neuronal connections
The Purpose of Sleep: To forget, Scientists say  sleep may help the brain prune back unneeded synapses.
By Carl Zimmer

A PET scan of a brain during normal sleep.

by Carl Zimmer

Over the years, scientists have come up with a lot of ideas about why we sleep.

Some have argued that it’s a way to save energy. Others have suggested that slumber provides an opportunity to clear away the brain’s cellular waste. Still others have proposed that sleep simply forces animals to lie still, letting them hide from predators.

A pair of papers published on Thursday in the journal Science offer evidence for another notion: We sleep to forget some of the things we learn each day.

In order to learn, we have to grow connections, or synapses, between the neurons in our brains. These connections enable neurons to send signals to one another quickly and efficiently. We store new memories in these networks.

In 2003, Giulio Tononi and Chiara Cirelli, biologists at the University of Wisconsin-Madison, proposed that synapses grew so exuberantly during the day that our brain circuits got “noisy.” When we sleep, the scientists argued, our brains pare back the connections to lift the signal over the noise.

In the years since, Dr. Tononi and Dr. Cirelli, along with other researchers, have found a great deal of indirect evidence to support the so-called synaptic homeostasis hypothesis.

(excerpt - click the link for the complete article) 

anonymous asked:

there is no difference between the brains of men and women. try harder, misogynist.

Female brains have a higher percentage of grey matter.

“While measuring brain activity with magnetic resonance imaging during blood pressure trials, UCLA researchers found that men and women had opposite responses in the right front of the insular cortex.”

“The female brain appears to have increased connection between neurons in the right and left hemispheres of the brain, and males seem to have increased neural communication within hemispheres from frontal to rear portions of the organ.”

Here are some other links with information on the differences between male and female brains:

But I guess science is just misogynistic.

The human brain is the most complicated thing in the universe. Hundreds of billions of neurons; literal quadrillions of connections between them; Even now, our incredibly advanced science is barely scratching the surface of its true complexity. So complicated is it that some have posited that we never will understand it, not because we won’t be trying but simply because doing so would be theoretically impossible. Whatever the truth may be, it certainly stands as the greatest intellectual challenge to confront humankind and it will take thousands of geniuses hundreds of years to etc etc

anyways yours is fucking up and if you can’t explain to me why and how in a way i can understand i’m going to assume that you’re lying to me about your needs

Repetition Physically Changes Your Brain

Have you ever wondered what a memory is exactly and how it gets   formed? You have hundreds, thousands, perhaps millions of memories in   your brain. Songs you remember how to sing. Scenes from movies. Memories  of last year’s holiday. Facts such as the names of all the planets, and  on and on. Do you know what a memory is and how it gets created?

Neurons firing – There are 10 billion neurons in   your brain that store information. Electrical impulses flow through a   neuron and are moved by neuron-transmitting chemicals across the   synaptic gap between neurons. Neurons in your brain fire every time you repeat a word, phrase, song, or phone number you are trying to memorize.  Memories are stored as patterns of connections between neurons.

Keep reading

anonymous asked:

Cyboy, that's just the thing- You CAN remember. You've already proven that you KNOW the name, so eventually, you might just be able to remember ALL of it. Please... Here, perhaps this will ring some bells- You rode a gigantic nuke into the middle of new york, all the while fighting with Akari before you two became lovers... You traveled back in time with Mare when you inadvertently killed Rachel, and changed the course of space-time... You did so many amazing things- And you CAN recall them.

*Neurons start connecting…memories start to be restored…slowly*
Wait…wait….WAIT! Ummm…uhmmm…I..uhh…I think I remember some of that stuff!
( @hexadecimalhell , cyboy is beginning to regain memories. Engage target?)

Supporting the damaged brain

A new study shows that embryonic nerve cells can functionally integrate into local neural networks when transplanted into damaged areas of the visual cortex of adult mice.

(Image caption: Neuronal transplants (blue) connect with host neurons (yellow) in the adult mouse brain in a highly specific manner, rebuilding neural networks lost upon injury. Credit: Sofia Grade, LMU/Helmholtz Zentrum München)

When it comes to recovering from insult, the adult human brain has very little ability to compensate for nerve-cell loss. Biomedical researchers and clinicians are therefore exploring the possibility of using transplanted nerve cells to replace neurons that have been irreparably damaged as a result of trauma or disease. Previous studies have suggested there is potential to remedy at least some of the clinical symptoms resulting from acquired brain disease through the transplantation of fetal nerve cells into damaged neuronal networks. However, it is not clear whether transplanted intact neurons can be sufficiently integrated to result in restored function of the lesioned network. Now researchers based at LMU Munich, the Max Planck Institute for Neurobiology in Martinsried and the Helmholtz Zentrum München have demonstrated that, in mice, transplanted embryonic nerve cells can indeed be incorporated into an existing network in such a way that they correctly carry out the tasks performed by the damaged cells originally found in that position. Such work is of importance in the potential treatment of all acquired brain disease including neurodegenerative illnesses such as Alzheimer‘s or Parkinson’s disease, as well as strokes and trauma, given each disease state leads to the large-scale, irreversible loss of nerve cells and the acquisition of a what is usually a lifelong neurological deficit for the affected person.

In the study published in Nature, researchers of the Ludwig Maximilians University Munich, the Max Planck Institute of Neurobiology, and the Helmholtz Zentrum München have specifically asked whether transplanted embryonic nerve cells can functionally integrate into the visual cortex of adult mice. “This region of the brain is ideal for such experiments,” says Magdalena Götz, joint leader of the study together with Mark Hübener. Hübener is a specialist in the structure and function of the mouse visual cortex in Professor Tobias Bonhoeffer’s Department (Synapses – Circuits – Plasticity) at the MPI for Neurobiology. As Hübener explains, “we know so much about the functions of the nerve cells in this region and the connections between them that we can readily assess whether the implanted nerve cells actually perform the tasks normally carried out by the network.” In their experiments, the team transplanted embryonic nerve cells from the cerebral cortex into lesioned areas of the visual cortex of adult mice. Over the course of the following weeks and months, they monitored the behavior of the implanted, immature neurons by means of two-photon microscopy to ascertain whether they differentiated into so-called pyramidal cells, a cell type normally found in the area of interest. “The very fact that the cells survived and continued to develop was very encouraging,” Hübener remarks. “But things got really exciting when we took a closer look at the electrical activity of the transplanted cells.” In their joint study, PhD student Susanne Falkner and Postdoc Sofia Grade were able to show that the new cells formed the synaptic connections that neurons in their position in the network would normally make, and that they responded to visual stimuli.

The team then went on to characterize, for the first time, the broader pattern of connections made by the transplanted neurons. Astonishingly, they found that pyramidal cells derived from the transplanted immature neurons formed functional connections with the appropriate nerve cells all over the brain. In other words, they received precisely the same inputs as their predecessors in the network. In addition, they were able to process that information and pass it on to the downstream neurons which had also differentiated in the correct manner. “These findings demonstrate that the implanted nerve cells have integrated with high precision into a neuronal network into which, under normal conditions, new nerve cells would never have been incorporated,” explains Götz, whose work at the Helmholtz Zentrum and at LMU focuses on finding ways to replace lost neurons in the central nervous system. The new study reveals that immature neurons are capable of correctly responding to differentiation signals in the adult mammalian brain and can close functional gaps in an existing neural network.

The human brain has 100 billion neurons, each neuron connected to 10 thousand other neurons. Sitting on your shoulders is the most complicated object in the known universe.
—  Michio Kaku
Researchers Shed Light on How Neurons Exchange Neurotransmitters

For more than a century, neuroscientists have known that nerve cells talk to one another across the small gaps between them, a process known as synaptic transmission (synapses are the connections between neurons). Information is carried from one cell to the other by neurotransmitters such as glutamate, dopamine, and serotonin, which activate receptors on the receiving neuron to convey excitatory or inhibitory messages.

But beyond this basic outline, the details of how this crucial aspect of brain function occurs have remained elusive. Now, new research by scientists at the University of Maryland School of Medicine (UM SOM) has for the first time elucidated details about the architecture of this process. The paper was published in the journal Nature.

Synapses are very complicated molecular machines. They are also tiny: only a few millionths of an inch across. They have to be incredibly small, since we need a lot of them; the brain has around 100 trillion of them, and each is individually and precisely tuned to convey stronger or weaker signals between cells.

To visualize features on this sub-microscopic scale, the researchers turned to an innovative technology known as single-molecule imaging, which can locate and track the movement of individual protein molecules within the confines of a single synapse, even in living cells. Using this approach, the scientists identified an unexpected and precise pattern in the process of neurotransmission. The researchers looked at cultured rat synapses, which in terms of overall structure are very similar to human synapses.

(Image caption: Synapses visualized in live neurons. The overall structure of one cell in a dense network of interconnected neurons is visible from expression of a red and green fluorescent protein that fills that cell entirely)

“We are seeing things that have never been seen before. This is a totally new area of investigation,” said Thomas Blanpied, PhD, Associate Professor in the Department of Physiology, and leader of the group that performed the work. “For many years, we’ve had a list of the many types of molecules that are found at synapses, but that didn’t get us very far in understanding how these molecules fit together, or how the process really works structurally. Now by using single-molecule imaging to map where many of the key proteins are, we have finally been able to reveal the core architectural structure of the synapse.”

In the paper, Blanpied describes an unexpected aspect to this architecture that may explain why synapses are so efficient, but also susceptible to disruption during disease: at each synapse, key proteins are organized very precisely across the gap between cells. “The neurons do a better job than we ever imagined of positioning the release of neurotransmitter molecules near their receptors,” Blanpied says. “The proteins in the two different neurons are aligned with incredible precision, almost forming a column stretching between the two cells.” This proximity optimizes the power of the transmission, and also suggests new ways that this transmission can be modified.

Blanpied’s lab has created a video representation of the process.

Understanding this architecture will help clarify how communication within the brain works, or, in the case of psychiatric or neurological disease, how it fails to work. Blanpied is also focusing on the activity of “adhesion molecules,” which stretch from one cell to the other and may be important pieces of the “nano-column.” He suspects that if adhesion molecules are not placed correctly at the synapse, synapse architecture will be disrupted, and neurotransmitters won’t be able to do their jobs. Blanpied hypothesizes that in at least some disorders, the issue may be that even though the brain has the right amount of neurotransmitter, the synapses don’t transmit these molecules efficiently.

Blanpied says that this improved comprehension of synaptic architecture could lead to a better understanding of brain diseases such as depression, schizophrenia and Alzheimer’s disease, and perhaps suggest new ideas for treatments.

Blanpied and his colleagues will next explore whether the synaptic architecture changes in certain disorders: they will begin by looking at a synapses in a mouse model of the pathology in schizophrenia.

“The complexity of the human brain seems overwhelming. But Dr. Blanpied and his colleagues have taken an important step in helping us understand this system,” said UM SOM Dean E. Albert Reece MD, PhD, MBA, who is also vice president for medical affairs at the University of Maryland and the John Z. and Akiko K. Bowers Distinguished Professor. “This study is impressive scientifically, and it is just the first step of what I am sure will be a long series of important discoveries about the brain and its 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.”

Here’s the thing: The brain is a complex thing, but it is horrifically badly designed.

In terms of how signals pass through from input to output, it’s sort of like an ant colony. An ant going from point A to point B will probably manage to do so in a reasonable time, but it’s almost never going to be a simple, straight-forward route. Neurons connect to neurons without concern for what those other neurons process, neurochemicals are released by completely unrelated processes that affect calculations, and even the engineering of neurons themselves leaves them open to error.

Your brain adapts to this by learning, but it’s a case of evolutionary engineering in real-time. New calculations are built on top of old ones, and few are ever rewritten cleanly.

What this amounts to is that the human brain is terrible at certainty, it’s awful at consistency, and in general it’s kind of a miracle it does anything reliably outside of homeostasis (which it still occasionally fouls up).

Your opinions will change. Your ideas will change. Your tastes will change. Your sexuality, your gender, what you thought of Terminator 3, everything can change and probably will at least a little bit over time.

Few things in the brain are static.

This does not mean they were wrong then or even that they are now right, only that they have changed and probably will again later down the road, maybe a day or maybe decades later. Don’t mistake change for error.

We are creatures of water, and like water, we flow.