neural function

  • Apples - the peel of the apples includes a powerful antioxidant called quercetin that enhances memory function
  • Avocados - promotes brain health and contributes to healthy blood flow
  • Berries - such as blueberries, cherries and even grapes have a direct effects on brain function. It contains antioxidants that improve blood flow to the brain and enhance neural activity
  • Broccoli - great source of vitamin K - enhance cognitive function and improve brainpower
  • Dark chocolate - has a powerful antioxidant which includes several natural stimulants that enhance focus and concentration
  • Extra Virgin Olive Oil - has a powerful antioxidants known as polyphenols that improve learning and memory
  • Eggs - more specifically the yolks, leading source of choline which is a precursor for acetylcholine - neurotransmitter involved in helping you remember things
  • Fish - have Omega-3 fatty acids that are essential to proper neural function. According American Journal of Clinical Nutrition - reduce risk of dementia as you get older
  • Nuts - rich source of vitamin E
  • Onions - ability to improve important brain function like memory and focus
  • Oatmeal - reduce risk for heart disease and promotes good flow to the organ system which includes the brain
  • Rosemary - contains carnosic acid that helps protect the brain from neurodegeneration; protects the brain against chemical free radicals
  • Salmon - omega-3 fatty acids to help keep your brain running smoothy and improve memory
  • Tomatoes - contains lycopene that could help protect against the kind of free radical damage to cells which occurs in the development of dementia
  • Turmeric - helps boost antioxidant levels and keep your immune system healthy; improves brain’s oxygen intake, keeping  you alert and able to process information
  • Yerba Mate - can enhance short term brain power
Balancing Time and Space in the Brain: A New Model Holds Promise for Predicting Brain Dynamics

For as long as scientists have been listening in on the activity of the brain, they have been trying to understand the source of its noisy, apparently random, activity. In the past 20 years, “balanced network theory” has emerged to explain this apparent randomness through a balance of excitation and inhibition in recurrently coupled networks of neurons. A team of scientists has extended the balanced model to provide deep and testable predictions linking brain circuits to brain activity.

Lead investigators at the University of Pittsburgh say the new model accurately explains experimental findings about the highly variable responses of neurons in the brains of living animals. On Oct. 31, their paper, “The spatial structure of correlated neuronal variability,” was published online by the journal Nature Neuroscience.

The new model provides a much richer understanding of how activity is coordinated between neurons in neural circuits. The model could be used in the future to discover neural “signatures” that predict brain activity associated with learning or disease, say the investigators.

“Normally, brain activity appears highly random and variable most of the time, which looks like a weird way to compute,” said Brent Doiron, associate professor of mathematics at Pitt, senior author on the paper, and a member of the University of Pittsburgh Brain Institute (UPBI). “To understand the mechanics of neural computation, you need to know how the dynamics of a neuronal network depends on the network’s architecture, and this latest research brings us significantly closer to achieving this goal.”

Earlier versions of the balanced network theory captured how the timing and frequency of inputs—excitatory and inhibitory—shaped the emergence of variability in neural behavior, but these models used shortcuts that were biologically unrealistic, according to Doiron.

“The original balanced model ignored the spatial dependence of wiring in the brain, but it has long been known that neuron pairs that are near one another have a higher likelihood of connecting than pairs that are separated by larger distances. Earlier models produced unrealistic behavior—either completely random activity that was unlike the brain or completely synchronized neural behavior, such as you would see in a deep seizure. You could produce nothing in between.”

In the context of this balance, neurons are in a constant state of tension. According to co-author Matthew Smith, assistant professor of ophthalmology at Pitt and a member of UPBI, “It’s like balancing on one foot on your toes. If there are small overcorrections, the result is big fluctuations in neural firing, or communication.”

The new model accounts for temporal and spatial characteristics of neural networks and the correlations in the activity between neurons—whether firing in one neuron is correlated with firing in another. The model is such a substantial improvement that the scientists could use it to predict the behavior of living neurons examined in the area of the brain that processes the visual world.

After developing the model, the scientists examined data from the living visual cortex and found that their model accurately predicted the behavior of neurons based on how far apart they were. The activity of nearby neuron pairs was strongly correlated. At an intermediate distance, pairs of neurons were anticorrelated (When one responded more, the other responded less.), and at greater distances still they were independent.

“This model will help us to better understand how the brain computes information because it’s a big step forward in describing how network structure determines network variability,” said Doiron. “Any serious theory of brain computation must take into account the noise in the code. A shift in neuronal variability accompanies important cognitive functions, such as attention and learning, as well as being a signature of devastating pathologies like Parkinson’s disease and epilepsy.”

While the scientists examined the visual cortex, they believe their model could be used to predict activity in other parts of the brain, such as areas that process auditory or olfactory cues, for example. And they believe that the model generalizes to the brains of all mammals. In fact, the team found that a neural signature predicted by their model appeared in the visual cortex of living mice studied by another team of investigators.

“A hallmark of the computational approach that Doiron and Smith are taking is that its goal is to infer general principles of brain function that can be broadly applied to many scenarios. Remarkably, we still don’t have things like the laws of gravity for understanding the brain, but this is an important step for providing good theories in neuroscience that will allow us to make sense of the explosion of new experimental data that can now be collected,” said Nathan Urban, associate director of UPBI.

Blue Brain team finds 'Multi-dimensional universe' in brain networks

For most people, it is a stretch of the imagination to understand the world in four dimensions but a new study has discovered structures in the brain with up to eleven dimensions – ground-breaking work that is beginning to reveal the brain’s deepest architectural secrets.

Using algebraic topology in a way that it has never been used before in Neuroscience, a team from the Blue Brain Project has uncovered a universe of multi-dimensional geometrical structures and spaces within the networks of the brain.

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Colors of Dissonance (pt. 13)

Part 12

Nathan sighs. “Fine, I’ll help you. What do you need me to do?”

Mat rubs his hands together and ushers Nate over to a Tube in the corner. “Just go about your regularly scheduled streaming, and allow me a chance to observe your vitals in the process.”

“You want me to get back in the death trap that is slowly driving me insane?” Nate shakes his head. “No way!”

Mathew crosses his arms over his chest. “This is the only way. I need someone to monitor, Nate, otherwise there’s going to be no way of stopping this.” He pulls another three overflowing files out of a cabinet to his right. “This is all the research I’ve done so far, and it’s taken me a year.” He sighs and pinches the bridge of his nose. “And we’re running out of time before we all lose it.”

Nate nods, sighing to himself. “Alright. I’ll do it.”

“Thank you,” Mat says, offering Nate a hand.

Nate stares at it and instead walks over to the Tube, getting it ready to go and set to his streaming frequency. “Anything special that you need me to do?”

Mathew grabs a few extra sensors from a cabinet and attaches them to either side of Nate’s head and to the pulse point on his neck. “Make sure your neural cam is functioning properly. I need that video feed in order to properly gauge how much interference you’re experiencing once under the immersion. If for any reason you feel that you might possibly be in any danger, just let me know, and I’ll hit the eject button, have you out of it as quickly as possible. Got that?”

“Yeah,” Nate nods, adjusting his wrist sensors again because of the irritation from the scrapes there.

Mathew sees them and sighs. “Nate, I’m really sorry about all of this.”

“Just sorry that I don’t blindly trust you anymore.” Nate starts the final preparations for the immersion and checks the clock. He’s already ten minutes late, and Mando is not going to be happy about that.

Mat grabs his arm. “You know that’s not what I meant. Things are… things are hard for me, ok? All the crap you deal with is even worse for me, and this thing in my head… it’s started to take over even when I try to fight him.” Mathew pushes a hand through his hair and sighs as Nate turns to listen. “And there’s so much at stake here, too many lives…”

Nathan rubs at his forehead and sighs. “You know what? Alright, I’ll accept that I don’t understand all of this, but there’s no reason to put yourself under all this pressure.” He smirks at his friend and shrugs his shoulders. “If we find a cure, good for us. Maybe they’ll give me a vacation for once. If we don’t, well…” Nate reaches up and punches Mat in the shoulder. “We’ll all go crazy together. Right?”

“Eloquently put,” Mat says with a little huff. “Now, you should get started if you don’t want to disappoint those fans.”

Nate nods and steps into the Tube, sealing it shut and waiting for the gas to surround him. “Here goes nothing…”


Sean tastes blood. It’s in his mouth, all over his arms and torso, and on the floor. There are several bodies, some of them in pieces, littered around the room as Anti finally relents control with a crackle of static and a whisper of, “U̳ͅn̩̳̞̖t̻į͉l̩̤̺̹̺̯ ̨̤͕͙̝n̙̪̖͕͚̯e͇̟͎͞x̡͈̩̼̗̭ț͉̠̬͜ ̫͔̬̜̰͎̞t̳̻̀i̻̮̺̼͙̹̞̕m̪̗e̖̰̼̼̱͖̫,̫̤̹̞ͅ ͙͇̺͕̭͚̪I̼̹͇̝ͅ'͙l̫͈͇l̹̺̜ ̀b̭̻̥̳̭̦̩e̲͘ ̢̜̺̯w͏̟̤͖̱̳̲a͖i̖͉t̩̪̺͠i̕n̜̟̗̦̺g̼͎̫̻͇̜.̛̜̳ͅ”

Sean staggers, sagging against a wall and retching every last bit of food in his stomach. He runs to the bathroom and washes his face and hands. He just wants to free himself of that awful smell. He strips out of the bloodied clothes as well and finds a fresh pair of jeans and a t-shirt crammed into a box in one of the back rooms. There’s a black beanie too, to hide his hair.

Sean knows that he probably doesn’t have much longer before Corporate sends reinforcements, so he tries to come up with a plan.

He takes a hoverboard and flies out to look for Mark and Amy. or He leaves on foot, hoping not to draw any attention.

Neuro chip records brain cell activity at higher resolution

Brain functions are controlled by millions of brain cells. However, in order to understand how the brain controls functions, such as simple reflexes or learning and memory, we must be able to record the activity of large networks and groups of neurons. Conventional methods have allowed scientists to record the activity of neurons for minutes, but a new technology, developed by University of Calgary researchers, known as a bionic hybrid neuro chip, is able to record activity in animal brain cells for weeks at a much higher resolution. The technological advancement was published in the journal Scientific Reports.

“These chips are 15 times more sensitive than conventional neuro chips,” says Naweed Syed, PhD, scientific director of the University of Calgary, Cumming School of Medicine’s Alberta Children’s Hospital Research Institute, member of the Hotchkiss Brain Institute and senior author on the study. “This allows brain cell signals to be amplified more easily and to see real time recordings of brain cell activity at a resolution that has never been achieved before.”

The development of this technology will allow researchers to investigate and understand in greater depth, in animal models, the origins of neurological diseases and conditions such as epilepsy, as well as other cognitive functions such as learning and memory.

“Recording this activity over a long period of time allows you to see changes that occur over time, in the activity itself,” says Pierre Wijdenes, a PhD student in the Biomedical Engineering Graduate Program and the study’s first author. “This helps to understand why certain neurons form connections with each other and why others won’t.”

The cross-faculty team created the chip to mimic the natural biological contact between brain cells, essentially tricking the brain cells into believing that they are connecting with other brain cells. As a result, the cells immediately connect with the chip, thereby allowing researchers to view and record the two-way communication that would go on between two normal functioning brain cells.

“We simulated what Mother Nature does in nature and provided brain cells with an environment where they feel as if they are at home,” says Syed. “This has allowed us to increase the sensitivity of our readings and help neurons build a long-term relationship with our electronic chip.”

While the chip is currently used to analyze animal brain cells, this increased resolution and the ability to make long-term recordings is bringing the technology one step closer to being effective in the recording of human brain cell activity.

“Human brain cell signals are smaller and therefore require more sensitive electronic tools to be designed to pick up the signals,” says Colin Dalton, adjunct professor in the Department of Electrical and Computer Engineering at the Schulich School of Engineering and a co-author on this study. Dalton is also the facility manager of the University of Calgary’s Advanced Micro/nanosystems Integration Facility (AMIF), where the chips were designed and fabricated.

Researchers hope the technology will one day be used as a tool to bring personalized therapeutic options to patients facing neurological disease.

Do No Harm - Chapter 9

I will abstain from all intentional wrong-doing and harm

Wanna read previous chapters?: Ch. 1, Ch. 2, Ch. 3, Ch. 4, Ch. 5, Ch.6, Ch.7, Ch.8

6866 Words

Read it on AO3!

Angela thought about putting up a fight when the other doctors shooed her out of the room, but she instead decided that wouldn’t get her anywhere positive. She would be gracious in her success. She could be.

Besides, Amélie was a bit too out of it to want to talk to her much. She spent a lot of time staring at her hands and offering brief answers to the long questions she was being asked.

So when a parade of more doctors came in, followed by a team of lawyers, Angela was content to leave the crowded room. She allowed herself one little glance back, and could swear she saw those golden eyes lift from examining cyanotic skin to follow her to the door.

Angela could hold on to that a while. She could wait. She could.

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More (Detailed) Neuroscience and Behavior Notes

Other Neuroscience and Behavior Notes (with pics!)
What’s not included in that^ post is here and vice versa. Also some things might repeat.


Neurons: The Basic Elements of Behavior
The Structure of the Neuron

  • Neurons: Nerve cells, the basic elements of the nervous system
  • Perhaps as many as trillion neurons throughout the body are involved in the control of behavior.
  • The nucleus incorporates heredity material that determines how a cell will function.
  • Neurons are physically held in place by glial cells. Glial cells provide nourishment to neutrons, insulate them, help repair damage, and generally support neural functioning.
  • Terminal Buttons AKA Terminal Branches
  • Myelin Sheath: made up of fat and protein
  • Neural impulses generally move across neurons in one direction only

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anonymous asked:

Boys go to Jupiter to get more stupider BC the atmosphere of Jupiter stops all neural function (stupiter)and

And girls go to college to get more knowledge because thats where the knowledge is

Pictured above is a remembrancer image of the Primarchs of the XIII  and II Legion’s just moments after victory at Ullanor was assured. 

Heimvald Aonghusson depicted on the right was known as the Ursen Lord or the Bear of Man. Third Primarch found by the Emperor of mankind he was noted upon being found having conquered a small empire of worlds that would be comparable to the Realm of Ultramar in size, the Primarch met with the Emperor at the border of this realm known as the ‘Tamin Dominion’. Upon meeting the Emperor Heimvald swore an oath of fealty to his father and new Lord. The master of mankind gave to his newfound son the II legion of Space Marines and due to his son’s emotional promise the Emperor declared that the legion would be known forevermore as ‘The Oathsworn’. Heimvald was shadowed by Leman Russ the previous Primarch found when he first received his legion, from him the new Primarch gained knowledge of strategy and warfare as well as some influence on his own legion’s internal structuring. 

Later in the Great Crusade when the Primarch Angron Thal’kyr was discovered and subsequently abandoned shortly after by the Emperor, the Solare Alise beseeched Heimvald for assistance and informed him of the gravity of his brother’s plight. Spurred on by the knowledge of Angron’s terminal condition, Heimvald sent scouts from his legion who scoured over 9 worlds in five different systems of space for anything they could find. His scouts returned with news that the solution to the Red Angel’s woes was on the Ork held manufactorum world of Geryl’s Forge which reports say had at one point in its planetary history acquired either a copy of the original Butcher’s Nails STC, or somehow obtained the original. Regardless with this they had created a piece of technology based upon the original implants known as ‘The Foundation’, it was used as a multi-functional neural pathway for technology to integrate with the nervous system. 

The Ursen Lord brought the might of his Legion upon the world with assistance from both the World Eaters Legion and the Solare Alise Romero who was accompanied by a cadre of Sisters of Silence. The Orks although initially confident were weakened in a series of assault campaigns to retake the world with minimal collateral damage, this world acted as the first joint campaign both legions had undertaken and it would not be their last together. With assistance from the XIII Legion’s Fleet Captain Lotara Sarrin in orbit and the joint task force of two legions alongside a cadre of sisters of silence proved too effective for the Orks. After only two conflicts the Warboss known as Spinekraka was lured out and slain, the Greenskins could not recoup from the loss of their leader quick enough and control of the world was returned to the Imperium. A unique form of the Foundation was created for Angron, designed to overlap and take over the Butcher’s Nails. Consent for the surgery took some time as the Primarch was loathe to have anyone in his head again, though for some reason he changed his mind and consented to the Magos and Dominion medical engineers.

Angron was put into a medical coma and mentally assuaged by the Solare while the Foundation was installed, the procedure although grueling was a success. The Primarch’s terminal status was rescinded with great joy and with time his unique physiology would hopefully begin to regenerate parts of his brain that the Butcher’s nails had damaged or destroyed outright. The surgery the Primarch undertook was mirrored and performed on Alise with her consent, the Foundation acting as a bridge for the Solare to manually hook up to the Primarch and act as a transitionary limbic system. The hope being that eventually Angron’s mind would repair itself and no longer need the Solare, though by this point the two had begun to foster a relationship that Heimvald was keen to encourage as he saw it as a wonderful thing for his brother to find someone who cared so much for his well being. 

(Hello all! @syberfab is the one who I commissioned for this work! I thought I might as well make a blog and post to share my headcanons about my Primarch. Look forward to more stuff from me in the future! @asklotarasarrin @askangron40k @ask-solare-alise)

A quick guide to neural implants in Halo for RVB fans

  1. Standard - The standard neural interface has basic functions. It acts as a “friend or foe” indicator, so that radar signatures will pick up the owner’s signature and identify it as friendly. It is easily removed and is basically intended to prevent friendly fire.
  2. Command Neural Interface (CNI)-  implanted in the brain of every UNSC ship commander. In addition to the duties of a standard, they also have several purposes specific to a ship commander.They cannot be removed without killing the host or doing permanent damage to the host’s brain. Their main use is the storage of data codes, NAV data, and also for receiving telemetry from outside sources. AI can access info from here or enter info into there, but only with permission. The commander can also lace with the ship itself to get data.
  3. Spartan Neural Interface (probably what Freelancers have a similar interface to) -an upgrade of the standard that SPARTANs received when fitted for MJOLNIR Mark V. They cannot be removed without killing the host or doing permanent damage to the host’s brain. the Spartan Neural Interface is unique in that it is designed to allow an AI to directly interface with the Spartan’s brain. The AI is said to reside both inside the armor and inside the wearer’s mind. Essentially, it is in both places at once. The interface allows the AI access to most of the suit’s internal systems, though the Spartan has override control.

Basically anyone would have a standard neural interface. The Freelancer one was special for the fact that the AI could interface even while the armor was off, and in that specific AI could jump into it without a chip somehow. But most likely it would be closer to the Spartan interface.

Any other character from the UNSC would have a basic version at least, though. Which is basically a tiny chip. They can be removed easily

I wouldnt be surprised if the Director had a Command interface but he was never shown to have it probably because he was mostly a civilian and not military really. Id imagine he might have considered it at some point though.

People who would have Freelancer Project implants:

  1. The reds
  2. the blues
  3. the freelancers
  4. maybe someone like Niner or the Counselor we’re not really sure
  5. Any freelancer grunts

If the character is not in this group they dont have Freelancer implants. They have something else. This includes Felix, Locus, Kimball, Doyle, Dr Grey, the LTs, and any other Fed or New character.

Fun Fact: Our brains account for 3% of our body weight but use 20% of our energy resources. Also the idea that we only use 10% of our brain is complete nonsense. We use 100% of our brains; however, due to a process known as neural plasticity, we can function even if large portions of our brain are missing.

I was doing some random reading and apparently ADD/ADHD is caused by abnormalities in the frontal lobe of our brains. The frontal lobe controls speech, language, and motor function (I kind of fell in love with medical science while I was self diagnosing my ADHD). As I’ve gotten older, my ADHD symptoms have multiplied. At the same time I seem to have lost the perfect balance and coordination I loved when I was a kid. I’m not just talking getting old, here. I’m only 18 and yet I walk into walls/doorways, trip over thin air, and drop things all the time. Now either I have MS without the #1 symptom of weakness, or a theory that could explain it. The same damage that causes the ADHD could cause balance/coordination issues. I have a friend who’s got combined ADHD and she’s as clumsy as I am (though she blames it on her tiny feet). Since the frontal lobe controls language, it also explains why some of us mix up words and have trouble understanding speech. Again, it’s just a theory, but it makes sense to me. Anyone else unusually clumsy?


You’re talking about dyspraxia, which is a common comorbid disorder with ADHD. The frontal lobe also manages your executive functions, which are to do with things like impulsive behaviours and making plans and stuff like that.


While it’s true that many of the functional deficits in ADHD are localized in the frontal lobes, it’s a huge over-simplification to say that ADHD is caused by frontal lobe abnormalities. Yes, the frontal lobes are involved in motor function and language processing (as well as executive functions like J said) but these processes are controlled through interaction with other areas of the brain. Different aspects of motor function are also controlled by the parietal lobe, basal ganglia and striatal pathways, and the cerebellum. Speech production happens in the frontal lobes while understanding speech and language processing largely happens in the temporal lobes. 

Although studies on ADHD have found abnormalities in the frontal lobes like smaller volume, less activation and less blood flow, this is not necessarily the case for everyone with ADHD. It is far more likely that ADHD is caused by interaction between genetics, neural anatomy, and environmental factors rather than just one thing like frontal lobe abnormalities.  Even then it’s not damage (unless of course ADHD symptoms were caused by an injury, which is also possible), just differences in neural structure and functions. 

It is possible that symptoms of dyspraxia appear with ADHD symptoms, but this is more likely because of differences in connectivity between the frontal lobes and areas that are actually more involved with balance and fine motor control, such as the cerebellum and basal ganglia than damage or abnormalities in the frontal lobes. 


Two new studies uncover key players responsible for learning and memory formation

One of the most fascinating properties of the mammalian brain is its capacity to change throughout life. Experiences, whether studying for a test or experiencing a traumatic situation, alter our brains by modifying the activity and organization of specific neural circuitry, thereby modifying subsequent feelings, thoughts, and behavior. These changes take place in and among synapses, communication junctions between neurons. This experience-driven alteration of brain structure and function is called synaptic plasticity and it is considered the cellular basis for learning and memory.

Many research groups across the globe are dedicated to advancing our understanding of the fundamental principles of learning and memory formation. This understanding is dependent upon identifying the molecules involved in learning and memory and the roles they play in the process. Hundreds of molecules appear to be involved in the regulation of synaptic plasticity, and understanding the interactions among these molecules is crucial to fully understand how memory works.

There are several underlying mechanisms that work together to achieve synaptic plasticity, including changes in the amount of chemical signals released into a synapse and changes in how sensitive a cell’s response is to those signals. In particular, the protein BDNF, its receptor TrkB, and GTPase proteins are involved in some forms of synaptic plasticity, however, very little is known regarding when and where they are activated in the process.

By using sophisticated imaging techniques to monitor the spatiotemporal activation patterns of these molecules in single dendritic spines, the research group led by Dr. Ryohei Yasuda at Max Planck Florida Institute for Neuroscience and Dr. James McNamara at Duke University Medical Center have uncovered critical details of the interplay of these molecules during synaptic plasticity. These exciting findings were published online ahead of print in September 2016 as two independent publications in Nature (1, 2).

A surprising signaling system within the spine

In one of the publications (Harward and Hedrick et al.), the authors identified an autocrine signaling system – a system where molecules act on the same cells that produce them – within single dendritic spines. This autocrine signaling system is achieved by rapid release of the protein, BDNF, from a stimulated spine and subsequent activation of its receptor, TrkB, on the same spine, which further activates signaling inside the spine. This in turn leads to spine enlargement, the process essential for synaptic plasticity. In other words, signaling initiated inside the spine goes outside the spine and activates a receptor on the external surface of the spine, thereby evoking additional signals inside the spine. This finding of an autocrine signaling process within the dendritic spines surprised the scientists.

What are the consequences of the autocrine signaling within the spine?

The second publication (Hedrick and Harward et al.) reports that the autocrine signaling leads to activation of an additional set of signaling molecules called small GTPase proteins. The findings reveal a three-molecule model of structural plasticity, which implicates the localized, coincident activation of three GTPase proteins Rac1, Cdc42, and RhoA, as a causal feature of structural plasticity. It is known that these proteins regulate the shape of dendritic spines, however, how they work together to control spine structure has remained unclear. The researchers monitored the spatiotemporal activation patterns of these molecules in single dendritic spines during synaptic plasticity and found that all three proteins are activated simultaneously, but their activation patterns differed significantly. One of the differences is that RhoA and Rac1, when activated, spread beyond the stimulated spine to the surrounding dendrite, which facilitates plasticity of surrounding spines. Another difference is that Cdc42 activity was restricted to the stimulated spine, what seems to be necessary to produce spine-specific plasticity. Furthermore, the autocrine BDNF signaling is required for activation of Cdc42 and Rac1, but not for RhoA.

Unprecedented insights into the regulation of synaptic plasticity

These two studies provide unprecedented insights into the regulation of synaptic plasticity. One study revealed for the first time an autocrine signaling system and the second study presented a unique form of biochemical computation in dendrites involving the controlled complementation of three molecules. According to Dr. Yasuda, understanding the molecular mechanisms that are responsible for the regulation of synaptic strength is critical for understanding how neural circuits function, how they form, and how they are shaped by experience. Dr. McNamara noted that disorder of these signaling systems likely underlies dysfunction of synapses that cause epilepsy and a diversity of other diseases of the brain. Because hundreds of species of proteins are involved in the signal transduction that regulates synaptic plasticity, it is essential to investigate the dynamics of more proteins to better understand the signaling mechanisms in dendritic spines.

Future research in the Yasuda and McNamara Labs is expected to lead to significant advances in the understanding of intracellular signaling in neurons and will provide key insights into the mechanisms underlying synaptic plasticity and memory formation and brain diseases. These insights will hopefully lead to the development of drugs that could enhance memory and prevent or more effectively treat epilepsy and other brain disorders.

The Brain’s Gardeners: Immune Cells ‘Prune’ Connections Between Neurons

A new study, published in the journal Nature Communications, shows that cells normally associated with protecting the brain from infection and injury also play an important role in rewiring the connections between nerve cells. While this discovery sheds new light on the mechanics of neuroplasticity, it could also help explain diseases like autism spectrum disorders, schizophrenia, and dementia, which may arise when this process breaks down and connections between brain cells are not formed or removed correctly.

(Image caption: Microglia (green) with purple representing the P2Y12 receptor which the study shows is a critical regulator in the process of pruning connections between nerve cells)

“We have long considered the reorganization of the brain’s network of connections as solely the domain of neurons,” said Ania Majewska, Ph.D., an associate professor in the Department of Neuroscience at the University of Rochester Medical Center (URMC) and senior author of the study. “These findings show that a precisely choreographed interaction between multiple cells types is necessary to carry out the formation and destruction of connections that allow proper signaling in the brain.”

The study is another example of a dramatic shift in scientists’ understanding of the role that the immune system, specifically cells called microglia, plays in maintaining brain function. Microglia have been long understood to be the sentinels of the central nervous system, patrolling the brain and spinal cord and springing into action to stamp out infections or gobble up dead cell tissue. However, scientists are now beginning to appreciate that, in addition to serving as the brain’s first line of defense, these cells also have a nurturing side, particularly as it relates to the connections between neurons.

The formation and removal of the physical connections between neurons is a critical part of maintaining a healthy brain and the process of creating new pathways and networks among brain cells enables us to absorb, learn, and memorize new information.  

“The brain’s network of connections is like a garden,” said Rebecca Lowery, a graduate student in Majewska’s lab and co-author of the study. “Not only does it require nourishment and a healthy environment, but every once in a while you need to prune dead branches and pull up weeds in order to allow new flowers to grow.”

While this constant reorganization of neural networks – called neuroplasticity – has been well understood for some time, the basic mechanisms by which connections between brain cells are made and broken has eluded scientists.

Performing experiments in mice, the researchers employed a well-established model of measuring neuroplasticity by observing how cells reorganize their connections when visual information received by the brain is reduced from two eyes to one.

The researchers found that in the mice’s brains microglia responded rapidly to changes in neuronal activity as the brain adapted to processing information from only one eye. They observed that the microglia targeted the synaptic cleft – the business end of the connection that transmits signals between neurons. The microglia “pulled up” the appropriate connections, physically disconnecting one neuron from another, while leaving other important connections intact.

This is similar to what occurs during an infection or injury, in which microglia are activated, quickly navigate towards the injured site, and remove dead or diseased tissue while leaving healthy tissue untouched.

The researchers also pinpointed one of the key molecular mechanisms in this process and observed that when a single receptor – called P2Y12 – was turned off the microglia ceased removing the connections between neurons.

These findings may provide new insight into disorders that are the characterized by sensory or cognitive dysfunction, such as autism spectrum disorders, schizophrenia, and dementia. It is possible that when the microglia’s synapse pruning function is interrupted or when the cells mistakenly remove the wrong connections – perhaps due to genetic factors or because the cells are too occupied elsewhere fighting an infection or injury – the result is impaired signaling between brain cells.

“These findings demonstrate that microglia are a dynamic and integral component of the complex machinery that allows neurons to reorganize their connections in the healthy mature brain,” said Grayson Sipe, a graduate student in Majewska’s lab and co-author of the study. “While more work needs to be done to fully understand this process, this study may help us understand how genetics or disruption of the immune system contributes to neurological disorders.”

DAY 2655

Jalsa, Mumbai                 July 19/20,  2015                Sun/Mon  12:22 am

You rest, you wake up, you bathe and dress, you wonder what was worn the previous Sunday, you decide what would be most appealing for the well wishers today, you make changes, you check from the office below - people in place, steps in place, ok … walking down to the masses … what will they do today .. will they scream, will they push and crush, will some petition, will some seek autograph and pictures .. how long should I remain there .. are they happy .. some Ef noticed .. acknowledging them with special smiles and waves and namaskaars … turing back .. close the gates .. a last look .. a last wave .. and back to the room ..

Now as the pictures get loaded, one sees the faces of elation and joy, of the keen vantage positions taken, of the poor little children riding piggy back on parent’s shoulders wondering why they are being subjected to this ordeal, of traffic snarls and irritated motorists who honk for space and desire to move on … of traffic sufferers, who write in as a response on FB, their disgust at this fake appreciation for a celebrity, and how the celebrity should care about the traffic, of how he should not hold these travellers to discomfort by coming out of his home, of how he should prevent this by hiring a ground near by and meet his fans or “whatever they are called” ( his words, not mine ), instead of causing this trouble for those that do not wish to see this old aged actor, of suggesting that the actor go to Juhu beach every Sunday and hold his “ meetings “ there since there is a “lot of space” and avoid the delays that he has to go through waiting for the crowds to clear so he can pass by on the road, for he has ‘no intention of seeing or meeting this third rate actor’ …

I would entirely agree with this responder on FB. This celebrity actor is indeed an old aged man, and most certainly a third rate actor .. 

BUT .. Mr Suffering Motorist .. I am in no way going to leave my house to locations that you so generously suggest, to meet my well wishers .. they are like family to me, and I shall meet my family at home not on the beach .. !!!

GOT IT … !!

It is a foregone conclusion in the minds of some - you cannot have the benefit of celebrity and be correct and good. Celebrity comes along with arrogance and rudeness, of disrespect and discourtesy, rudeness, impoliteness, incivility, unmannerliness, lack of respect, lack of civility, ungraciousness, irreverence, lack of consideration, ill/bad manners; insolence, impudence, impertinence, cheek, flippancy, churlishness … !!!

And the slightest wrong done, must certainly be the work of them that categorise themselves with celeb status. Always .. anywhere, any place, any incident .. GET THAT BLOODY CELEBRITY ! THEY ARE THE BANE OF OUR EXISTENCE … THEY ARE THE ONES THAT CAUSE GRIEF AND PROBLEM ..!!

Errors and mistakes are not just the prerogatives of those that be common. They that are supposedly ‘uncommon’ are in it as well. We are all human and possess human tendencies of error .. we too are vulnerable and filled with inaccuracy .. but NOT with all the error and inaccuracy that transpires everywhere. 

Be not quick in your judgement. Be of some value of balance. Be of patient learning of fact. Give room. Give opportunity. Give required space before closing all the doors of your cerebrum - the portion of the brain .. responsible for the integration of complex sensory and neural functions and the initiation and coordination of voluntary activity in the body .. give life a chance .. you may be right, I agree, but you may also be entirely wrong ! What then !!??

Shall thou be in position or state to remove the crucifix. To extract the nails through the flesh of the innocent. To wipe away the blood of human blamelessness. Tell me .. THE NATION WANTS TO KNOW !!!

In life .. two things are perennial, constant, certain - DEATH and INCOME TAX ! Death has a period, Tax does not. One can perish and be removed from the earth, but not the tax. I wrote earlier about my regard and respect for the Revenue Department, and my encounters with them - some of trial and great discomfort, but mostly of fairness and exemplary gratitude.

I recently was sent a missive from the Department, which demonstrated the elegance with which they respect those that respect the law. The Commissioner of Service Tax sent a letter commending my payments and complimenting me for being among the top individuals in following the rules and regulations of the authority, of the correct maintenance of my books of accounts and wishing me well for this impeccable work, one among the many many others ..

Officers of the Establishment often come under fire for their attitude. I have always acknowledged that they are the most proficient learned and consummate managers of the nation. When we do bad, they will and have authority to penalise, prosecute and seek corrective measures. But .. when we do good, they also have the grace to acknowledge it. As they have done for me, and for which I am eternally grateful ..

Communication in today’s times is faster than most brains are able to even think. Responses are therefore needed to be in as rapid a manner as possible. Missing some, may result in rapid belief and subsequent accusation or opinion. Defeating formed or perceived opinion, is a trip to Pluto or Mars .. and at times one to the Sun - impossible to get close, and if you do, not a hope in hell to get back .. SINGED, BURNT AND EVAPORATED IN VACUOUS SPACE !! 

Some remark on the bare feet as I step out to greet the well wishers, and its relevance .. its nothing what many think it to be .. its just a state I am in .. 

And at times its good to feel what most ‘soles’ feel every day otherwise .. !!

Amitabh Bachchan

pringolio-deactivated20151026  asked:

About what the discussion you and the INFPs were having: I think what you guys were getting onto was the development of cognitive functions or neural connections in general. Neural plasticity is a thing and can be learned from the people around you; that's probably yet another reason mistypes happen and why MBTI as a system tends to be viewed nowadays as flawed. People in even this community are always saying how complex humans are - well, duh. There needs to be deeper analysis.

Whoa, hold on. Let me sort this out.

  1. Neural plasticity is a thing - yes. Fully endorse.
  2. Humans are complex - yes. Fully endorse.
  3. Neural plasticity is somehow related to MBTI - no. Disagree.

MBTI is not a science. It was the brainchild of two women who loved Jung but who were not even psychologists in their own right. Jung’s theories, in turn, are like many of the theories emerging from psychoanalysis around Freud’s time. In short, they are interesting and utterly unprovable. I am all for learning MBTI for fun, for a means of interpreting people and characters, for memes - but let’s not pretend that cognitive functions are scientifically sound. That’s like trying to prove the Oedipus Complex is a legitimate phenomenon: it’s always possible to say that someone is not accessing their unconscious if they don’t behave the way your theory dictates, or that they are simply unaware of their own cognitive functions.

Neural plasticity, on the other hand, is a scientific phenomenon. The brain is an incredible organ, capable of learning new things and overcoming severe injury to regain old skills. This is documented and accounted for statistically, with real evidence. It is biologically explainable and visible in the subjects’ brain scans. Take a look at the way phantom limbs work, for instance.

You should think of MBTI as a framework, but not a framework that your brain somehow inherently has. Your brain is not ‘an INFP brain,’ it’s just your brain, the functioning of which can be classified as INFP according to MBTI theory. It’s like assuming that all artists will produce more or less the same kind of artwork, when the label of ‘artist’ is actually just a convenient term for a group of people who have a common interest (art). You can think of your type, then, as a convenient term for a group of people who have a common way of thinking.

I will be perfectly clear about my beliefs: I love MBTI. I love that it has made me feel part of a sixteen-part whole, that it is elegant and relatively simple to learn. But I acknowledge that it is very flawed. What we need is not deeper analysis, it is to understand the limits of the theory so that we don’t overextend ourselves trying to make it apply to areas where it doesn’t belong. MBTI is a theory, a philosophy, an art - but not a science. If we want to continue to deal honestly with personality typology, we must recognize this fact and not tread on the toes of quantifiable psychology.

Fic: Attempt Number Nine

Android!Kurt au based off this piece of fanart by @i-wanna-be-a-klaine-ship-ranger. ~3.7k, AO3

It’s his ninth attempt. Three years of research and scrounging parts have led to this, and countless days before that, daydreaming, sketching, imagining. He’s spent a good portion of his inheritance. He barely goes out of the house anymore. His sleep schedule is fucked and he doesn’t really pay much attention to what he eats.

But if this works, it will be so worth it.

He presses record. “Android K-05, neural loop test, attempt number nine. This is Blaine Anderson speaking at–” he glances at his watch– “2:09 am EST, Wednesday 13th October, 2028. Commencing charging now.”

Blaine cranks the dial to the right, fingers hovering above the switch on his dashboard, headset on and ears covered. He feels static electricity crackle in the air around him.

“Complete,” he mutters as he reaches maximum charge power. “Here we go.” He drops his hand and flicks the switch, hoping beyond hope that this time, it will work.

In a second, a bright blue light glares among the wires and machinery of his workshop, throwing everything into deep highlights and shadows. He squeezes his eyes shut against the glare and winces when the loud squeal of the android energy turbines manages to break through his thick earmuffs. The thrum and throb of the power coursing through the network of cables reverberates right down to his feet. He cautiously squints his eyes open a little more–it’s never lasted this long before.

His heart is pounding in his chest as he reaches up to shield his eyes from the light, daring to hope–is it–could it actually be–

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