How We Recall the Past

How We Recall the Past

Summary: Researchers have identified a neural circuit that is critical for memory retrieval.

Source: MIT.

Neuroscientists discover a brain circuit dedicated to retrieving memories.

When we have a new experience, the memory of that event is stored in a neural circuit that connects several parts of the hippocampus and other brain structures. Each cluster of neurons may store different aspects of the memory, such as the location where the event occurred or the emotions associated with it.

Neuroscientists who study memory have long believed that when we recall these memories, our brains turn on the same hippocampal circuit that was activated when the memory was originally formed. However, MIT neuroscientists have now shown, for the first time, that recalling a memory requires a “detour” circuit that branches off from the original memory circuit.

“This study addresses one of the most fundamental questions in brain research — namely how episodic memories are formed and retrieved — and provides evidence for an unexpected answer: differential circuits for retrieval and formation,” says Susumu Tonegawa, the Picower Professor of Biology and Neuroscience, the director of the RIKEN-MIT Center for Neural Circuit Genetics at the Picower Institute for Learning and Memory, and the study’s senior author.

This distinct recall circuit has never been seen before in a vertebrate animal, although a study published last year found a similar recall circuit in the worm Caenorhabditis elegans.

Dheeraj Roy, a recent MIT PhD recipient, and research scientist Takashi Kitamura are the lead authors of the paper, which appears in the Aug. 17 online edition of Cell. Other MIT authors are postdocs Teruhiro Okuyama and Sachie Ogawa, and graduate student Chen Sun. Yuichi Obata and Atsushi Yoshiki of the RIKEN Brain Science Institute are also authors of the paper.

Parts unknown

The hippocampus is divided into several regions with different memory-related functions — most of which have been well-explored, but a small area called the subiculum has been little-studied. Tonegawa’s lab set out to investigate this region using mice that were genetically engineered so that their subiculum neurons could be turned on or off using light.

The researchers used this approach to control memory cells during a fear-conditioning event — that is, a mild electric shock delivered when the mouse is in a particular chamber.

Previous research has shown that encoding these memories involves cells in a part of the hippocampus called CA1, which then relays information to another brain structure called the entorhinal cortex. In each location, small subsets of neurons are activated, forming memory traces known as engrams.

“It’s been thought that the circuits which are involved in forming engrams are the same as the circuits involved in the re-activation of these cells that occurs during the recall process,” Tonegawa says.

However, scientists had previously identified anatomical connections that detour from CA1 through the subiculum, which then connects to the entorhinal cortex. The function of this circuit, and of the subiculum in general, was unknown.

In one group of mice, the MIT team inhibited neurons of the subiculum as the mice underwent fear conditioning, which had no effect on their ability to later recall the experience. However, in another group, they inhibited subiculum neurons after fear conditioning had occurred, when the mice were placed back in the original chamber. These mice did not show the usual fear response, demonstrating that their ability to recall the memory was impaired.

This provides evidence that the detour circuit involving the subiculum is necessary for memory recall but not for memory formation. Other experiments revealed that the direct circuit from CA1 to the entorhinal cortex is not necessary for memory recall, but is required for memory formation.

“Initially, we did not expect the outcome would come out this way,” Tonegawa says. “We just planned to explore what the function of the subiculum could be.”

“This paper is a tour de force of advanced neuroscience techniques, with an intriguing core result showing the existence and importance of different pathways for formation and retrieval of hippocampus-dependent memories,” says Karl Deisseroth, a professor of bioengineering and psychiatry and behavioral sciences at Stanford University, who was not involved in the study.

Editing memories

Why would the hippocampus need two distinct circuits for memory formation and recall? The researchers found evidence for two possible explanations. One is that interactions of the two circuits make it easier to edit or update memories. As the recall circuit is activated, simultaneous activation of the memory formation circuit allows new information to be added.

Image shows CA1 hippocampal neurons.

“We think that having these circuits in parallel helps the animal first recall the memory, and when needed, encode new information,” Roy says. “It’s very common when you remember a previous experience, if there’s something new to add, to incorporate the new information into the existing memory.”

Another possible function of the detour circuit is to help stimulate longer-term stress responses. The researchers found that the subiculum connects to a pair of structures in the hypothalamus known as the mammillary bodies, which stimulates the release of stress hormones called corticosteroids. That takes place at least an hour after the fearful memory is recalled.

While the researchers identified the two-circuit system in experiments involving memories with an emotional component (both positive and negative), the system is likely involved in any kind of episodic memory, the researchers say.

The findings also suggest an intriguing possibility related to Alzheimer’s disease, according to the researchers. Last year, Roy and others in Tonegawa’s lab found that mice with a version of early-stage Alzheimer’s disease have trouble recalling memories but are still able to form new memories. The new study suggests that this subiculum circuit may be affected in Alzheimer’s disease, although the researchers have not studied this.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Funding: The research was funded by the RIKEN Brain Science Institute, the Howard Hughes Medical Institute, and the JPB Foundation.

Source: Anne Trafton – MIT
Image Source: NeuroscienceNews.com image is credited to Dheeraj Roy/Tonegawa Lab, MIT.
Original Research: Abstract for “Distinct Neural Circuits for the Formation and Retrieval of Episodic Memories” by Dheeraj S. Roy, Takashi Kitamura, Teruhiro Okuyama, Sachie K. Ogawa, Chen Sun, Yuichi Obata, Atsushi Yoshiki, and Susumu Tonegawa in Cell. Published online August 17 2017 doi:10.1016/j.cell.2017.07.013

MIT “How We Recall the Past.” NeuroscienceNews. NeuroscienceNews, 17 August 2017.
<http://neurosciencenews.com/memory-retrieval-neural-network-7321/&gt;.

Abstract

Distinct Neural Circuits for the Formation and Retrieval of Episodic Memories

Highlights

•dSub and the circuit, CA1→dSub→EC5, are required for hippocampal memory retrieval
•The direct CA1→EC5 circuit is essential for hippocampal memory formation
•The dSub→MB circuit regulates memory-retrieval-induced stress hormone responses
•The dSub→EC5 circuit contributes to context-dependent memory updating

Summary
The formation and retrieval of a memory is thought to be accomplished by activation and reactivation, respectively, of the memory-holding cells (engram cells) by a common set of neural circuits, but this hypothesis has not been established.

The medial temporal-lobe system is essential for the formation and retrieval of episodic memory for which individual hippocampal subfields and entorhinal cortex layers contribute by carrying out specific functions.

One subfield whose function is poorly known is the subiculum. Here, we show that dorsal subiculum and the circuit, CA1 to dorsal subiculum to medial entorhinal cortex layer 5, play a crucial role selectively in the retrieval of episodic memories. Conversely, the direct CA1 to medial entorhinal cortex layer 5 circuit is essential specifically for memory formation.

Our data suggest that the subiculum-containing detour loop is dedicated to meet the requirements associated with recall such as rapid memory updating and retrieval-driven instinctive fear responses.

“Distinct Neural Circuits for the Formation and Retrieval of Episodic Memories” by Dheeraj S. Roy, Takashi Kitamura, Teruhiro Okuyama, Sachie K. Ogawa, Chen Sun, Yuichi Obata, Atsushi Yoshiki, and Susumu Tonegawa in Cell. Published online August 17 2017 doi:10.1016/j.cell.2017.07.013

My scientist friend asked how to detox or clean his body from toxins

Over the years, I have experienced family and friends dying of cancer. I observed their lifestyle and toxins they are exposed to. So to answer my friend’s question on how to detox and the mechanism of cleaning our body or getting rid of toxins, I listed some items for Dos and Donts.

Our lymphatic system which travels opposite our blood is responsible for cleaning our blood.  Search for lymphatic, massage and detox in this site http://www.clubalthea.com

When we clean the many bad foods or toxins that entered our body, we must clean our liver first, our laboratory.  It is closely linked to our heart that during our last breath, our liver is the first and last signal that our heart gets to shut down.

Detox or cleaning our cells from toxins is the key to living longer, the anti-aging process we all are seeking for. In my 50s, I could have died long time ago if I was born centuries ago with no clean water, fresh produce and raising a dozen children. Each child is minus 5 years of a woman’s age.

Detox is like cleaning the toilet. The following are detox tips and anti-aging tips to clean your cells:

Dos in cleansing your body from toxin, also detoxes your liver

  • Massage
  • Adequate sleep
  • Filtered water
  • Lemon
  • Baking soda (pinch in your drinking water)
  • Activated charcoal
  • Digestive enzymes from pineapple and papaya
  • Apple cider vinegar
  • Wash produce with salt or diluted vinegar
  • No over ripe fruits and left over foods or 3-day old rice ( aflatoxin , mycotoxin )
  • No charred BBQ
  • Whole foods ; sulfur rich as they are anti-inflammatory (ginger, garlic, turmeric, coconut, walnuts)
  • Deep breathing thru nose and blow out thru mouth
  • Prayer: May God’s light energy be with you and say Amen to accept it.
  • Resveratrol from Berries, kiwi, citrus fruit
  • Fasting
  • Activated charcoal
  • Clean air

Donts are ways that when practiced or consumed can kills our nerve cells and produce toxins in our cells.

  • Avoidance of too much caffeine, iron and sugar, these are food for cancer
  • Other metal toxins
  • TRANS fat
  • Processed
  • Plastics in food
  • Stress
  • Shift work: not sleeping from 10pm to 4 am
  • Radiation
  • Over medications, chemo, other carcinogens
  • Avoid exposure to fumes, chemicals (formaldehydes,carcinogens,toxins)

 

——-

Hi Connnie,

And what is your recipe for liver detox and the mechanism by which it works to accomplish that?

From: Male friend in his late 50s whose brother died of pancreatic cancer

Pain is Not Just a Matter of Nerves

Summary: Researchers reveal the role glial cells play in the sensation of pain.

Source: Medical University of Vienna.

The sensation of pain occurs when neural pathways conduct excitation generated by tissue damage to the spinal cord, where the nociceptive information is extensively pre-processed. From there, the information is transmitted to the human brain, where the sensation of “pain” is finally created. This is the general belief. However, researchers from the Division of Neurophysiology at MedUni Vienna’s Center for Brain Research have now discovered that pain is not just a matter of nerves but that non-neuronal cells, the glial cells, are also involved in clinically relevant pain models and their activation is sufficient to amplify pain. The study has now been published in the leading journal “Science”.

Glial cells are the commonest type of cells in the human brain and spinal cord. They surround neurons but are distinct from them and play an important supporting role – for example, in material transport and metabolism or the fluid balance in the brain and spinal cord.

Novel explanation for puzzling pain phenomena

At the same time, however, when they are activated – by pain processes, for example ­– glial cells are themselves able to release messenger substances, such as inflammatory cytokines. Glial cells therefore have two modes: a protective and a pro-inflammatory mode. “The activation of glial cells results in a pain-amplifying effect, as well as spreading the pain to previously unaffected parts of the body. For the very first time, our study provides a biological explanation for this and for other hitherto unexplained pain phenomena in medicine,” says Jürgen Sandkühler, Head of the Division of Neurophysiology at MedUni Vienna’s Center for Brain Research.

Image shows neurons.

Over-activation of glial cells in the spinal cord can, for example, be caused by strong pain stimuli from a wound or surgical intervention, or even by opiates. Sandkühler: “This could also explain why opiates are initially very good at relieving pain but then often cease to be effective. Another example is the phenomenon of “withdrawal” in drug addicts, where activated glial cells cause severe pain throughout the body.”

A healthy lifestyle can beneficially impact the glial cell system

According to Sandkühler, neuroinflammatory diseases of the brain, environmental factors and even the person’s own lifestyle can lead to activation of glial cells. Examples from the current literature are: depression, anxiety disorders and chronic stress, multiple sclerosis or Alzheimer’s and diabetes, as well as lack of exercise and poor diet. Sandkühler: “Glial cells are an important factor in ensuring the equilibrium of a person’s neuroinflammatory system.” The study results give grounds for speculation that improvements in a person’s lifestyle could have a beneficial impact upon this system and ensure that they generally suffer less pain or “minor niggles”, says Sandkühler: “It is therefore in our own hands: thirty minutes of moderate exercise three or four times a week, a healthy diet and avoiding putting on excess weight can make a huge difference.”

ABOUT THIS PAIN RESEARCH ARTICLE

Source: Medical University of Vienna
Image Source: This NeuroscienceNews.com image is adapted from the Medical University of Vienna press release.
Original Research: Abstract for “Gliogenic LTP Spreads Widely in Nociceptive Pathways” by M.T. Kronschläger, R. Drdla-Schutting, M. Gassner, S.D. Honsek, H.L. Teuchmann, and J. Sandkühler in Science. Published online November 10 2016 doi:10.1002/da.22577

CITE THIS NEUROSCIENCENEWS.COM ARTICLE
Medical University of Vienna. “Pain is Not Just a Matter of Nerves.” NeuroscienceNews. NeuroscienceNews, 11 November 2016.
<http://neurosciencenews.com/neurons-pain-amplification-5489/&gt;.

Abstract

Gliogenic LTP Spreads Widely in Nociceptive Pathways

Learning and memory formation involve long-term potentiation of synaptic strength (LTP). A fundamental feature of LTP induction in the brain is the need for coincident pre- and postsynaptic activity. This restricts LTP expression to activated synapses only (homosynaptic LTP) and leads to its input specificity. In the spinal cord, we discovered a fundamentally different form of LTP that is induced by glial cell activation and mediated by diffusible, extracellular messengers, including D-serine and tumor necrosis factor (TNF), and that travel long distances via the cerebrospinal fluid, thereby affecting susceptible synapses at remote sites. The properties of this gliogenic LTP resolve unexplained findings of memory traces in nociceptive pathways and may underlie forms of widespread pain hypersensitivity.

“Gliogenic LTP Spreads Widely in Nociceptive Pathways” by M.T. Kronschläger, R. Drdla-Schutting, M. Gassner, S.D. Honsek, H.L. Teuchmann, and J. Sandkühler in Science. Published online November 10 2016 doi:10.1002/da.22577

Babies Exposed to Stimulation Get a Brain Boost

Summary: Contrary to popular belief, exposing children to stimuli early can help to boost their development, researchers report.

Source: NTNU.

Many new parents still think that babies should develop at their own pace, and that they shouldn’t be challenged to do things that they’re not yet ready for. Infants should learn to roll around under their own power, without any “helpful” nudges, and they shouldn’t support their weight before they can stand or walk on their own. They mustn’t be potty trained before they are ready for it.

According to neuroscientist Audrey van der Meer, a professor at the Norwegian University of Science and Technology (NTNU) this mindset can be traced back to the early 1900s, when professionals were convinced that our genes determine who we are, and that child development occurred independently of the stimulation that a baby is exposed to. They believed it was harmful to hasten development, because development would and should happen naturally.

Early stimulation in the form of baby gym activities and early potty training play a central role in Asia and Africa. The old development theory also contrasts with modern brain research that shows that early stimulation contributes to brain development gains even in the wee ones among us.

Using the body and senses

Van der Meer is a professor of neuropsychology and has used advanced EEG technology for many years to study the brain activity of hundreds of babies.

The results show that the neurons in the brains of young children quickly increase in both number and specialization as the baby learns new skills and becomes more mobile. Neurons in very young children form up to a thousand new connections per second.

Van der Meer’s research also shows that the development of our brain, sensory perception and motor skills happen in sync. She believes that even the smallest babies must be challenged and stimulated at their level from birth onward. They need to engage their entire body and senses by exploring their world and different materials, both indoors and out and in all types of weather. She emphasizes that the experiences must be self-produced; it is not enough for children merely to be carried or pushed in a stroller.

Unused brain synapses disappear

“Many people believe that children up to three years old only need cuddles and nappy changes, but studies show that rats raised in cages have less dendritic branching in the brain than rats raised in an environment with climbing and hiding places and tunnels. Research also shows that children born into cultures where early stimulation is considered important, develop earlier than Western children do,” van der Meer says.

She adds that the brains of young children are very malleable, and can therefore adapt to what is happening around them. If the new synapses that are formed in the brain are not being used, they disappear as the child grows up and the brain loses some of its plasticity.

Van der Meer mentions the fact that Chinese babies hear a difference between the R and L sounds when they are four months old, but not when they get older. Since Chinese children do not need to distinguish between these sounds to learn their mother tongue, the brain synapses that carry this knowledge disappear when they are not used.

Loses the ability to distinguish between sounds

Babies actually manage to distinguish between the sounds of any language in the world when they are four months old, but by the time they are eight months old they have lost this ability, according to van der Meer.

In the 1970s, it was believed that children could only learn one language properly. Foreign parents were advised not to speak their native language to their children, because it could impede the child’s language development. Today we think completely differently, and there are examples of children who speak three, four or five languages fluently without suffering language confusion or delays.

Brain research suggests that in these cases the native language area in the brain is activated when children speak the languages. If we study a foreign language after the age of seven, other areas of the brain are used when we speak the language, explains Van der Meer.

She adds that it is important that children learn languages by interacting with real people.

“Research shows that children don’t learn language by watching someone talk on a screen, it has to be real people who expose them to the language,” says van der Meer.

Early intervention with the very young

Since a lot is happening in the brain during the first years of life, van der Meer says that it is easier to promote learning and prevent problems when children are very young.

The term “early intervention” keeps popping up in discussions of kindergartens and schools, teaching and learning. Early intervention is about helping children as early as possible to ensure that as many children as possible succeed in their education and on into adulthood – precisely because the brain has the greatest ability to change under the influence of the ambient conditions early in life.

“When I talk about early intervention, I’m not thinking of six-year-olds, but even younger children from newborns to age three. Today, 98 per cent of Norwegian children attend kindergarten, so the quality of the time that children spend there is especially important. I believe that kindergarten should be more than just a holding place – it should be a learning arena – and by that I mean that play is learning,” says van der Meer.

Too many untrained staff

She adds that a two-year old can easily learn to read or swim, as long as the child has access to letters or water. However, she does not want kindergarten to be a preschool, but rather a place where children can have varied experiences through play.

“This applies to both healthy children and those with different challenges. When it comes to children with motor challenges or children with impaired vision and hearing, we have to really work to bring the world to them,” says van der Meer.

“One-year-olds can’t be responsible for their own learning, so it’s up to the adults to see to it. Today untrained temporary staff tend to be assigned to the infant and toddler rooms, because it’s ‘less dangerous’ with the youngest ones since they only need cuddles and nappy changes. I believe that all children deserve teachers who understand how the brains of young children work. Today, Norway is the only one of 25 surveyed OECD countries where kindergarten teachers do not constitute 50 per cent of kindergarten staffing,” she said.

More children with special needs

Lars Adde is a specialist in paediatric physical therapy at St. Olavs Hospital and a researcher at NTNU’s Department of Laboratory Medicine, Children’s and Women’s Health. He works with young children who have special needs, in both his clinical practice and research.

Image shows a baby playing.

He believes it is important that all children are stimulated and get to explore the world, but this is especially important for children who have special challenges. He points out that a greater proportion of children that are now coming into the world in Norway have special needs.

“This is due to the rapid development in medical technology, which enables us to save many more children – like extremely premature babies and infants who get cancer. These children would have died 50 years ago, and today they survive – but often with a number of subsequent difficulties,” says Adde.

New knowledge offers better treatment

Adde says that the new understanding of brain development that has been established since the 1970s has given these children far better treatment and care options.

For example, the knowledge that some synapses in the brain are strengthened while others disappear has led to the understanding that we have to work at what we want to be good at – like walking. According to the old mindset, any general movement would provide good general motor function.

Babies who are born very prematurely at St. Olavs Hospital receive follow-up by an interdisciplinary team at the hospital and a municipal physiotherapist in their early years. Kindergarten staff where the child attends receive training in exactly how this child should be stimulated and challenged at the appropriate level. The follow-up enables a child with developmental delays to catch up quickly, so that measures can be implemented early – while the child’s brain is still very plastic.

A child may, for example, have a small brain injury that causes him to use his arms differently. Now we know that the brain connections that govern this arm become weaker when it is used less, which reinforces the reduced function.

“Parents may then be asked to put a sock on the “good” hand when their child uses his hands to play. Then the child is stimulated and the brain is challenged to start using the other arm,” says Adde.

Shouldn’t always rush development

Adde stresses that it is not always advisable to speed up the development of children with special needs who initially struggle with their motor skills.

A one–year old learning to walk first has to learn to find her balance. If the child is helped to standing position, she will eventually learn to stand – but before she has learned how to sit down again. If the child loses her balance, she’ll fall like a stiff cane, which can be both scary and counterproductive.

In that situation, “we might then ask the parents to instead help their child up to kneeling position while it holds onto something. Then the child will learn to stand up on its own. If the child falls, it will bend in the legs and tumble on its bum. Healthy children figure this out on their own, but children with special challenges don’t necessarily do this,” says Adde.

ABOUT THIS NEURODEVELOPMENT RESEARCH ARTICLE

Source: NTNU
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Full open access research for “Development of Visual Motion Perception for Prospective Control: Brain and Behavioral Studies in Infants” by Seth B. Agyei, F. R. (Ruud) van der Weel and Audrey L. H. van der Meer in Frontiers in Psychology. Published online February 9 2016 doi:10.3389/fpsyg.2016.00100

Abstract for “Longitudinal study of preterm and full-term infants: High-density EEG analyses of cortical activity in response to visual motion” bySeth B. Agyei, F.R. (Ruud) van der Weel, Audrey L.H. van der Meer in Neuropsychologia. Published online April 2016 doi:10.1016/j.neuropsychologia.2016.02.001

CITE THIS NEUROSCIENCENEWS.COM ARTICLE
NTNU “Babies Exposed to Stimulation Get a Brain Boost.” NeuroscienceNews. NeuroscienceNews, 30 January 2017.
<http://neurosciencenews.com/baby-stimulation-neurodevelopment-5844/&gt;.

Abstract

Development of Visual Motion Perception for Prospective Control: Brain and Behavioral Studies in Infants

During infancy, smart perceptual mechanisms develop allowing infants to judge time-space motion dynamics more efficiently with age and locomotor experience. This emerging capacity may be vital to enable preparedness for upcoming events and to be able to navigate in a changing environment. Little is known about brain changes that support the development of prospective control and about processes, such as preterm birth, that may compromise it. As a function of perception of visual motion, this paper will describe behavioral and brain studies with young infants investigating the development of visual perception for prospective control. By means of the three visual motion paradigms of occlusion, looming, and optic flow, our research shows the importance of including behavioral data when studying the neural correlates of prospective control.

“Development of Visual Motion Perception for Prospective Control: Brain and Behavioral Studies in Infants” by Seth B. Agyei, F. R. (Ruud) van der Weel and Audrey L. H. van der Meer in Frontiers in Psychology. Published online February 9 2016 doi:10.3389/fpsyg.2016.00100


Abstract

Longitudinal study of preterm and full-term infants: High-density EEG analyses of cortical activity in response to visual motion

Electroencephalogram (EEG) was used to investigate brain electrical activity of full-term and preterm infants at 4 and 12 months of age as a functional response mechanism to structured optic flow and random visual motion. EEG data were recorded with an array of 128-channel sensors. Visual evoked potentials (VEPs) and temporal spectral evolution (TSE, time-dependent amplitude changes) were analysed. VEP results showed a significant improvement in full-term infants’ latencies with age for forwards and reversed optic flow but not random visual motion. Full-term infants at 12 months significantly differentiated between the motion conditions, with the shortest latency observed for forwards optic flow and the longest latency for random visual motion, while preterm infants did not improve their latencies with age, nor were they able to differentiate between the motion conditions at 12 months. Differences in induced activities were also observed where comparisons between TSEs of the motion conditions and a static non-flow pattern showed desynchronised theta-band activity in both full-term and preterm infants, with synchronised alpha-beta band activity observed only in the full-term infants at 12 months. Full-term infants at 12 months with a substantial amount of self-produced locomotor experience and neural maturation coupled with faster oscillating cell assemblies, rely on the perception of structured optic flow to move around efficiently in the environment. The poorer responses in the preterm infants could be related to impairment of the dorsal visual stream specialized in the processing of visual motion.

“Longitudinal study of preterm and full-term infants: High-density EEG analyses of cortical activity in response to visual motion” bySeth B. Agyei, F.R. (Ruud) van der Weel, Audrey L.H. van der Meer in Neuropsychologia. Published online April 2016 doi:10.1016/j.neuropsychologia.2016.02.001

A Link Between Gut Bacteria and Neurogenesis: Mouse Study

Summary: According to a new mouse study, antibotics that are strong enough to kill gut bacteria can also halt the growth of hippocampal neurons.

Source: Cell Press.

Antibiotics strong enough to kill off gut bacteria can also stop the growth of new brain cells in the hippocampus, a section of the brain associated with memory, reports a study in mice published May 19 in Cell Reports. Researchers also uncovered a clue to why– a type of white blood cell seems to act as a communicator between the brain, the immune system, and the gut.

“We found prolonged antibiotic treatment might impact brain function,” says senior author Susanne Asu Wolf of the Max-Delbrueck-Center for Molecular Medicine in Berlin, Germany. “But probiotics and exercise can balance brain plasticity and should be considered as a real treatment option.”

Wolf first saw clues that the immune system could influence the health and growth of brain cells through research into T cells nearly 10 years ago. But there were few studies that found a link from the brain to the immune system and back to the gut.

In the new study, the researchers gave a group of mice enough antibiotics for them to become nearly free of intestinal microbes. Compared to untreated mice, the mice who lost their healthy gut bacteria performed worse in memory tests and showed a loss of neurogenesis (new brain cells) in a section of their hippocampus that typically produces new brain cells throughout an individual’s lifetime. At the same time that the mice experienced memory and neurogenesis loss, the research team detected a lower level of white blood cells (specifically monocytes) marked with Ly6Chi in the brain, blood, and bone marrow. So researchers tested whether it was indeed the Ly6Chi monocytes behind the changes in neurogenesis and memory.

In another experiment, the research team compared untreated mice to mice that had healthy gut bacteria levels but low levels of Ly6Chi either due to genetics or due to treatment with antibodies that target Ly6Chi cells. In both cases, mice with low Ly6Chi levels showed the same memory and neurogenesis deficits as mice in the other experiment who had lost gut bacteria. Furthermore, if the researchers replaced the Ly6Chi levels in mice treated with antibiotics, then memory and neurogenesis improved.

“For us it was impressive to find these Ly6Chi cells that travel from the periphery to the brain, and if there’s something wrong in the microbiome, Ly6Chi acts as a communicating cell,” says Wolf.

Luckily, the adverse side effects of the antibiotics could be reversed. Mice who received probiotics or who exercised on a wheel after receiving antibiotics regained memory and neurogenesis. “The magnitude of the action of probiotics on Ly6Chi cells, neurogenesis, and cognition impressed me,” she says.

But one result in the experiment raised more questions about the gut’s bacteria and the link between Ly6Chi and the brain. While probiotics helped the mice regain memory, fecal transplants to restore a healthy gut bacteria did not have an effect.

Image show the impact of prolonged antibiotic treatment on brain cell plasticity and cognitive function.

“It was surprising that the normal fecal transplant recovered the broad gut bacteria, but did not recover neurogenesis,” says Wolf. “This might be a hint towards direct effects of antibiotics on neurogenesis without using the detour through the gut. To decipher this we might treat germ free mice without gut flora with antibiotics and see what is different.”

In the future, researchers also hope to see more clinical trials investigating whether probiotic treatments will improve symptoms in patients with neurodegenerative and psychiatric disorders.”We could measure the outcome in mood, psychiatric symptoms, microbiome composition and immune cell function before and after probiotic treatment,” says Wolf.

ABOUT THIS NEUROPHARMACOLOGY RESEARCH ARTICLE

Funding: This project was funded by the German Research Council.

Source: Joseph Caputo – Cell Press
Image Source: This NeuroscienceNews.com image is credited to Möhle et al./Cell Reports 2016.
Original Research: Full open access research for “Ly6Chi Monocytes Provide a Link between Antibiotic-Induced Changes in Gut Microbiota and Adult Hippocampal Neurogenesis” by Luisa Möhle, Daniele Mattei, Markus M. Heimesaat, Stefan Bereswill, André Fischer, Marie Alutis, Timothy French, Dolores Hambardzumyan, Polly Matzinger, Ildiko R. Dunay, and Susanne A. Wolf in Cell Reports. Published online May 19 2016 doi:10.1016/j.celrep.2016.04.074

CITE THIS NEUROSCIENCENEWS.COM ARTICLE
Cell Press. “A Link Between Gut Bacteria and Neurogenesis: Mouse Study.” NeuroscienceNews. NeuroscienceNews, 19 May 2016.
<http://neurosciencenews.com/neurogenesis-gut-bacteria-4253/&gt;.

Abstract

Ly6Chi Monocytes Provide a Link between Antibiotic-Induced Changes in Gut Microbiota and Adult Hippocampal Neurogenesis

Highlights
•Antibiotics decrease neurogenesis and cognitive function
•Probiotics or exercise rescues neurogenesis and cognitive function
•Ly6Chi monocytes are crucial for brain homeostasis

Summary
Antibiotics, though remarkably useful, can also cause certain adverse effects. We detected that treatment of adult mice with antibiotics decreases hippocampal neurogenesis and memory retention. Reconstitution with normal gut flora (SPF) did not completely reverse the deficits in neurogenesis unless the mice also had access to a running wheel or received probiotics. In parallel to an increase in neurogenesis and memory retention, both SPF-reconstituted mice that ran and mice supplemented with probiotics exhibited higher numbers of Ly6Chi monocytes in the brain than antibiotic-treated mice. Elimination of Ly6Chi monocytes by antibody depletion or the use of knockout mice resulted in decreased neurogenesis, whereas adoptive transfer of Ly6Chi monocytes rescued neurogenesis after antibiotic treatment. We propose that the rescue of neurogenesis and behavior deficits in antibiotic-treated mice by exercise and probiotics is partially mediated by Ly6Chi monocytes.

“Ly6Chi Monocytes Provide a Link between Antibiotic-Induced Changes in Gut Microbiota and Adult Hippocampal Neurogenesis” by Luisa Möhle, Daniele Mattei, Markus M. Heimesaat, Stefan Bereswill, André Fischer, Marie Alutis, Timothy French, Dolores Hambardzumyan, Polly Matzinger, Ildiko R. Dunay, and Susanne A. Wolf in Cell Reports. Published online May 19 2016 doi:10.1016/j.celrep.2016.04.074

Low glucose and low stress to go to sleep

There are many factors that will help you go to sleep. There are two most important factors.  One is that if you eat (few bites) sugary snacks (couple it with fish oil or omega 3), it should be 6 to 8 hrs before your sleep time. And the other one is that your stress level should be very low.

The pituitary gland is responsible for sleep, stress, sex hormones and food cravings.

Our gut microbiome (bacteria and microbes in our intestines) also communicates to our brain to tell us that they are busy or hungry.

When we have food cravings during the day, it is because we did not get quality sleep the night before.

When we are grumpy or stressed out that day, it also means that we did not get good sleep.

Our liver was not able to detox properly, so we have not so healthy skin as a result of poor quality sleep.

Our bedroom must be dimmed since lights tell our pituitary gland that it is not night time yet.

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So what did I do to go to sleep at 12 midnight after working making egg rolls until 9pm and eating chocolate desserts at that time? I have to wait till I calm my body and waited till 12midnight to go to sleep. I repeated some prayers to tell my brain to stop worrying or de-stress.  All these even after I took some important dietary supplements to go to sleep (melatonin, calcium and magnesium, Vit D3, zinc, Zyflamend night time caps).

Lesson: Our body needs low glucose and low stress to go to sleep.


Adrenal fatigue

Adrenal fatigue or hypoadrenia are terms used in alternative medicine to describe the unscientificbelief that the adrenal glands are exhausted and unable to produce adequate quantities of hormones, primarily the glucocorticoid cortisol, due to chronic stress or infections.[1] Adrenal fatigue should not be confused with recognized forms of adrenal dysfunction such as adrenal insufficiency or Addison’s Disease.[2]

The term “adrenal fatigue”, which was coined in 1998 by James Wilson, a chiropractor,[3] may be applied to a collection of mostly nonspecific symptoms.[1] There is no scientific evidence supporting the concept of adrenal fatigue and it is not recognized as a diagnosis by the medical community.[1][2]

Blood or salivary testing is sometimes offered but there is no evidence that adrenal fatigue exists or can be tested.


Pituitary gland

In vertebrate anatomy, the pituitary gland, or hypophysis, is an endocrine gland about the size of a pea and weighing 0.5 grams (0.018 oz) in humans. It is a protrusion off the bottom of the hypothalamus at the base of the brain. The hypophysis rests upon the hypophysial fossa of the sphenoid bone in the center of the middle cranial fossa and is surrounded by a small bony cavity (sella turcica) covered by a dural fold (diaphragma sellae).[2] The anterior pituitary (or adenohypophysis) is a lobe of the gland that regulates several physiological processes (including stress, growth, reproduction, and lactation). The intermediate lobe synthesizes and secretes melanocyte-stimulating hormone. The posterior pituitary (or neurohypophysis) is a lobe of the gland that is functionally connected to the hypothalamus by the median eminence via a small tube called the pituitary stalk (also called the infundibular stalk or the infundibulum).

Hormones secreted from the pituitary gland help control: growth, blood pressure, certain functions of the sex organs, thyroid glands and metabolism as well as some aspects of pregnancy, childbirth, nursing, water/salt concentration at the kidneys, temperature regulation and pain relief.