helpfully, that the “genetics are complex.”)
During the week, everyone is expected to get to the office more or less at the same time—let’s say 9 a.m. This suits larks just fine. Owls know they ought to go to bed at a reasonable time, but they can’t—they’re owls. So they end up having to get up one, two, or, in extreme cases, three hours earlier than their internal clock would dictate. This is what Roenneberg refers to as “social jet lag”—each workday, owls fall asleep in one time zone and, in effect, wake up in another. By the time the week is over, they’re exhausted. They “fly back” to their internal time zone on weekends and sleep in on Saturday and Sunday. Then, on Monday, they start the process all over again.
For larks, the problem is reversed. Social life is arranged so that it’s hard to have one unless you stay out late on Friday and Saturday nights. But, even when larks have partied till 3 a.m., they can’t sleep in the following day—they’re larks. So they stagger through until Monday, when they can finally get some rest.
….One of the great riddles of sleep is why we do it. Clearly, any animal that could get preyed upon is better off being alert, and even predators, when they’re snoozing, are losing time that otherwise could be used searching for victims. Yet sleep has a very long evolutionary history. It’s hard to measure a fruit fly’s brain waves, but even insects, which have been around for some four hundred million years, appear to need shut-eye. (Drosophila melanogaster, when they’re tired, creep away from their food, crouch down on their abdomens, and remain immobile for up to two and a half hours at a time.)
In the nineteen-eighties, Allan Rechtschaffen and Bernard Bergmann, both, like Kleitman, sleep researchers at the University of Chicago, performed what is now considered to be one of the classic experiments in the field. It showed that rats, when totally deprived of sleep, would, after two or three weeks, drop dead. But Rechtschaffen and Bergmann could never figure out the precise cause of the rats’ deaths, and so, they wrote in a follow-up paper in 2002, even “that dramatic symptom did not tell us much about why sleep was necessary.” Rechtschaffen has observed that “if sleep doesn’t serve an absolutely vital function, it is the greatest mistake evolution ever made…”
(Source: Elizabeth Kolbert, The New Yorker)
Brainbeauty: Cerebral Cortex
…May’s image shows progress on this work with three cell types being clearly labeled. What you are looking at are the lovely and complex branching astrocytes of the brain in yellow. These star-like glial cells surround the neurons of the brain and perform a wide variety of functions in the body including repair of injuries to the brain and protection of the brain’s neurons. In cyan we see the nuclei of each of the surrounding neurons in the brain. And in red, we see the blood vessels that provide blood supply to the brain. The brain studied here is a rat model.
The image was created using a confocal microscope. Confocal microscopy take a three dimensional sample and creates an in-focus image of small layers of the larger image (60-70 layers are viewed in this image alone). It then piles the images to create a clear image of the structure of the entire sample. This provides researchers with important information on how the different materials are arranged in the sample. They can also scroll through the different layers to get a closer look at a given area….
(Source: Gabrielle Demarco, The Approach)
Want to make your brain smarter? Slow down and dig deeper, advises Dr. Sandra Bond Chapman, a neuroscientist who has spent nearly 30 years studying this question….
Q: Why do you think it’s important to change what we mean by the word “smart”?
A: We tend to think that the smart person is the one who knows the most and retrieves the facts the quickest, but that’s rote and rigid learning. You can create a robot that can do the same thing and in fact will surpass us. What really makes us smart is our ability to synthesize, abstract and process information.
Q: Why do the frontal lobes play such a key role in your research?
A: Our frontal lobes pull together all the information from all the sources we have and help us figure out what to do with it. The frontal lobes have the most complex and vast connections across brain regions and are the last part of the brain to fully develop, usually in our 20s, but they are also the first to decline because in our 40s we tend to go on automatic pilot in our thinking.
Q: So, you are saying the frontal lobes don’t have to decline?
A: That’s right. Our brains have neuroplasticity, which means that they are the most changeable part of our body. If I go on automatic pilot, I lose brain power. But if I work the organ, it can get better every single year. A lot of people have this idea that IQ is fixed and you’re born smart or you’re not. IQ was designed to see if kids had learning problems, to see their strengths and weaknesses. It was never meant to define the potential of the human mind or to say how far you’re going to reach.
Q: Are you also saying, then, that the frontal lobes don’t automatically reach their potential?
A: Yes. If children don’t learn to weigh information rather than just take it in, if they don’t learn how to see both sides and try to come up with ways to solve problems, then they aren’t engaged in the higher order of thinking. If they’re doing rote learning instead of using these deeper thinking skills, they may not build what they are supposed to build, which means that they may not end up with the discernment to make good judgments in other areas as well.
Q: Is technology good or bad for our brains?
A: Yes, it is. (She laughs.) There is some good to staying connected. The problem is that we’re letting technology manage us more than we manage it. The more we keep ourselves in shallow, busy levels, the more our thinking gets fragmented, the more we are building a distracted brain that can’t focus; we’re building an ADD (attention-deficit disorder) brain. The frontal lobes require deeper-level thinking.
Q: What are the first steps we can take right now to build a smarter brain?
A: Do one thing at a time and hyperfocus, instead of multitask. Try to think of two important things you do that have been on automatic pilot and repeated in the same way far too long and brainstorm ways to shake them up. Be creative. When you go to a movie, ask yourself what the messages are and how can you apply them to yourself. Every time you do something new or understand something new, that stretches and builds complex frontal-lobe connections. All of these are exercises for above the neck that help you think smarter, not harder….
(Source: Nancy Churnin, Medical Xpress)
Neuronews: Psychologists uncover brain-imaging inaccuracies
Traditional methods of fMRI analysis systematically skew which regions of the brain appear to be activating, potentially invalidating hundreds of papers that use the technique.
….Functional magnetic resonance imaging measures changes in blood flow in the brain. It’s a powerful tool, but the signal fMRI actually detects – the result of the magnetic differences between oxygenated and deoxygenated blood – is noisy.
Researchers need to statistically process the data in order to make the resulting data interpretable. One of the most common approaches is known as “spatial smoothing,” which involves averaging the activity of each brain region with that of its neighbors.
But fMRI has only been in use since the mid-1990s. Many of the most common analyses in use today are holdovers from older, lower-resolution types of imaging and seem to have some undesired effects on the finer-grained signals fMRI can provide.
Knutson and Sacchet found that when researchers process fMRI data with a traditional “smoothing kernel” of 8mm, they end up averaging their images over too large an area. Activity in smaller brain structures can then be overlooked, or even shifted to areas that receive more blood flow and where the blood oxygenation level-dependent signal is stronger.
"It might seem strange that a systematic bias like that could bias the whole field," Knutson said. "But if half the people use 8mm and half use 4mm, you might end up with very different results, and it could add up…."
(Source: Max McClure, Standford News)
Neuronews: Star-shaped glial cells act as the brain’s ‘motherboard’
The transistors and wires that power our electronic devices need to be mounted on a base material known as a “motherboard.” Our human brain is not so different—neurons, the cells that transmit electrical and chemical signals, are connected to one another through synapses, similar to transistors and wires, and they need a base material too.
But the cells serving that function in the brain may have other functions as well. PhD student Maurizio De Pittà of Tel Aviv University’s Schools of Physics and Astronomy and Electrical Engineering says that astrocytes, the star-shaped glial cells that are predominant in the brain, not only control the flow of information between neurons but also connect different neuronal circuits in various regions of the brain.
Using models designed to mimic brain signalling, De Pittà’s research, led by his TAU supervisor Prof. Eshel Ben-Jacob, determined that astrocytes are actually “smart” in addition to practical. They integrate all the different messages being transferred through the neurons and multiplexing them to the brain’s circuitry. Published in the journal Frontiers in Computational Neuroscience and sponsored by the Italy-Israel Joint Neuroscience Lab, this research introduces a new framework for making sense of brain communications – aiding our understanding of the diseases and disorders that impact the brain….
(Source: Medical Xpress)
How do neurons store information about past events? In the Nencki Institute of Experimental Biology of the Polish Academy of Sciences in Warsaw, a previously unknown mechanism of memory trace formation has been discovered. It appears that at least some events are remembered thanks to… geometry…
"While conducting experiments on rats after epileptic seizures we have observed that a gene may permanently move deeper into the neuron’s cell nucleus. Since modification of the geometrical structure of the nucleus leads to changes in gene expression, this is how the neuron remembers, what happened," explains Prof. Grzegorz Wilczyński from the Laboratory of Molecular and Systemic Neuromorphology at the Nencki Institute…
In the case of neurons the epigenetic processes during which gene expression is decided by the environment, to date have been associated only with chemical reactions within the chromatin. Research done at the Nencki Institute has shown that in neurons we deal with yet another type of epigenetic effects: changes to the spatial structure of the cell’s nucleus resulting in the formation of permanent memory traces. This is possible for two reasons. First of all because of the presence of the nuclear membrane: genes can attach or detach from it, which impacts their expression. The second reason is related to the specific structure of the cell nucleus…
(Source: Science Daily; Image: Nencki Institute)
Neuronews: Is this peptide a key to happiness?
What makes us happy? Family? Money? Love? How about a peptide? The neurochemical changes underlying human emotions and social behavior are largely unknown. Now though, for the first time in humans, scientists at UCLA have measured the release of a specific peptide, a neurotransmitter called hypocretin, that greatly increased when subjects were happy but decreased when they were sad.
The finding suggests that boosting hypocretin could elevate both mood and alertness in humans, thus laying the foundation for possible future treatments of psychiatric disorders like depression by targeting measureable abnormalities in brain chemistry.
In addition, the study measured for the first time the release of another peptide, this one called melanin concentrating hormone, or MCH. Researchers found that its release was minimal in waking but greatly increased during sleep, suggesting a key role for this peptide in making humans sleepy….
(Source: Mark Wheeler, Medical Xpress; Image Credit: Jimmy Turnball)
Neuronews: Some brain cells are better virus fighters
Viruses often spread through the brain in patchwork patterns, infecting some cells but missing others. New research at Washington University School of Medicine in St. Louis helps explain why. The scientists showed that natural immune defenses that resist viral infection are turned on in some brain cells but switched off in others.
The cells that a pathogen infects can be a major determinant of the seriousness of brain infections,” says senior author Michael Diamond, MD, PhD, professor of medicine. “To understand the basis of disease, it is important to understand which brain regions are more susceptible and why.” While some brain infections are caused by bacteria, fungi or parasites, often the cause is a virus, such as West Nile virus, herpesvirus or enteroviruses. For their study, now available online in Nature Medicine, the researchers focused on granule cell neurons, a cell type that rarely becomes infected. They compared gene profiles in granule cells from the cerebellum with the activity in cortical neurons in the cerebral cortex, which are more vulnerable to infection….
Image: The white arrows highlight infected cells in a mouse brain. Scientists at Washington University School of Medicine in St. Louis have discovered that genetic programming makes some brain cells more resistant to infection. Image credit: Hyelim Cho.
(Source: Michael C. Purdy, Medical Xpress)
Brainbeauty: Medium spiny neurons
Medium spiny neurons (MSNs) are indeed “medium sized” with a cell body between 15 and 18 μm and dendritic fields that range from 200 to 300 μm in diameter. These neurons are marked by expansive dendrite trees with an abundant scattering of short spines. MSNs are the primary output of the striatum, a subcortical part of the forebrain that is the chief input region of the basal ganglia system. MSNs make up about 96% of the striatum and receive input from cortex, thalamus, and substantia nigra (1).
MSNs are GABAergic and therefore have an inhibitory influence on the neurons they project to, and are mostly modulated by dopamine and glutamate. Numerous tonically active cholinergic interneurons are closely positioned to the medium spiny neurons’ cell body in order to closely regulate their volatility. As a result, medium spiny neurons are normally quiet and tend not to exhibit spontaneous activity unless adequately activated (2).
Within the basal ganglia, complex neuronal loops are formed by MSNs that are important for the control of action, cognition, and emotion. In particular, these neurons have a critical role in motor control, habit formation, and motivated behavior. Further research of the medium spiny neuron is paramount due to their role in major neuropsychiatric disorders stretching from Parkinson’s disease and Huntington’s disease to schizophrenia and addiction (3).
Neuronerds: Your Brain by the Numbers
by Dwayne Godwin and Jorge Cham
Neuroscience has entered the public consciousness, and changed the way we talk about ourselves. But much of what passes as knowledge is inaccurate.
…This is sad but, perhaps, inevitable. As neuroscience has gained authority over previous ways of explaining human nature, it is not surprising that people will be compelled to use it if they want to try and make persuasive claims about how people are or should be – regardless of its accuracy. Folk neuroscience has become Freud for Freud-phobes, everyday psychology for the skeptical although in reality, rarely more helpful than either.
…Yet instead of revealing the beautiful complexity at our core, we live in a culture where dull biological platitudes make headlines and irritating scientific cliches win arguments. In response, we do not need a simpler culture but one that embraces complexity.
Neuroscience holds a prism up to human nature. Be suspicious of anyone who says there are no colours to be seen.
FOLK NEUROSCIENCE Popular misconceptions
■ The “left-brain” is rational, the “right-brain” is creative
The hemispheres have different specialisations (the left usually has key language areas, for example) but there is no clear rational-creative split and you need both hemispheres to be successful at either. You can no more do right-brain thinking than you can do rear-brain thinking.
■ Dopamine is a pleasure chemical
Dopamine has many functions in the brain, from supporting concentration to regulating the production of breast milk. Even in its most closely associated functioning it is usually considered to be involved in motivation (wanting) rather than the feeling of pleasure itself.
■ Low serotonin causes depression
A concept almost entirely promoted by pharmaceutical companies in the 1980s and 90s to sell serotonin-enhancing drugs like Prozac. No consistent evidence for it.
■ Video games, TV violence, porn or any other social spectre of the moment “rewires the brain”
Everything “rewires the brain” as the brain works by making and remaking connections. This is often used in a contradictory fashion to suggest that the brain is both particularly susceptible to change but once changed, can’t change back.
■ We have no control over our brain but we can control our mind
The mind and the brain are the same thing described in different ways and they make us who we are. Trying to suggest one causes the other is like saying wetness causes water.
(Source: Vaughnn Bell, The Guardian)