Theory for so long. Now a little evidence. Awesome.

medicalschool:

A Short Video About the Life of Neurons

radiopaedia:

Case of the day: Pericallosal lipoma. VIEW CASE: http://goo.gl/KKWuC via our Facebook page

radiopaedia:

Case of the day: Pericallosal lipoma. VIEW CASE: http://goo.gl/KKWuC

via our Facebook page

ucsdhealthsciences:

Rewriting a Receptor’s RoleSynaptic molecule works differently than thought; may mean new therapeutic targets for treating Alzheimer’s disease
In a pair of new papers, researchers at the University of California, San Diego School of Medicine and the Royal Netherlands Academy of Arts and Sciences upend a long-held view about the basic functioning of a key receptor molecule involved in signaling between neurons, and describe how a compound linked to Alzheimer’s disease impacts that receptor and weakens synaptic connections between brain cells.
The findings are published in the Feb. 18 early edition of the Proceedings of the National Academy of Sciences.
Long the object of study, the NMDA receptor is located at neuronal synapses – the multitudinous junctions where brain cells trade electrical and chemical messages. In particular, NMDA receptors are ion channels activated by glutamate, a major “excitatory” neurotransmitter associated with cognition, learning and memory.
“NMDA receptors are well known to allow the passage of calcium ions into cells and thereby trigger biochemical signaling,” said principal investigator Roberto Malinow, MD, PhD professor of neurosciences at UC San Diego School of Medicine.
The new research, however, indicates that NMDA receptors can also operate independent of calcium ions. “It turns upside down a view held for decades regarding how NMDA receptors function,” said Malinow, who holds the Shiley-Marcos Endowed Chair in Alzheimer’s Disease Research in Honor of Dr. Leon Thal (a renowned UC San Diego Alzheimer’s disease researcher who died in a single-engine airplane crash in 2007).
Specifically, Malinow and colleagues found that glutamate binding to the NMDA receptor caused conformational changes in the receptor that ultimately resulted in a weakened synapse and impaired brain function.
They also found that beta amyloid – a peptide that comprises the neuron-killing plaques associated with Alzheimer’s disease – causes the NMDA receptor to undergo conformational changes that also lead to the weakening of synapses.
“These new findings overturn commonly held views regarding synapses and potentially identify new targets in the treatment of Alzheimer’s disease,” said Malinow.

ucsdhealthsciences:

Rewriting a Receptor’s Role
Synaptic molecule works differently than thought; may mean new therapeutic targets for treating Alzheimer’s disease

In a pair of new papers, researchers at the University of California, San Diego School of Medicine and the Royal Netherlands Academy of Arts and Sciences upend a long-held view about the basic functioning of a key receptor molecule involved in signaling between neurons, and describe how a compound linked to Alzheimer’s disease impacts that receptor and weakens synaptic connections between brain cells.

The findings are published in the Feb. 18 early edition of the Proceedings of the National Academy of Sciences.

Long the object of study, the NMDA receptor is located at neuronal synapses – the multitudinous junctions where brain cells trade electrical and chemical messages. In particular, NMDA receptors are ion channels activated by glutamate, a major “excitatory” neurotransmitter associated with cognition, learning and memory.

“NMDA receptors are well known to allow the passage of calcium ions into cells and thereby trigger biochemical signaling,” said principal investigator Roberto Malinow, MD, PhD professor of neurosciences at UC San Diego School of Medicine.

The new research, however, indicates that NMDA receptors can also operate independent of calcium ions. “It turns upside down a view held for decades regarding how NMDA receptors function,” said Malinow, who holds the Shiley-Marcos Endowed Chair in Alzheimer’s Disease Research in Honor of Dr. Leon Thal (a renowned UC San Diego Alzheimer’s disease researcher who died in a single-engine airplane crash in 2007).

Specifically, Malinow and colleagues found that glutamate binding to the NMDA receptor caused conformational changes in the receptor that ultimately resulted in a weakened synapse and impaired brain function.

They also found that beta amyloid – a peptide that comprises the neuron-killing plaques associated with Alzheimer’s disease – causes the NMDA receptor to undergo conformational changes that also lead to the weakening of synapses.

“These new findings overturn commonly held views regarding synapses and potentially identify new targets in the treatment of Alzheimer’s disease,” said Malinow.

5 Scientific Reasons Why Breakups Are Devastating

Link to Original Article

image

Raise your hand if you’ve never heard any of the following lines, in one form or another:

  • Let’s be friends
  • I think we should see other people.
  • It’s not you. It’s me
  • I just don’t love you anymore.

If you’ve finished reading this list and your hand is raised, please bring it down to face level. Cup your hand to your cheek. Pull it back three to five inches, and, traveling at an increased velocity, slap yourself firmly on the face. Why? If you haven’t experienced rejection from a breakup, this exercise serves as a simulation of what rejection feels like. Actually, a slap in the face is much more pleasant than rejection.

Chances are, though, you didn’t raise your hand. I’m willing to bet that if you are reading this article, you are, unfortunately, familiar with the pain of rejection from a breakup.

Rejection Is Physiologically Heart-Breaking

"Rejection" comes from Latin, meaning thrown back. When we are rejected, we feel not only halted, but pushed back in the opposite direction of which we were headed. Now consider this: When rejected, how do we describe the event? We tend to say, "I was rejected." Notice what is going on here. We are using passive voice. This indicates how we feel about the part we play in rejection. We view ourselves as passive, as being the victim of an action, as inactive, as non-participative.

Read More

Scientists read dreams

from: Nature 

Brain scans during sleep can decode visual content of dreams.

19 October 2012

Scientists have learned how to discover what you are dreaming about while you sleep.

A team of researchers led by Yukiyasu Kamitani of the ATR Computational Neuroscience Laboratories in Kyoto, Japan, used functional neuroimaging to scan the brains of three people as they slept, simultaneously recording their brain waves using electroencephalography (EEG).

Researchers in Japan can predict certain features of dreams by looking at the brain activity of sleeping volunteers.

The researchers woke the participants whenever they detected the pattern of brain waves associated with sleep onset, asked them what they had just dreamed about, and then asked them to go back to sleep.

This was done in three-hour blocks, and repeated between seven and ten times, on different days, for each participant. During each block, participants were woken up ten times per hour. Each volunteer reported having visual dreams six or seven times every hour, giving the researchers a total of around 200 dream reports.

Perchance to dream

Most of the dreams reflected everyday experiences, but some contained unusual content, such as talking to a famous actor. The researchers extracted key words from the participants’ verbal reports, and picked 20 categories — such as ‘car’, ‘male’, ‘female’, and ‘computer’ — that appeared most frequently in their dream reports.

Kamitani and his colleagues then selected photos representing each category, scanned the participants’ brains again while they viewed the images, and compared brain activity patterns with those recorded just before the participants were woken up.

The researchers analysed activity in brain areas V1, V2 and V3, which are involved in the earliest stages of visual processing and encode basic features of visual scenes, such as contrast and the orientation of edges. They also looked at several other regions that are involved in higher order visual functions, such as object recognition.

In 2008, Kamitani and his colleagues reported that they could decode brain activity associated with the earliest stages of visual processing to reconstruct images shown to participants. Now, they have found that activity in the higher order brain regions could accurately predict the content of the participants’ dreams.

“We built a model to predict whether each category of content was present in the dreams,” says Kamitani. “By analysing the brain activity during the nine seconds before we woke the subjects, we could predict whether a man is in the dream or not, for instance, with an accuracy of 75–80%.”

The findings, presented at the annual meeting of the Society for Neuroscience in New Orleans, Louisiana, earlier this week, suggest that dreaming and visual perception share similar neural representations in the higher order visual areas of the brain.

“This is an interesting and exciting piece of work,” says neuroscientist Jack Gallant at the University of California, Berkeley, of the work presented at the meeting. “It suggests that dreaming involves some of the same higher level visual brain areas that are involved in visual imagery.”

“It also seems to suggest that our recall of dreams is based on short-term memory, because dream decoding was most accurate in the tens of seconds before waking,” he adds.

Kamitani and his colleagues are now trying to collect the same kind of data from the rapid eye movement (REM) stage of sleep, which is also associated with dreaming. “This is more challenging because we have to wait at least one hour before sleeping subjects reach that stage,” Kamitani says.

But the extra effort will be worth it, he says. “Knowing more about the content of dreams and how it relates to brain activity may help us to understand the function of dreaming.”

Central and peripheral nervous system. Thanks imgur.

Central and peripheral nervous system. Thanks imgur.

ucsdhealthsciences:

Neural Stem Cells Regenerate Axons in Severe Spinal Cord InjuryNew relay circuits, formed across sites of complete spinal transaction, result in functional recovery in ratsIn a study at the University of California, San Diego and VA San Diego Healthcare, researchers were able to regenerate “an astonishing degree” of axonal growth at the site of severe spinal cord injury in rats.  Their research revealed that early stage neurons have the ability to survive and extend axons to form new, functional neuronal relays across an injury site in the adult central nervous system (CNS).   The study also proved that at least some types of adult CNS axons can overcome a normally inhibitory growth environment to grow over long distances.  Importantly, stem cells across species exhibit these properties. The work will be published in the journal Cell on September 14. (For a history of spinal cord repair science and the significance of this latest work, read Ohio State University neuroscientist Phillip Popovich’s review here.) The UC San Diego-led team embedded neural stem cells in a matrix of fibrin (a protein key to blood-clotting that is already used in human neuron procedures), mixed with growth factors to form a gel.  The gel was then applied to the injury site in rats with completely severed spinal cords.“Using this method, after six weeks, the number of axons emerging from the injury site exceeded by 200-fold what had ever been seen before,” said Mark Tuszynski, MD, PhD, professor in the UC San Diego Department of Neurosciences and director of the UCSD Center for Neural Repair, who headed the study. “The axons also grew 10 times the length of axons in any previous study and, importantly, the regeneration of these axons resulted in significant functional improvement.”In addition, adult cells above the injury site regenerated into the neural stem cells, establishing a new relay circuit that could be measured electrically. “By stimulating the spinal cord four segments above the injury and recording this electrical stimulation three segments below, we detected new relays across the transaction site,” said Tuszynski. To confirm that the mechanism underlying recovery was due to formation of new relays, when rats recovered, their spinal cords were re-transected above the implant.  The rats lost motor function – confirming formation of new relays across the injury.  The grafting procedure resulted in significant functional improvement: On a 21-point walking scale, without treatment, the rats score was only 1.5; following the stem cell therapy, it rose to 7 – a score reflecting the animals’ ability to move all joints of affected legs.Results were then replicated using two human stem cell lines, one already in human trials for ALS.  “We obtained the exact results using human cells as we had in the rat cells,” said Tuszynski.The study made use of green fluorescent proteins (GFP), a technique that had never before been used to track neural stem cell growth. “By tagging the cells with GFP, we were able to observe the stem cells grow, become neurons and grow axons, showing us the full ability of these cells to grow and make connections with the host neurons,” said first author Paul Lu, PhD, assistant research scientist at UCSD’s Center for Neural Repair. “This is very exciting, because the technology didn’t exist before.”Pictured: Artist’s rendering of neurons

ucsdhealthsciences:

Neural Stem Cells Regenerate Axons in Severe Spinal Cord Injury
New relay circuits, formed across sites of complete spinal transaction, result in functional recovery in rats

In a study at the University of California, San Diego and VA San Diego Healthcare, researchers were able to regenerate “an astonishing degree” of axonal growth at the site of severe spinal cord injury in rats.  Their research revealed that early stage neurons have the ability to survive and extend axons to form new, functional neuronal relays across an injury site in the adult central nervous system (CNS).  

The study also proved that at least some types of adult CNS axons can overcome a normally inhibitory growth environment to grow over long distances.  Importantly, stem cells across species exhibit these properties. The work will be published in the journal Cell on September 14.

(For a history of spinal cord repair science and the significance of this latest work, read Ohio State University neuroscientist Phillip Popovich’s review here.)

The UC San Diego-led team embedded neural stem cells in a matrix of fibrin (a protein key to blood-clotting that is already used in human neuron procedures), mixed with growth factors to form a gel.  The gel was then applied to the injury site in rats with completely severed spinal cords.

“Using this method, after six weeks, the number of axons emerging from the injury site exceeded by 200-fold what had ever been seen before,” said Mark Tuszynski, MD, PhD, professor in the UC San Diego Department of Neurosciences and director of the UCSD Center for Neural Repair, who headed the study. “The axons also grew 10 times the length of axons in any previous study and, importantly, the regeneration of these axons resulted in significant functional improvement.”

In addition, adult cells above the injury site regenerated into the neural stem cells, establishing a new relay circuit that could be measured electrically. “By stimulating the spinal cord four segments above the injury and recording this electrical stimulation three segments below, we detected new relays across the transaction site,” said Tuszynski.

To confirm that the mechanism underlying recovery was due to formation of new relays, when rats recovered, their spinal cords were re-transected above the implant.  The rats lost motor function – confirming formation of new relays across the injury. 

The grafting procedure resulted in significant functional improvement: On a 21-point walking scale, without treatment, the rats score was only 1.5; following the stem cell therapy, it rose to 7 – a score reflecting the animals’ ability to move all joints of affected legs.

Results were then replicated using two human stem cell lines, one already in human trials for ALS.  “We obtained the exact results using human cells as we had in the rat cells,” said Tuszynski.

The study made use of green fluorescent proteins (GFP), a technique that had never before been used to track neural stem cell growth. “By tagging the cells with GFP, we were able to observe the stem cells grow, become neurons and grow axons, showing us the full ability of these cells to grow and make connections with the host neurons,” said first author Paul Lu, PhD, assistant research scientist at UCSD’s Center for Neural Repair. “This is very exciting, because the technology didn’t exist before.”

Pictured: Artist’s rendering of neurons

Liquefactive necrosis of the brain. Liquefactive necrosis is a type of tissue necrosis (cell death) which occurs primarily in brain tissue and abscesses. This type of necrosis is characterized by the degradation of tissue and replacement by a viscous mass. Here, you can see the liquid quality of the necrosis. While many other tissues will scar, the brain does not have the necessary machinery to generate a fibrotic scar. 

Liquefactive necrosis of the brain. Liquefactive necrosis is a type of tissue necrosis (cell death) which occurs primarily in brain tissue and abscesses. This type of necrosis is characterized by the degradation of tissue and replacement by a viscous mass. Here, you can see the liquid quality of the necrosis. While many other tissues will scar, the brain does not have the necessary machinery to generate a fibrotic scar. 

Cerebral atrophy.
Death of neurons and other CNS tissues leads to cerebral atrophy. Here you can clearly see the increasing size of the sulci (valleys) as well as narrowing gyri (hills). Cerebral atrophy often occurs as the result of neurodegenerative diseases such as Alzheimer’s. It can also arise following a cerebral infarction. 

Cerebral atrophy.

Death of neurons and other CNS tissues leads to cerebral atrophy. Here you can clearly see the increasing size of the sulci (valleys) as well as narrowing gyri (hills). Cerebral atrophy often occurs as the result of neurodegenerative diseases such as Alzheimer’s. It can also arise following a cerebral infarction.