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)
“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.”
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
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
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?)
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.
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.
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.
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
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.
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 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
“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.”
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
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.
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.
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
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
“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.