m i c r o b a t d y n a m o
  • April 17th
    1,130 notes
    Source

    scipsy:

    Images produced with Diffusion spectrum magnetic resonance imaging (DSI) a new tool developed by Van J Wedeen. Here’s an interview, and here’s a slide show.

    (via freshphotons)

  • August 30th
    264 notes
    Source
    fuckyeahneuroscience:

Neurons: Animated Cellular and Molecular Concepts
This is a really great illustrated (free!) online textbook of sorts that describes the basic neuron, from its anatomy to ion channels and neurotransmitter activity. The 8 chapters listed are:
Anatomy of a Neuron
Axonal Transport
Ions and Ion Channels
Resting Membrane Potential
Action Potential
Neurotransmitter Release
Postsynaptic Mechanisms
Removal of Neurotransmitter
Each section has illustrations and diagrams to help supplement your studies! Whether you want to start your foundation in neuroscience or give it a small refresher, definitely bookmark this resource.
fuckyeahneuroscience:

Neurons: Animated Cellular and Molecular Concepts
This is a really great illustrated (free!) online textbook of sorts that describes the basic neuron, from its anatomy to ion channels and neurotransmitter activity. The 8 chapters listed are:
Anatomy of a Neuron
Axonal Transport
Ions and Ion Channels
Resting Membrane Potential
Action Potential
Neurotransmitter Release
Postsynaptic Mechanisms
Removal of Neurotransmitter
Each section has illustrations and diagrams to help supplement your studies! Whether you want to start your foundation in neuroscience or give it a small refresher, definitely bookmark this resource.

    fuckyeahneuroscience:

    Neurons: Animated Cellular and Molecular Concepts

    This is a really great illustrated (free!) online textbook of sorts that describes the basic neuron, from its anatomy to ion channels and neurotransmitter activity. The 8 chapters listed are:

    • Anatomy of a Neuron
    • Axonal Transport
    • Ions and Ion Channels
    • Resting Membrane Potential
    • Action Potential
    • Neurotransmitter Release
    • Postsynaptic Mechanisms
    • Removal of Neurotransmitter

    Each section has illustrations and diagrams to help supplement your studies! Whether you want to start your foundation in neuroscience or give it a small refresher, definitely bookmark this resource.

    (via section5)

  • July 26th
    14 notes
    Modeling neuron death with real and simulated decapitations
One of the guiding principles of animal research is to minimize suffering. Care for your animals well, don’t carry out needless procedures, and, when it is time, kill them as painlessly as possible. With the strict ethical oversight within the university system, these ideals are rigorously enforced. But some questions are difficult to answer. For instance, what is the best way to kill an animal? Is a death that is presumed to be quick and relatively painless really so? 
A group of researchers from Radboud University of Nijmegen set out to answer this question for decapitation. Decapitation is sometimes preferred for euthanizing lab animals because the brain is not perfused with anesthetics during death, making it easier to analyze brain tissue post mortem.
But, if the death isn’t quick or nearly painless, then it shouldn’t be used. To get a bead on this question, the researchers observed the electro encephalograms (EEGs) from rats as they were decapitated. In line with previous research, they found that the amount of activity in the brain appeared to decrease rapidly. They reached this conclusion by analyzing the amount of power in the EEG signal, which decreased by half every 6 seconds after decapitation. After 30 seconds the EEG was recording nothing but noise, and you would think that nothing more interesting would happen.
But you would be wrong. At about the one minute mark, a single, low frequency pulse appeared. The Nijmegen group speculated that this is the time at which the neurons’ membrane potential fails, blocking further transmission of sodium ions. The nature of the EEG pulse indicated that a large portion of all the neurons in the brain were failing at the same time, leading to what the researchers referred to as a “wave of death.” They then went on to claim that this could be the basis for determining brain death, because, at that point, presumably, there is no return for the neurons.

(via Ars Technica) Modeling neuron death with real and simulated decapitations
One of the guiding principles of animal research is to minimize suffering. Care for your animals well, don’t carry out needless procedures, and, when it is time, kill them as painlessly as possible. With the strict ethical oversight within the university system, these ideals are rigorously enforced. But some questions are difficult to answer. For instance, what is the best way to kill an animal? Is a death that is presumed to be quick and relatively painless really so? 
A group of researchers from Radboud University of Nijmegen set out to answer this question for decapitation. Decapitation is sometimes preferred for euthanizing lab animals because the brain is not perfused with anesthetics during death, making it easier to analyze brain tissue post mortem.
But, if the death isn’t quick or nearly painless, then it shouldn’t be used. To get a bead on this question, the researchers observed the electro encephalograms (EEGs) from rats as they were decapitated. In line with previous research, they found that the amount of activity in the brain appeared to decrease rapidly. They reached this conclusion by analyzing the amount of power in the EEG signal, which decreased by half every 6 seconds after decapitation. After 30 seconds the EEG was recording nothing but noise, and you would think that nothing more interesting would happen.
But you would be wrong. At about the one minute mark, a single, low frequency pulse appeared. The Nijmegen group speculated that this is the time at which the neurons’ membrane potential fails, blocking further transmission of sodium ions. The nature of the EEG pulse indicated that a large portion of all the neurons in the brain were failing at the same time, leading to what the researchers referred to as a “wave of death.” They then went on to claim that this could be the basis for determining brain death, because, at that point, presumably, there is no return for the neurons.

(via Ars Technica)

    Modeling neuron death with real and simulated decapitations

    One of the guiding principles of animal research is to minimize suffering. Care for your animals well, don’t carry out needless procedures, and, when it is time, kill them as painlessly as possible. With the strict ethical oversight within the university system, these ideals are rigorously enforced. But some questions are difficult to answer. For instance, what is the best way to kill an animal? Is a death that is presumed to be quick and relatively painless really so? 

    A group of researchers from Radboud University of Nijmegen set out to answer this question for decapitation. Decapitation is sometimes preferred for euthanizing lab animals because the brain is not perfused with anesthetics during death, making it easier to analyze brain tissue post mortem.

    But, if the death isn’t quick or nearly painless, then it shouldn’t be used. To get a bead on this question, the researchers observed the electro encephalograms (EEGs) from rats as they were decapitated. In line with previous research, they found that the amount of activity in the brain appeared to decrease rapidly. They reached this conclusion by analyzing the amount of power in the EEG signal, which decreased by half every 6 seconds after decapitation. After 30 seconds the EEG was recording nothing but noise, and you would think that nothing more interesting would happen.

    But you would be wrong. At about the one minute mark, a single, low frequency pulse appeared. The Nijmegen group speculated that this is the time at which the neurons’ membrane potential fails, blocking further transmission of sodium ions. The nature of the EEG pulse indicated that a large portion of all the neurons in the brain were failing at the same time, leading to what the researchers referred to as a “wave of death.” They then went on to claim that this could be the basis for determining brain death, because, at that point, presumably, there is no return for the neurons.

    (via Ars Technica)

  • July 8th
    21 notes
    In Eyes, a Clock Calibrated by Wavelengths of Light
Just as the ear has two purposes — hearing and telling you which way is up — so does the eye. It receives the input necessary for vision, but the retina also houses a network of sensors that detect the rise and fall of daylight. With light, the body sets its internal clock to a 24-hour cycle regulating an estimated 10 percent of our genes.
The workhorse of this system is the light-sensitive hormone melatonin, which is produced by the body every evening and during the night. Melatonin promotes sleep and alerts a variety of biological processes to the approximate hour of the day.
Light hitting the retina suppresses the production of melatonin — and there lies the rub. In this modern world, our eyes are flooded with light well after dusk, contrary to our evolutionary programming. Scientists are just beginning to understand the potential health consequences. The disruption of circadian cycles may not just be shortchanging our sleep, they have found, but also contributing to a host of diseases.
“Light works as if it’s a drug, except it’s not a drug at all,” said George Brainard, a neurologist at Thomas Jefferson University in Philadelphia and one of the first researchers to study light’s effects on the body’s hormones and circadian rhythms.
Any sort of light can suppress melatonin, but recent experiments have raised novel questions about one type in particular: the blue wavelengths produced by many kinds of energy-efficient light bulbs and electronic gadgets.
Dr. Brainard and other researchers have found that light composed of blue wavelengths slows the release of melatonin with particular effectiveness. Until recently, though, few studies had directly examined how blue-emitting electronics might affect the brain.

(via NYTimes.com) In Eyes, a Clock Calibrated by Wavelengths of Light
Just as the ear has two purposes — hearing and telling you which way is up — so does the eye. It receives the input necessary for vision, but the retina also houses a network of sensors that detect the rise and fall of daylight. With light, the body sets its internal clock to a 24-hour cycle regulating an estimated 10 percent of our genes.
The workhorse of this system is the light-sensitive hormone melatonin, which is produced by the body every evening and during the night. Melatonin promotes sleep and alerts a variety of biological processes to the approximate hour of the day.
Light hitting the retina suppresses the production of melatonin — and there lies the rub. In this modern world, our eyes are flooded with light well after dusk, contrary to our evolutionary programming. Scientists are just beginning to understand the potential health consequences. The disruption of circadian cycles may not just be shortchanging our sleep, they have found, but also contributing to a host of diseases.
“Light works as if it’s a drug, except it’s not a drug at all,” said George Brainard, a neurologist at Thomas Jefferson University in Philadelphia and one of the first researchers to study light’s effects on the body’s hormones and circadian rhythms.
Any sort of light can suppress melatonin, but recent experiments have raised novel questions about one type in particular: the blue wavelengths produced by many kinds of energy-efficient light bulbs and electronic gadgets.
Dr. Brainard and other researchers have found that light composed of blue wavelengths slows the release of melatonin with particular effectiveness. Until recently, though, few studies had directly examined how blue-emitting electronics might affect the brain.

(via NYTimes.com)

    In Eyes, a Clock Calibrated by Wavelengths of Light

    Just as the ear has two purposes — hearing and telling you which way is up — so does the eye. It receives the input necessary for vision, but the retina also houses a network of sensors that detect the rise and fall of daylight. With light, the body sets its internal clock to a 24-hour cycle regulating an estimated 10 percent of our genes.

    The workhorse of this system is the light-sensitive hormone melatonin, which is produced by the body every evening and during the night. Melatonin promotes sleep and alerts a variety of biological processes to the approximate hour of the day.

    Light hitting the retina suppresses the production of melatonin — and there lies the rub. In this modern world, our eyes are flooded with light well after dusk, contrary to our evolutionary programming. Scientists are just beginning to understand the potential health consequences. The disruption of circadian cycles may not just be shortchanging our sleep, they have found, but also contributing to a host of diseases.

    “Light works as if it’s a drug, except it’s not a drug at all,” said George Brainard, a neurologist at Thomas Jefferson University in Philadelphia and one of the first researchers to study light’s effects on the body’s hormones and circadian rhythms.

    Any sort of light can suppress melatonin, but recent experiments have raised novel questions about one type in particular: the blue wavelengths produced by many kinds of energy-efficient light bulbs and electronic gadgets.

    Dr. Brainard and other researchers have found that light composed of blue wavelengths slows the release of melatonin with particular effectiveness. Until recently, though, few studies had directly examined how blue-emitting electronics might affect the brain.

    (via NYTimes.com)

  • June 29th
     
Micro Machinist Takes on Bug Brains

Wired: What is it that you do?
Gus Lott: I think of it as reverse robotics. We’re dealing with organisms that have evolved circuits and adaptive-learning algorithms—mostly worms, fruit flies, and rodents—and we’re trying to develop tools that reverse-engineer how these natural machines work. We’re trying to figure out how nature built its own algorithm.

(via Wired Magazine)  
Micro Machinist Takes on Bug Brains

Wired: What is it that you do?
Gus Lott: I think of it as reverse robotics. We’re dealing with organisms that have evolved circuits and adaptive-learning algorithms—mostly worms, fruit flies, and rodents—and we’re trying to develop tools that reverse-engineer how these natural machines work. We’re trying to figure out how nature built its own algorithm.

(via Wired Magazine)

    Micro Machinist Takes on Bug Brains

    Wired: What is it that you do?

    Gus Lott: I think of it as reverse robotics. We’re dealing with organisms that have evolved circuits and adaptive-learning algorithms—mostly worms, fruit flies, and rodents—and we’re trying to develop tools that reverse-engineer how these natural machines work. We’re trying to figure out how nature built its own algorithm.

    (via Wired Magazine)

  • June 21st
    9 notes
    Growing a Brain in a Dish
Source.
That doughnut shape decorated with bright green spots, some connected by red pathways, amidst sky blue neighbors could be an artist’s creation, but is the result of a creative scientific attempt to grow an active brain in a dish, complete with memories. Really.

Researchers at the University of Pittsburgh published this stunning study in the journal Lab on a Chip {the full paper can be accessed here.} When I first learned how to grow cells in a lab, the technique of tissue culture, the idea of even growing brain cells was a far-fetched dream, much less brain cells capable of forming networks, complete with biological signals.
How did they do it?
To produce the models, the Pitt team stamped adhesive proteins onto silicon discs. Once the proteins were cultured and dried, cultured hippocampus cells from embryonic rats were fused to the proteins and then given time to grow and connect to form a natural network. The researchers disabled the cells’ inhibitory response and then excited the neurons with an electrical pulse.
Zeringue and his colleagues were able to sustain the resulting burst of network activity for up to what in neuronal time is 12 long seconds. Compared to the natural duration of .25 seconds at most, the model’s 12 seconds permitted an extensive observation of how the neurons transmitted and held the electrical charge, Zeringue said.


(via Dean’s Corner
) Growing a Brain in a Dish
Source.
That doughnut shape decorated with bright green spots, some connected by red pathways, amidst sky blue neighbors could be an artist’s creation, but is the result of a creative scientific attempt to grow an active brain in a dish, complete with memories. Really.

Researchers at the University of Pittsburgh published this stunning study in the journal Lab on a Chip {the full paper can be accessed here.} When I first learned how to grow cells in a lab, the technique of tissue culture, the idea of even growing brain cells was a far-fetched dream, much less brain cells capable of forming networks, complete with biological signals.
How did they do it?
To produce the models, the Pitt team stamped adhesive proteins onto silicon discs. Once the proteins were cultured and dried, cultured hippocampus cells from embryonic rats were fused to the proteins and then given time to grow and connect to form a natural network. The researchers disabled the cells’ inhibitory response and then excited the neurons with an electrical pulse.
Zeringue and his colleagues were able to sustain the resulting burst of network activity for up to what in neuronal time is 12 long seconds. Compared to the natural duration of .25 seconds at most, the model’s 12 seconds permitted an extensive observation of how the neurons transmitted and held the electrical charge, Zeringue said.


(via Dean’s Corner
)

    Growing a Brain in a Dish

    Source.

    That doughnut shape decorated with bright green spots, some connected by red pathways, amidst sky blue neighbors could be an artist’s creation, but is the result of a creative scientific attempt to grow an active brain in a dish, complete with memories. Really.

    Researchers at the University of Pittsburgh published this stunning study in the journal Lab on a Chip {the full paper can be accessed here.} When I first learned how to grow cells in a lab, the technique of tissue culture, the idea of even growing brain cells was a far-fetched dream, much less brain cells capable of forming networks, complete with biological signals.

    How did they do it?

    To produce the models, the Pitt team stamped adhesive proteins onto silicon discs. Once the proteins were cultured and dried, cultured hippocampus cells from embryonic rats were fused to the proteins and then given time to grow and connect to form a natural network. The researchers disabled the cells’ inhibitory response and then excited the neurons with an electrical pulse.

    Zeringue and his colleagues were able to sustain the resulting burst of network activity for up to what in neuronal time is 12 long seconds. Compared to the natural duration of .25 seconds at most, the model’s 12 seconds permitted an extensive observation of how the neurons transmitted and held the electrical charge, Zeringue said.

    (via Dean’s Corner

    )

  • May 31st
    1 note
    Ads Implant False Memories

It turns out that vivid commercials are incredibly good at tricking the hippocampus (a center of long-term memory in the brain) into believing that the scene we just watched on television actually happened. And it happened to us…scientists refer to this as the “false experience effect,” since the ads are slyly weaving fictional experiences into our very real lives.

(via Wired.com) Ads Implant False Memories

It turns out that vivid commercials are incredibly good at tricking the hippocampus (a center of long-term memory in the brain) into believing that the scene we just watched on television actually happened. And it happened to us…scientists refer to this as the “false experience effect,” since the ads are slyly weaving fictional experiences into our very real lives.

(via Wired.com)

    Ads Implant False Memories

    It turns out that vivid commercials are incredibly good at tricking the hippocampus (a center of long-term memory in the brain) into believing that the scene we just watched on television actually happened. And it happened to us…scientists refer to this as the “false experience effect,” since the ads are slyly weaving fictional experiences into our very real lives.

    (via Wired.com)

  • May 19th
    95 notes
    Source
    Similarities between actual structures is entirely contextual.

Maybe Similarities between actual structures is entirely contextual.

Maybe

    Similarities between actual structures is entirely contextual.

    Maybe

    (via physicsphysics)

  • December 2nd
    Get Better At Math By Disrupting Your Brain

How the study worked: Over six days, 15 adult subjects were asked to learn the association between nine arbitrary symbols without knowing the quantity that had been assigned to them. The learning phase lasted for nearly two hours each day, and for the first 20 minutes of each daily session, subjects were exposed to transcranial direct current stimulation of their parietal lobes.
The parietal lobes are thought to be critical regions in the processing of magnitudes and the representation of numbers. Individuals who have difficulties with numbers have been found to have anomalies of the right parietal lobe, and the right parietal lobe is also thought to be critical for the development of numerical understanding during childhood.
At the end of the learning phase, the subjects’ newly created number sense was measured using various tests. The goal of the study was to assess whether modifying activity in the parietal lobes affected the acquisition of number competence.
If the brain functions by optimizing behavior, it might be possible to worsen numerical competence by disrupting parietal function, but it should not be possible to enhance it that way. However, that is precisely what Cohen Kadosh’s team found. Remarkably, this improvement was still present six months after the training.
What are we to make of this? It has become increasingly apparent that complex brain functions — such as coordinated movement, memory, language, or mathematical thinking — depend critically on dynamic interactions between brain areas. This is the concept of “functional connectivity networks” — distributed brain regions transiently interacting to perform a particular neural function.
(via Get Better At Math By Disrupting Your Brain: Scientific American)
Get Better At Math By Disrupting Your Brain

How the study worked: Over six days, 15 adult subjects were asked to learn the association between nine arbitrary symbols without knowing the quantity that had been assigned to them. The learning phase lasted for nearly two hours each day, and for the first 20 minutes of each daily session, subjects were exposed to transcranial direct current stimulation of their parietal lobes.
The parietal lobes are thought to be critical regions in the processing of magnitudes and the representation of numbers. Individuals who have difficulties with numbers have been found to have anomalies of the right parietal lobe, and the right parietal lobe is also thought to be critical for the development of numerical understanding during childhood.
At the end of the learning phase, the subjects’ newly created number sense was measured using various tests. The goal of the study was to assess whether modifying activity in the parietal lobes affected the acquisition of number competence.
If the brain functions by optimizing behavior, it might be possible to worsen numerical competence by disrupting parietal function, but it should not be possible to enhance it that way. However, that is precisely what Cohen Kadosh’s team found. Remarkably, this improvement was still present six months after the training.
What are we to make of this? It has become increasingly apparent that complex brain functions — such as coordinated movement, memory, language, or mathematical thinking — depend critically on dynamic interactions between brain areas. This is the concept of “functional connectivity networks” — distributed brain regions transiently interacting to perform a particular neural function.
(via Get Better At Math By Disrupting Your Brain: Scientific American)

    Get Better At Math By Disrupting Your Brain

    How the study worked: Over six days, 15 adult subjects were asked to learn the association between nine arbitrary symbols without knowing the quantity that had been assigned to them. The learning phase lasted for nearly two hours each day, and for the first 20 minutes of each daily session, subjects were exposed to transcranial direct current stimulation of their parietal lobes.

    The parietal lobes are thought to be critical regions in the processing of magnitudes and the representation of numbers. Individuals who have difficulties with numbers have been found to have anomalies of the right parietal lobe, and the right parietal lobe is also thought to be critical for the development of numerical understanding during childhood.

    At the end of the learning phase, the subjects’ newly created number sense was measured using various tests. The goal of the study was to assess whether modifying activity in the parietal lobes affected the acquisition of number competence.

    If the brain functions by optimizing behavior, it might be possible to worsen numerical competence by disrupting parietal function, but it should not be possible to enhance it that way. However, that is precisely what Cohen Kadosh’s team found. Remarkably, this improvement was still present six months after the training.

    What are we to make of this? It has become increasingly apparent that complex brain functions — such as coordinated movement, memory, language, or mathematical thinking — depend critically on dynamic interactions between brain areas. This is the concept of “functional connectivity networks” — distributed brain regions transiently interacting to perform a particular neural function.

    (via Get Better At Math By Disrupting Your Brain: Scientific American)

  • August 12th
    This is a rather interesting article.
Inception and the Neuroscience of Sleep | Science Not Fiction

…Due to its need for invasive experiments, neuroscience typically works with non-human animals, which raises a significant difficulty: how do you know that a rat is dreaming? You can’t wake it up from REM sleep and ask. (Well, you can, but don’t expect a cogent response.) There’s no accepted objective indicator that a person or animal is having a dream, as opposed to sleeping. But, we can still learn something useful by looking at the neuroscience of sleep.
The neuroscience of sleep has told us a few important things over the years. For example, we know that our pattern of sleep and wakefulness (the “circadian rhythm”) has much of its basis in the activity of the suprachiasmatic nucleus, a rice-grained-sized group of cells just above where the optic nerves from our eyes crossover. We know that our free running rhythm—what we go to if we are completely in the dark, with no indicator of solar activity—is slightly over 24 hours, and that the length of the rhythm can be affected by things like cannabinoids found in pot. We know that the brain activity of a person dreaming is very similar to that of an awake person—were it not for the fact that our body is paralyzed during dreaming, we’d probably do a lot of things we’d regret.
While we’ve made a lot of progress in understanding sleep, we’ve a long way to go to understand dreaming. What makes it a challenge, perhaps as big a challenge as understanding consciousness itself, is the subjective aspect of dreaming. For example, we know that vivid dreaming occurs during REM sleep in humans. We also know that other animals have REM sleep. Do they also dream? How can we know, since, as I mentioned above, we can’t wake them during REM sleep and ask (the way we determined this fact with humans)? How we can go from objective facts like the presence of REM sleep to subjective ones, like a dream of a pink elephant bouncing down along a high tension power line (from one of my own dreams) is as unclear as how we get from neurons firing to awareness. Nonetheless, significant work has occurred on some of the neuronal correlates of REM sleeping in rodents and songbirds.
The most intriguing result from recent work is that during sleeping, the brain appears to “play back” patterns of activity that occurred during the day. For example, Matt Wilson and colleagues have found that patterns of “place cell” activity — brain cells that light up, like crumbs left on Hansel and Gretel’s path in the woods, corresponding to a specific path that the animal (in these experiments, a rodent) took during the day — and this playback seems to be integral to the animal learning the path it took. In birdsong, from work by Dan Margoliash and others, we’ve learned that birds playback patterns of activity almost identical to singing while they sleep, and again, it seems to be integral to the bird learning its large repertoire of over a million syllables. Why does the brain play back patterns of daytime activity at night? It isn’t completely understood, but some backstory on memory research helps motivate one hypothesis.
It’s been known for some time that a structure called the hippocampus is responsible for acquisition of new memories. Without it, we still have our memories, but anything new that happens is completely lost (think of the movie Memento, one of Christpher Nolan’s previous films) — we are stuck in the continual present. Real-life patient HM taught us this many years ago, after he had this structure removed as part of an experimental operation to cure his epilepsy. He, and many similar cases, lose all memory but for those events that happened some time before the loss of their hippocampus, typically a few months. Over time, the idea has emerged that perhaps the hippocampus “trains” the neural networks in other regions of the brain to store memories through repeated playback during sleep. Like crickets trying to attract females in the night, in the world of memory nothing succeeds like persistent repetition.
This is a rather interesting article.
Inception and the Neuroscience of Sleep | Science Not Fiction

…Due to its need for invasive experiments, neuroscience typically works with non-human animals, which raises a significant difficulty: how do you know that a rat is dreaming? You can’t wake it up from REM sleep and ask. (Well, you can, but don’t expect a cogent response.) There’s no accepted objective indicator that a person or animal is having a dream, as opposed to sleeping. But, we can still learn something useful by looking at the neuroscience of sleep.
The neuroscience of sleep has told us a few important things over the years. For example, we know that our pattern of sleep and wakefulness (the “circadian rhythm”) has much of its basis in the activity of the suprachiasmatic nucleus, a rice-grained-sized group of cells just above where the optic nerves from our eyes crossover. We know that our free running rhythm—what we go to if we are completely in the dark, with no indicator of solar activity—is slightly over 24 hours, and that the length of the rhythm can be affected by things like cannabinoids found in pot. We know that the brain activity of a person dreaming is very similar to that of an awake person—were it not for the fact that our body is paralyzed during dreaming, we’d probably do a lot of things we’d regret.
While we’ve made a lot of progress in understanding sleep, we’ve a long way to go to understand dreaming. What makes it a challenge, perhaps as big a challenge as understanding consciousness itself, is the subjective aspect of dreaming. For example, we know that vivid dreaming occurs during REM sleep in humans. We also know that other animals have REM sleep. Do they also dream? How can we know, since, as I mentioned above, we can’t wake them during REM sleep and ask (the way we determined this fact with humans)? How we can go from objective facts like the presence of REM sleep to subjective ones, like a dream of a pink elephant bouncing down along a high tension power line (from one of my own dreams) is as unclear as how we get from neurons firing to awareness. Nonetheless, significant work has occurred on some of the neuronal correlates of REM sleeping in rodents and songbirds.
The most intriguing result from recent work is that during sleeping, the brain appears to “play back” patterns of activity that occurred during the day. For example, Matt Wilson and colleagues have found that patterns of “place cell” activity — brain cells that light up, like crumbs left on Hansel and Gretel’s path in the woods, corresponding to a specific path that the animal (in these experiments, a rodent) took during the day — and this playback seems to be integral to the animal learning the path it took. In birdsong, from work by Dan Margoliash and others, we’ve learned that birds playback patterns of activity almost identical to singing while they sleep, and again, it seems to be integral to the bird learning its large repertoire of over a million syllables. Why does the brain play back patterns of daytime activity at night? It isn’t completely understood, but some backstory on memory research helps motivate one hypothesis.
It’s been known for some time that a structure called the hippocampus is responsible for acquisition of new memories. Without it, we still have our memories, but anything new that happens is completely lost (think of the movie Memento, one of Christpher Nolan’s previous films) — we are stuck in the continual present. Real-life patient HM taught us this many years ago, after he had this structure removed as part of an experimental operation to cure his epilepsy. He, and many similar cases, lose all memory but for those events that happened some time before the loss of their hippocampus, typically a few months. Over time, the idea has emerged that perhaps the hippocampus “trains” the neural networks in other regions of the brain to store memories through repeated playback during sleep. Like crickets trying to attract females in the night, in the world of memory nothing succeeds like persistent repetition.

    This is a rather interesting article.

    Inception and the Neuroscience of Sleep | Science Not Fiction

    …Due to its need for invasive experiments, neuroscience typically works with non-human animals, which raises a significant difficulty: how do you know that a rat is dreaming? You can’t wake it up from REM sleep and ask. (Well, you can, but don’t expect a cogent response.) There’s no accepted objective indicator that a person or animal is having a dream, as opposed to sleeping. But, we can still learn something useful by looking at the neuroscience of sleep.

    The neuroscience of sleep has told us a few important things over the years. For example, we know that our pattern of sleep and wakefulness (the “circadian rhythm”) has much of its basis in the activity of the suprachiasmatic nucleus, a rice-grained-sized group of cells just above where the optic nerves from our eyes crossover. We know that our free running rhythm—what we go to if we are completely in the dark, with no indicator of solar activity—is slightly over 24 hours, and that the length of the rhythm can be affected by things like cannabinoids found in pot. We know that the brain activity of a person dreaming is very similar to that of an awake person—were it not for the fact that our body is paralyzed during dreaming, we’d probably do a lot of things we’d regret.

    While we’ve made a lot of progress in understanding sleep, we’ve a long way to go to understand dreaming. What makes it a challenge, perhaps as big a challenge as understanding consciousness itself, is the subjective aspect of dreaming. For example, we know that vivid dreaming occurs during REM sleep in humans. We also know that other animals have REM sleep. Do they also dream? How can we know, since, as I mentioned above, we can’t wake them during REM sleep and ask (the way we determined this fact with humans)? How we can go from objective facts like the presence of REM sleep to subjective ones, like a dream of a pink elephant bouncing down along a high tension power line (from one of my own dreams) is as unclear as how we get from neurons firing to awareness. Nonetheless, significant work has occurred on some of the neuronal correlates of REM sleeping in rodents and songbirds.

    The most intriguing result from recent work is that during sleeping, the brain appears to “play back” patterns of activity that occurred during the day. For example, Matt Wilson and colleagues have found that patterns of “place cell” activity — brain cells that light up, like crumbs left on Hansel and Gretel’s path in the woods, corresponding to a specific path that the animal (in these experiments, a rodent) took during the day — and this playback seems to be integral to the animal learning the path it took. In birdsong, from work by Dan Margoliash and others, we’ve learned that birds playback patterns of activity almost identical to singing while they sleep, and again, it seems to be integral to the bird learning its large repertoire of over a million syllables. Why does the brain play back patterns of daytime activity at night? It isn’t completely understood, but some backstory on memory research helps motivate one hypothesis.

    It’s been known for some time that a structure called the hippocampus is responsible for acquisition of new memories. Without it, we still have our memories, but anything new that happens is completely lost (think of the movie Memento, one of Christpher Nolan’s previous films) — we are stuck in the continual present. Real-life patient HM taught us this many years ago, after he had this structure removed as part of an experimental operation to cure his epilepsy. He, and many similar cases, lose all memory but for those events that happened some time before the loss of their hippocampus, typically a few months. Over time, the idea has emerged that perhaps the hippocampus “trains” the neural networks in other regions of the brain to store memories through repeated playback during sleep. Like crickets trying to attract females in the night, in the world of memory nothing succeeds like persistent repetition.

  • May 15th
    Magnetically Induced  Hallucinations Explain Ball Lightning, Say Physicists
Transcranial magnetic stimulation (TMS) is an extraordinary technique  pioneered by neuroscientists to explore the workings of the brain.  The  idea is to place a human in a rapidly changing magnetic field that is  powerful enough to induce currents in neurons in the brain. Then sit  back and see what happens.
Since TMS was invented in the 1980s, it has become a powerful way of  investigating how the brain works. Because the fields can be tightly  focused, it is possible to generate currents in very specific areas of  the brain to see what they do.
Focus the field in the visual cortex, for example, and the induced  eddys cause the subject to ‘see’ lights that appear as discs and lines.  Move the the field within the cortex and the subject sees the lights  move too.
All that much is repeatable in the lab using giant superconducting  magnets capable of creating fields of as much as 0.5 Tesla inside the  brain.
But if this happens in the lab, then why not in the real world too,  say Joseph Peer and Alexander Kendl at the University of Innsbruck in  Austria. They calculate that the rapidly changing fields associated with  repeated lightning strikes  are powerful enough to cause a similar  phenomenon in humans within 200 metres.
(via) Magnetically Induced  Hallucinations Explain Ball Lightning, Say Physicists
Transcranial magnetic stimulation (TMS) is an extraordinary technique  pioneered by neuroscientists to explore the workings of the brain.  The  idea is to place a human in a rapidly changing magnetic field that is  powerful enough to induce currents in neurons in the brain. Then sit  back and see what happens.
Since TMS was invented in the 1980s, it has become a powerful way of  investigating how the brain works. Because the fields can be tightly  focused, it is possible to generate currents in very specific areas of  the brain to see what they do.
Focus the field in the visual cortex, for example, and the induced  eddys cause the subject to ‘see’ lights that appear as discs and lines.  Move the the field within the cortex and the subject sees the lights  move too.
All that much is repeatable in the lab using giant superconducting  magnets capable of creating fields of as much as 0.5 Tesla inside the  brain.
But if this happens in the lab, then why not in the real world too,  say Joseph Peer and Alexander Kendl at the University of Innsbruck in  Austria. They calculate that the rapidly changing fields associated with  repeated lightning strikes  are powerful enough to cause a similar  phenomenon in humans within 200 metres.
(via)

    Magnetically Induced Hallucinations Explain Ball Lightning, Say Physicists

    Transcranial magnetic stimulation (TMS) is an extraordinary technique pioneered by neuroscientists to explore the workings of the brain. The idea is to place a human in a rapidly changing magnetic field that is powerful enough to induce currents in neurons in the brain. Then sit back and see what happens.

    Since TMS was invented in the 1980s, it has become a powerful way of investigating how the brain works. Because the fields can be tightly focused, it is possible to generate currents in very specific areas of the brain to see what they do.

    Focus the field in the visual cortex, for example, and the induced eddys cause the subject to ‘see’ lights that appear as discs and lines. Move the the field within the cortex and the subject sees the lights move too.

    All that much is repeatable in the lab using giant superconducting magnets capable of creating fields of as much as 0.5 Tesla inside the brain.

    But if this happens in the lab, then why not in the real world too, say Joseph Peer and Alexander Kendl at the University of Innsbruck in Austria. They calculate that the rapidly changing fields associated with repeated lightning strikes are powerful enough to cause a similar phenomenon in humans within 200 metres.

    (via)

  • September 3rd
    1 note
    Source
    whisperoftheshot:

Clemson University researcher Nina Zhang created brain-in-a-tube, a biogel that regrows injured brain tissue.  There is a possibility of human use in 3 years!
“These results that we are seeing in adult lab rats are the first of its kind and show a sustained functional recovery in the animal model of TBI (traumatic brain injury). It also represents one of very few in the traumatic brain injury field that attempts structural repair of the lesion cavity using a tissue-engineering approach.”
(via io9)

EXCITEMENT! whisperoftheshot:

Clemson University researcher Nina Zhang created brain-in-a-tube, a biogel that regrows injured brain tissue.  There is a possibility of human use in 3 years!
“These results that we are seeing in adult lab rats are the first of its kind and show a sustained functional recovery in the animal model of TBI (traumatic brain injury). It also represents one of very few in the traumatic brain injury field that attempts structural repair of the lesion cavity using a tissue-engineering approach.”
(via io9)

EXCITEMENT!

    whisperoftheshot:

    Clemson University researcher Nina Zhang created brain-in-a-tube, a biogel that regrows injured brain tissue.  There is a possibility of human use in 3 years!

    “These results that we are seeing in adult lab rats are the first of its kind and show a sustained functional recovery in the animal model of TBI (traumatic brain injury). It also represents one of very few in the traumatic brain injury field that attempts structural repair of the lesion cavity using a tissue-engineering approach.”

    (via io9)

    EXCITEMENT!

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