Posts tagged science

May 7, 2012

Erxi Wu, assistant professor of pharmaceutical sciences, and Shuang Zhou, a doctoral student in Wu’s lab, co-wrote the article, “Smilagenin Attenuates Beta Amyloid (25-35)-Induced Degeneration of Neuronal Cells via Stimulating the Gene Expression of Brain-Derived Neurotrophic Factor,” which will be published by Neuroscience. They collaborated with Yaer Hu lab at Shanghai Jiaotong University, China, for the publication.

According to the authors, the development of drugs that weaken neurodegeneration is important for the treatment of Alzheimer’s disease. They previously found that smilagenin, a steroidal sapogenin from traditional Chinese medicinal herbs that improves memory in animal models, is neither a cholinesterase inhibitor nor a glutamate receptor antagonist, but can significantly elevate the declined muscarinic receptor (M receptor density). In this paper, to clarify whether smilagenin represents a new approach for treating neurodegeneration disease, they first demonstrate that smilagenin pretreatment significantly attenuates the neurodegenerative changes induced by beta amyloid 25-35 (Aβ25-35) in cultured rat cortical neurons, including decreased cholinergic neuron number, shortened neurite outgrowth length and declined muscarinic receptor density. Brain-derived neurotrophic factor protein in the culture medium was also decreased by Aβ25-35 and significantly elevated by smilagenin. 

Parallel experiments revealed that when the trk receptors were inhibited by K252a or the action of brain-derived neurotrophic factor was inhibited by a neutralizing anti- brain-derived neurotrophic factor antibody, the effects of smilageninon the Aβ25-35 induced neurodegeneration in rat cortical neurons were almost completely abolished. In the all-trans retinoic acid-differentiated SH-SY5Y neuroblastoma cells, the brain-derived neurotrophic factortranscription rate measured by a nuclear run-on assay was significantly suppressed by Aβ25-35 and elevated by SMI, but the brain-derived neurotrophic factor degradation rate measured by half-life determination was unchanged by Aβ25-35 and smilagenin. Transcript analysis of the SH-SY5Y cells using quantitative RT-PCR showed that the IV and VI transcripts of brain-derived neurotrophic factor mRNA were significantly decreased by Aβ25-35 and elevated by smilagenin. 

“Taken together, this study concludes that smilagenin attenuates Aβ25-35-induced neurodegeneration in cultured rat cortical neurons and SH-SY5Y cells mainly through stimulating brain-derived neurotrophic factor mRNA transcription implicating that SMI may represent a novel therapeutic strategy for Alzheimer’s disease,” Wu said. “Collaborating with Dr. Hu at Shanghai Jiaotong University, China, we together would like to find better therapeutics and elucidate the mechanisms of the potential novel therapy for Alzheimer’s disease,” Wu said.

Provided by North Dakota State University

Source: medicalxpress.com

May 6, 2012

Gaining access to the inner workings of a neuron in the living brain offers a wealth of useful information: its patterns of electrical activity, its shape, even a profile of which genes are turned on at a given moment. However, achieving this entry is such a painstaking task that it is considered an art form; it is so difficult to learn that only a small number of labs in the world practice it.

Researchers at MIT and the Georgia Institute of Technology have developed a way to automate a process called whole-cell patch clamping, which involves bringing a tiny hollow glass pipette in contact with the cell membrane of a neuron, then opening up a small pore in the membrane to record the electrical activity within the cell. Credit: Sputnik Animation and MIT McGovern Institute

But that could soon change: Researchers at MIT and the Georgia Institute of Technology have developed a way to automate the process of finding and recording information from neurons in the living brain. The researchers have shown that a robotic arm guided by a cell-detecting computer algorithm can identify and record from neurons in the living mouse brain with better accuracy and speed than a human experimenter.

The new automated process eliminates the need for months of training and provides long-sought information about living cells’ activities. Using this technique, scientists could classify the thousands of different types of cells in the brain, map how they connect to each other, and figure out how diseased cells differ from normal cells.

The project is a collaboration between the labs of Ed Boyden, associate professor of biological engineering and brain and cognitive sciences at MIT, and Craig Forest, an assistant professor in the George W. Woodruff School of Mechanical Engineering at Georgia Tech.

"Our team has been interdisciplinary from the beginning, and this has enabled us to bring the principles of precision machine design to bear upon the study of the living brain," Forest says. His graduate student, Suhasa Kodandaramaiah, spent the past two years as a visiting student at MIT, and is the lead author of the study, which appears in the May 6 issue of Nature Methods.

The method could be particularly useful in studying brain disorders such as schizophrenia, Parkinson’s disease, autism and epilepsy, Boyden says. “In all these cases, a molecular description of a cell that is integrated with [its] electrical and circuit properties … has remained elusive,” says Boyden, who is a member of MIT’s Media Lab and McGovern Institute for Brain Research. “If we could really describe how diseases change molecules in specific cells within the living brain, it might enable better drug targets to be found.”

Read more …

May 6, 2012 

Brain networks may avoid traffic jams at their busiest intersections by communicating on different frequencies, researchers at Washington University School of Medicine in St. Louis, the University Medical Center at Hamburg-Eppendorf and the University of Tübingen have learned.

"Many neurological and psychiatric conditions are likely to involve problems with signaling in brain networks," says co-author Maurizio Corbetta, MD, the Norman J. Stupp Professor of Neurology at Washington University. "Examining the temporal structure of brain activity from this perspective may be especially helpful in understanding psychiatric conditions like depression and schizophrenia, where structural markers are scarce."

The research will be published May 6 in Nature Neuroscience.

Scientists usually study brain networks — areas of the brain that regularly work together — using magnetic resonance imaging, which tracks blood flow. They assume that an increase in blood flow to part of the brain indicates increased activity in the brain cells of that region.

"Magnetic resonance imaging is a useful tool, but it does have limitations," Corbetta says. "It only allows us to track brain cell activity indirectly, and it is unable to track activity that occurs at frequencies greater than 0.1 hertz, or once every 10 seconds. We know that some signals in the brain can cycle as high as 500 hertz, or 500 times per second."

For the new study, conducted at the University Medical Center at Hamburg-Eppendorf, the researchers used a technique called magnetoencephalography (MEG) to analyze brain activity in 43 healthy volunteers. MEG detects very small changes in magnetic fields in the brain that are caused by many cells being active at once. It can detect these signals at rates up to 100 hertz.

"We found that different brain networks ticked at different frequencies, like clocks ticking at different speeds," says lead author Joerg Hipp, PhD, of the University Medical Center at Hamburg-Eppendorf and the University of Tübingen, both in Germany.

For example, networks that included the hippocampus, a brain area critical for memory formation, tended to be active at frequencies around 5 hertz. Networks constituting areas involved in the senses and movement were active between 32 hertz and 45 hertz. Many other brain networks were active at frequencies between eight and 32 hertz. These “time-dependent” networks resemble different airline route maps, overlapping but each ticking at a different rate.

"There have been a number of fMRI studies of depression and schizophrenia showing ‘spatial’ changes in the organization of brain networks," Corbettta says. "MEG studies provide a window into a much richer ‘temporal’ structure. In the future, this might offer new diagnostic tests or ways to monitor the efficacy of interventions in these debilitating mental conditions."

Provided by Washington University School of Medicine

Source: medicalxpress.com

ScienceDaily (May 4, 2012) — Researchers in Spain have found that at least some of the individuals claiming to see the so-called aura of people actually have the neuropsychological phenomenon known as “synesthesia” (specifically, “emotional synesthesia”). This might be a scientific explanation of their alleged ability.

New research suggests that at least some of the individuals claiming to see the so-called aura of people actually have the neuropsychological phenomenon known as “synesthesia” (specifically, “emotional synesthesia”). This might be a scientific explanation of their alleged ability. (Credit: © Nikki Zalewski / Fotolia)

In synesthetes, the brain regions responsible for the processing of each type of sensory stimuli are intensely interconnected. Synesthetes can see or taste a sound, feel a taste, or associate people or letters with a particular color.

The study was conducted by the University of Granada Department of Experimental Psychology Óscar Iborra, Luis Pastor and Emilio Gómez Milán, and has been published in the journal Consciousness and Cognition. This is the first time that a scientific explanation has been provided for the esoteric phenomenon of the aura, a supposed energy field of luminous radiation surrounding a person as a halo, which is imperceptible to most human beings.

In basic neurological terms, synesthesia is thought to be due to cross-wiring in the brain of some people (synesthetes); in other words, synesthetes present more synaptic connections than “normal” people. “These extra connections cause them to automatically establish associations between brain areas that are not normally interconnected,” professor Gómez Milán explains. New research suggests that many healers claiming to see the aura of people might have this condition.

The case of the "Santón de Baza"

One of the University of Granada researchers remarked that “not all ‘healers’ are synesthetes, but there is a higher prevalence of this phenomenon among them. The same occurs among painters and artists, for example.” To carry out this study, the researchers interviewed some synesthetes including a ‘healer’ from Granada, “Esteban Sánchez Casas,” known as"El Santón de Baza".

Many local people attribute “paranormal powers” to El Santón, because of his supposed ability to see the aura of people “but, in fact, it is a clear case of synesthesia,” the researchers explained. According to the researchers, El Santón has face-color synesthesia (the brain region responsible for face recognition is associated with the color-processing region); touch-mirror synesthesia (when the synesthete observes a person who is being touched or is experiencing pain, s/he experiences the same); high empathy (the ability to feel what other person is feeling), and schizotypy (certain personality traits in healthy people involving slight paranoia and delusions). “These capacities make synesthetes have the ability to make people feel understood, and provide them with special emotion and pain reading skills,” the researchers explain.

In the light of the results obtained, the researchers remarked on the significant “placebo effect” that healers have on people, “though some healers really have the ability to see people’s ‘auras’ and feel the pain in others due to synesthesia.” Some healers “have abilities and attitudes that make them believe in their ability to heal other people, but it is actually a case of self-deception, as synesthesia is not an extrasensory power, but a subjective and ‘adorned’ perception of reality,” the researchers state.

Source: Science Daily

May 5, 2012 

In an effort to identify the underlying causes of neurological disorders that impair motor functions such as walking and breathing, UCLA researchers have developed a novel system to measure the communication between stem cell-derived motor neurons and muscle cells in a Petri dish.

The study provides an important proof of principle that functional motor circuits can be created outside of the body using stem cell-derived neurons and muscle cells, and that the level of communication, or synaptic activity, between the cells could be accurately measured by stimulating motor neurons with an electrode and then measuring the transfer of electrical activity into the muscle cells to which the motor neurons are connected.

When motor neurons are stimulated, they release neurotransmitters that depolarize the membranes of muscle cells, allowing the entry of calcium and other ions that cause them to contract. By measuring the strength of this activity, one can get a good estimation of the overall health of motor neurons. That estimation could shed light on a variety of neurodegenerative diseasessuch as spinal muscular atrophy and amyotrophic lateral sclerosis, or Lou Gehrig’s disease, in which the communication between motor neurons and muscle cells is thought to unravel, said study senior author Bennett G. Novitch, an assistant professor of neurobiology and a scientist with the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA.

The findings of the study appear May 4, 2012 in PLoS ONE, a peer-reviewed journal of the Public Library of Science.

"Now that we have this method to measure the strength of the communications between motor neurons and muscle cells, we may be able to begin exploring what happens in the earliest stages of motor neuron disease, before neuronal death becomes prevalent," Novitch said. "This can help us to pinpoint where things begin to go wrong and provide us with new clues into therapeutic interventions that could improve synaptic communication and promote neuronal survival."

Novitch said the synaptic communication activity his team was able to create and measure using mouse embryonic stem cell-derived motor neurons and muscle cells looks very similar what is seen in a mouse, validating that their model is a realistic representation of what is happening in a living organism.

"That gives us a good starting point to try to model what happens in cells that harbor genetic mutations that are associated with neurodegenerative diseases,. To do that, we had to first define an activity profile of normal synaptic communication," he said. "Some research suggests that a breakdown in this communication can be an early indication of disease progression or possibly an initiating event. Neurons that cannot effectively transmit information to muscle cells will eventually withdraw their contacts, causing both the neurons and muscle cells to degenerate over time. Hopefully, we can now create disease models that will allow us to study what is happening."

In this study, Novitch and his team, led by Joy Umbach, an associate professor of molecular and medical pharmacology, used mouse embryonic stem cells to create the motor neurons and previously established lines of muscle precursors to produce muscle fibers. They put both cells together in a Petri dish, and the cells were cultured in such a way to encourage communication. Novitch said the team wanted to see if they would naturally form synaptic contacts and whether or not there was neural transmission between them.

In less than a week, the neurons had reached out to the muscle cells and assembled the protein networks needed for synaptic communication, Novitch said.

To measure the connections between the cells, the scientists used a technique called dual patch clamp recording. Pipettes containing stimulating and recording electrodes are inserted into the membranes of the motor neurons and muscle cells, being careful not to injure them. With this method, they were able send an electrical current into the motor neurons and measure responses in the muscle cells, as well as visualize the muscular contractions.

"The in vitro system developed here might accordingly be expanded to assess the underlying cellular and molecular mechanisms that contribute to this decline in synaptic input to motor neurons," the study states. "Thus, in addition to their utility for helping to answer fundamental biological questions, these co-cultures have clear applications in addressing problems of medical significance."

Going forward, Novitch and his team hope to recreate and confirm the work using human stem cell-derived motor neurons and muscle cells and measure the synaptic communications with newly developed optical recording methods, which are less invasive than the patch clamp techniques used in this study.

Provided by University of California, Los Angeles

Source: medicalxpress.com

ScienceDaily (May 3, 2012) — Malfunctioning single proteins can cause disruptions in neuronal junctions leading to autistic forms of behavior. A current study, published in the scientific journal Nature, comes to this conclusion after examining genetically altered mice.

The study, in which scientists from Charité — Universitätsmedizin Berlin and the NeuroCure Cluster of Excellence contributed, thus supports the hypothesis that disruptions in neuronal junctions, i.e. synapses, could be the cause of the development of neuropsychiatric illnesses like autism. The international research team, that included scientists from Ulm University and the Institut Pasteur in Paris, ascribes a key role to the excitatory synapses. This finding could become an important step stone for future autism therapies.

Nerve cells communicate with each other via signal transmission to synaptic junctions. These junctions are stabilized through structural proteins, including the so-called ProSAP1/Shank2 protein. In order to understand the role that this protein has on synapses and ultimately in the development of autism, the researchers genetically modified mice and disabled the relevant protein. The choice of this protein was not arbitrary: In preparation for the current study, a number of the scientists involved found evidence that the mutation of this protein can lead to autism in humans. Various neuronal developmental disorders manifested through distinctive social and communicative behavioral features, as well as stereotyped behaviors are combined under the term of “autism.”

The absence of this structural protein in the mouse model also had visible implications: Animals with the mutated gene are hyperactive and demonstrate compulsive repetitions of particular features — like grooming, for example. In behavioral experiments, peculiarities in social and communicative interaction also become distinct. In the brains of the mice, researchers found noticeable mutations of synaptic junctions — specifically in excitatory synapses. When glutamate transmitters bind to glutamate receptors located at these junctions, the nerve cells become excitatory. If the mouse is lacking this structural protein, the transmitters increasingly find a related structural protein on the excitatory synapses, the ProSAP2/Shank3. This protein has also been implicated in the development of autism. At the same time, the composition of glutamate receptors mutates.

But what happens when this related structural protein in the mice is switched off? This is also examined in the study presented. The conclusion is that, in this case as well, mutations of the excitatory synapses occur. Obviously, both structural molecules alternate in fulfilling regular functions. “The study illustrates the significant role glutamatergic systems play in autism and thus contributes to understanding better synaptic changes in autism,” reports Stephanie Wegener, one of the participating scientists at Charité Berlin. The study is therefore an important part of the essential scientific foundation needed to develop possible therapies for autism.

Source: Science Daily

ScienceDaily (May 3, 2012) — The problems of living with bipolar have been well documented, but a new study by Lancaster University has captured the views of those who also report highly-valued, positive experiences of living with the condition.

Researchers at Lancaster’s Spectrum Centre, which is dedicated to the study of bipolar disorder, interviewed and recorded their views of ten people with a bipolar diagnosis, aged between 24 and 57. Participants in the study reported a number of perceived benefits to the condition ranging from to sharper senses to increased productivity.

The research was designed to explore growing evidence that some people with bipolar value their experiences and in some cases would prefer not to be without the condition.

Participants described a wide range of experiences and internal states that they believed they felt to a far greater intensity than those without the condition. These included increased perceptual sensitivity, creativity, focus and clarity of thought.

Some held (or had previously held) high functioning professional jobs or had been studying for higher level qualifications. They described in detail how they experienced times when tasks that are usually quite difficult or time consuming, would feel incredibly easy and the ability to achieve at a high level during these times was clearly immensely rewarding.

Others expressed the view that they felt ‘lucky’ or even ‘blessed’ to have the condition.

Alan, (not his real name) one of the interviewees, said: “It’s almost as if it opens up something in the brain that isn’t otherwise there, and I see colour much more vividly than I used to……So I think that my access to music and art are something for which I’m grateful to bipolar for enhancing. It’s almost as if it’s a magnifying glass that sits between that and myself.”

Researchers even found some people with bipolar reaped positive experiences from their lows such as greater empathy with the suffering of others.

Dr Fiona Lobban, who led the study, said: “Bipolar Disorder is generally seen as a severe and enduring mental illness with serious negative consequences for the people with this diagnosis and their friends and family. For some people this is very much the case. Research shows that long term unemployment rates are high, relationships are marred by high levels of burden on family and friends and quality of life is often poor. High rates of drug and alcohol misuse are reported for people with this diagnosis and suicide rates are twenty times that of the general population.

"However, despite all these factors researchers and clinicians are aware that that some aspects of bipolar experiences are also highly valued by some people. We wanted to find out what these positive experiences were.

"People were very keen to take part in this study and express views which some felt had to be hidden from the medical profession.

"It is really important that we learn more about the positives of bipolar as focusing only on negative aspects paints a very biased picture that perpetuates the view of bipolar as a wholly negative experience. If we fail to explore the positives of bipolar we also fail to understand the ambivalence of some people towards treatment."

Rita Long from Stockport was not part of the study but can identify with its findings. She was 40 when she was diagnosed with the condition but from her school days she was aware that she experienced the world differently to her twin sister.

"We were making Christmas cakes at school and I was so interested and excited by it and my sister says she remembers watching me and thinking, ‘I really wish I could get that excited about making a Christmas cake’. I noticed things, experienced them with a different level of intensity, we’d be on a walk and I’d be saying look at the colour of this, and my sister would be saying, ‘It’s just a berry’. Socially too, people with bipolar can be quite quick witted, humorous. Until much later in life I just presumed those things were part of my personality.

"I don’t want to underestimate how difficult the bad times can be that some people go through with bipolar but at the same time I feel very passionate about the positives. If we are going to move on as a society — in academia, in business, in entertainment — we need people who will push boundaries. People with bipolar can do that."

Source: Science Daily

ScienceDaily (May 3, 2012) — A team led by scientists at The Scripps Research Institute has shown that an extra copy of a brain-development gene, which appeared in our ancestors’ genomes about 2.4 million years ago, allowed maturing neurons to migrate farther and develop more connections.

A team led by Scripps Research Institute scientists has found evidence that, as humans evolved, an extra copy of a brain-development gene allowed neurons to migrate farther and develop more connections. (Credit: Photo courtesy of The Scripps Research Institute)

What genetic changes account for the vast behavioral differences between humans and other primates? Researchers so far have catalogued only a few, but now it seems that they can add a big one to the list. A team led by scientists at The Scripps Research Institute has shown that an extra copy of a brain-development gene, which appeared in our ancestors’ genomes about 2.4 million years ago, allowed maturing neurons to migrate farther and develop more connections.

Surprisingly, the added copy doesn’t augment the function of the original gene, SRGAP2, which makes neurons sprout connections to neighboring cells. Instead it interferes with that original function, effectively giving neurons more time to wire themselves into a bigger brain.

"This appears to be a major example of a genomic innovation that contributed to human evolution," said Franck Polleux, a professor at The Scripps Research Institute. "The finding that a duplicated gene can interact with the original copy also suggests a new way to think about how evolution occurs and might give us clues to human-specific developmental disorders such as autism and schizophrenia."

Read more …

ScienceDaily (May 3, 2012) — UCSF scientists have identified patterns of brain activity in the rat brain that play a role in the formation and recall of memories and decision-making. The discovery, which builds on the team’s previous findings, offers a path for studying learning, decision-making and post-traumatic stress syndrome.

Brain patterns through which the rats see rapid replays of past experiences are fundamental to their ability to make decisions. Disturbing those particular brain patterns impaired the animals’ ability to learn rules based on memories of things that had happened in the past. (Credit: © Oleg Kozlov / Fotolia)

The researchers previously identified patterns of brain activity in the rat hippocampus, a brain region critical for memory storage. The patterns sometimes represented where an animal was in space, and, at other times, represented fast-motion replays of places the animal had been, but no one knew whether these patterns indicated the process of memory formation and recollection.

In the journal Science this week (online May 3, 2012), the UCSF researchers demonstrated that the brain activity is critical for memory formation and recall. Moreover, they showed that the brain patterns through which the rats see rapid replays of past experiences are fundamental to their ability to make decisions. Disturbing those particular brain patterns impaired the animals’ ability to learn rules based on memories of things that had happened in the past.

"We think these memory-replay events are central to understanding how the brain retrieves past experiences and uses them to make decisions," said neuroscientist Loren Frank, PhD, a associate professor of physiology and a member of the Keck Center for Integrative Neuroscience at UCSF, who led the research with Shantanu Jadhav, PhD, a post-doctoral fellow. "They offer insight into how a past experience can have such a profound effect on how we think and feel."

The finding gives scientists a new way to investigate fundamental processes like learning and decision-making in animals and in people. It also may help shed light on memory disorders like post-traumatic stress disorder (PTSD), which is characterized by strong, disturbing and uncontrolled memories.

Without Links to the Past, Rats Face Indecision

Seeking to understand how the recall of specific memories in the brain guides our thinking, Frank and his colleagues built a system for detecting the underlying patterns of neuronal activity in rats. They fitted the animals with electrodes and built a system that enabled them to detect a specific pattern, called a sharp-wave ripple, in the hippocampus. Whenever they detected a ripple, they would send a small amount of electricity into another set of electrodes that would immediately interrupt the ripple event, in effect turning off all memory replay activity without otherwise affecting the brain.

The UCSF researchers knew that these sharp-wave ripples would be activated when the animals had to make choices about which direction to turn as they wended their way toward their reward: a few drops of sweetened condensed milk. These signals seem to be flashes of memory recall, said Frank, a rat’s past knowledge flooding back to inform it on what had happened in the past and where it might go in the future. Squashing the sharp-wave ripples, the UCSF team found, disrupted the recall and subverted the rat’s ability to correctly navigate the maze.

This shows, said Frank, that the sharp-wave ripples are critical for this type of memory recall. Through these brain waves, the rat reprocesses and replays old experiences in a fleeting instant — lessons from the past essential for shaping their perception of the present.

"We think these memory replay events are a fundamental constituent of memory retrieval and play a key role in human perspective and decision-making as well," he said. "These same events have been seen in memory tasks in humans, and now we know they are critical for memory in rats. We think that these fast-forward replays make up the individual elements of our own memories, which jump rapidly from event to event."

Next, the team wants to tease out information about how the rats actually use these memory replay events to make decisions and how amplifying or blocking specific replay events will change the way an animal learns and remembers. They also think that these events could be important for understanding memory problems, as when stressful memories intrude into daily life.

Source: Science Daily

May 3, 2012

Under some conditions, the brains of embryonic chicks appear to be awake well before those chicks are ready to hatch out of their eggs. That’s according to an imaging study published online on May 3 in Current Biology, a Cell Press publication, in which researchers woke chick embryos inside their eggs by playing loud, meaningful sounds to them. Playing meaningless sounds to the embryos wasn’t enough to rouse their brains.

This image shows an X-ray computed-tomography image of the chicken embryo skeleton inside an egg, which shows the developmental stage, together with a positron emission tomography image showing nervous system activity in the brain. Balaban et al., publishing in Current Biology, report the activity in chicken embryo brains is inversely related to behavioral activity, with different sleep-like states emerging for the first time. Playing meaningful sounds selectively induced patterns of embryonic brain activity similar to awake, post-hatching animals. Image 3D rendering by Carmen García-Villalba. Credit: Balaban et al. Current Biology

The findings may have implications not only for developing chicks and other animals, but also for prematurely born infants, the researchers say. Pediatricians have worried about the effects of stimulating brains that are still under construction, especially as modern medicine continues to push back the gestational age at which preemies can reliably survive.

"This work showed that embryo brains can function in a waking-like manner earlier than previously thought—well before birth," said Evan Balaban of McGill University. "Like adult brains, embryo brains also have neural circuitry that monitors the environment to selectively wake the brain up during important events."

That waking-like brain activity appears in a latent but inducible state during the final 20 percent of embryonic life, the researchers found. At that point, sleep-like brain activity patterns also emerge.

Before that major dividing line in development—for the first 80 percent of embryonic life— “embryos are in a state that is neither like sleep nor waking,” Balaban said. He suggests it may be useful to compare that state to what happens when people are comatose or under the influence of anesthesia.

This entire line of work was made possible by a new generation of molecular brain imagers developed by Balaban’s coauthors Juan-José Vaquero and Manuel Desco at the Universidad Carlos III in Madrid. Those state-of-the art machines can detect very small amounts of tracer molecules and pinpoint them to a tiny region of the brain (about 0.7 mm, or less than 3/100ths of an inch).

The researchers say they were surprised to capture waking-like activity before birth. And there were other surprises, too. The embryo brains they observed showed considerable variation in activity, for one.

Before the emergence of sleep and waking patterns of brain activity, the chick embryos in their study exhibited lots of spontaneous movement, even as their higher-brain regions remained inactive. Once the chicks reached that 80 percent mark in development, higher-brain regions began crackling with activity. At the same time, those physical movements ceased as the embryos entered a sleep-like state.

"The last 30 percent of fetal brain development is a more interesting time than we previously thought, because it’s when complex whole-brain functions that depend on coordination of widely separated brain areas first emerge," Balaban said. "Embryos begin to cycle through a variety of brain states and are even capable of showing waking-like brain activity."

That might explain instances of complex fetal and early neonatal learning. “It also raises questions about the longer-term developmental consequences that such brain activity may have, if it is induced before intrinsic brain wiring is sufficiently completed,” Balaban said, “for example, in babies born very prematurely. We are excited by the possibility that the techniques developed here can now be used to provide answers to these questions.”

Provided by Cell Press

Source: medicalxpress.com