“The scientists marked 63 cells called radial stem cells, which can divide to create new nerve cells. Researchers then watched these stem cells for up to two months, taking pictures every 12 or 24 hours.
“During that time, 42 of these stem cells underwent a spurt of division, churning out two kinds of cells: intermediate cells that would go on to produce nerve cells as well as mature nerve cells themselves. Once this burst of activity ended, the radial stem cells disappeared by dividing themselves into mature nerve cells that could no longer split.
“Many of these newly formed nerve cells had brief lives, dying either within the first four days, or 13 to 18 days after birth. It’s not clear what kills these newborn cells. Interspersed among the dying cells, survivors go on to knit themselves into the brain.”
Read Laura Sanders full article at Science News: Watch Nerve Cells Being Born in Living Mice
Watch the video: https://youtu.be/vW9FF6PRyBY
“Traumatic memories are often experienced as “relived” rather than remembered, which is why people experiencing them react as though they are re-experiencing the situations in which they were traumatized. When a traumatic memory is triggered, the somatosensory experience of the person reliving the memory can be powerful; the whole body “remembers” and replicates the sensations of the trauma, including sympathetic nervous system fight, flight, or freeze responses. The psychophysiological experience is of reliving the trauma, what we call a flashback. In this situation, the client often effectively dissociates from the present reality and is caught in the state of re-living the traumatic memory.
“Whereas memories of ordinary events, even those containing somatosensory and emotional components, do not have the somatosensory texture and depth of flashbacks, making it much easier to remain connected to external stimuli and to experience being present in the moment while simultaneously feeling (remembered) sensations or emotions.”
[The article continues with remarks from Til Luchau, who I desperately want to train with some day. I have to be content with his Advance Trainings fb group for the time being.]
“The state-dependant memory model discussed above [not included in this excerpt, read the full article] is more nuanced and sophisticated, and so arguably more useful. It brings to mind a book I’m currently reading: Lisa Feldman Barrett’s How Emotions are Made (2017, Houghton Mifflin Harcourt. ISBN 9780544133310). In her “theory of constructed emotions,” Barrett builds on the idea that our brains are structured to predict what we will see, taste, here, and feel. Apparently, there’s good evidence that the brain only processes things it does not predict. In this model, preloaded but widely networked caches of information (concepts) and meaning (valence) are used to minimize the brain’s energy use and maximize processing time.
“Interestingly, she writes that the brain’s wiring causes internal sensation and body signals (interoception and proprioception) to reach the brain’s processing centers before external perceptions (exteroception), such as sight, hearing etc. This sets up the brain to rapidly predict what it’ll perceive exteroceptively, based largely on past bodily experience (as well as language) what’s going to happen outside. In other words, we take in sensory information only until our brains can predict what will happen.
“This is the proposed mechanism behind both perceptions and emotion: for example, in this model, we are not reacting to our perceptions with emotions, we are neurologically predicting what will happen, and it is our predictions that shape our perceptions, emotions, and actions.”
Read the full article (and Til’s full commentary, plus comments from Walt Fritz) from Fascia & Fitness: Where Does Somatic Memory in the Body Reside?
“The study was a randomized-controlled single-blinded study with 40 healthy right-handed adult participants. The effect of touch on the client’s brain was monitored using functional magnetic resonance imaging (fMRI).
“The clients were randomly assigned to one of the two touch treatment groups:
- Therapist focusing on tactile perception from the hands (mindful touch group)
- Therapist focusing on auditory stimuli (non-mindful touch group/sound focused group).
“The therapists in the mindful touch group were asked to focus their attention on the feeling/perception from the hands that were contacting the client, i.e., the therapist had to feel the client’s tissue regarding its consistency, density, temperature, responsiveness, and motility (e.g., myofascial movements).
“The therapists in the sound-focused (non-mindful touch) group were asked to direct their attention toward acoustic stimuli (beeps) that were delivered through headphones. These beeps were delivered at a random interval between 0.5 seconds and 2.0 seconds; and the therapist had to count the number of beeps per session.
“The results revealed that sustained static touch applied by a therapist resulted in significant differences in brain activity of the person receiving the touch depending on whether the person giving the touch was focused on the touch or focused instead of random beeping sounds. Tthese changes were noted in connectivity between regions of the clients’ brains known as the posterior cingulate cortex, insula, and inferior-frontal gyrus.
“These functional connectivity changes are markedly different only after 15 min of touching. In other words, if the therapist is mindful and sustained over time, it can elicit significant effects in the client’s functional brain connectivity between areas processing the interoceptive and attentional value of touch.”
Read the full article at Fascia & Fitness, plus commentary from Joseph E. Muscolino: Mindful Touch Can Modify the Brain’s Functional Connectivity
“This is the first study to find that TBI in mice can trigger delayed, long-term changes in the colon and that subsequent bacterial infections in the gastrointestinal system can increase posttraumatic brain inflammation and associated tissue loss. The findings were published recently in the journal Brain, Behavior, and Immunity.
“These results indicate strong two-way interactions between the brain and the gut that may help explain the increased incidence of systemic infections after brain trauma and allow new treatment approaches,” said the lead researcher, Alan Faden, MD, the David S. Brown Professor in Trauma in the Departments of Anesthesiology, Anatomy & Neurobiology, Psychiatry, Neurology, and Neurosurgery at UMSOM, and director of the UMSOM Shock, Trauma and Anesthesiology Research Center.
“Researchers have known for years that TBI has significant effects on the gastrointestinal tract, but until now, scientists have not recognized that brain trauma can make the colon more permeable, potentially allowing allow harmful microbes to migrate from the intestine to other areas of the body, causing infection.. People are 12 times more likely to die from blood poisoning after TBI, which is often caused by bacteria, and 2.5 times more likely to die of a digestive system problem, compared with those without such injury.
“In this study, the researchers examined mice that received an experimental TBI. They found that the intestinal wall of the colon became more permeable after trauma, changes that were sustained over the following month.
“It is not clear how TBI causes these gut changes. A key factor in the process may be enteric glial cells (EGCs), a class of cells that exist in the gut. These cells are similar to brain astroglial cells, and both types of glial cells are activated after TBI. After TBI, such activation is associated with brain inflammation that contributes to delayed tissue damage in the brain. Researchers don’t know whether activation of ECGs after TBI contributes to intestinal injury or is instead an attempt to compensate for the injury.”
Read the full article at Neuroscience News: Traumatic Brain Injury Causes Intestinal Damage
“For some neuroscientists, new studies have changed the way they think about the brain.
“One of the skeptics at that Alzheimer’s meeting was Sangram Sisodia, a neurobiologist at the University of Chicago. He wasn’t swayed by Dr. Cryan’s talk, but later he decided to put the idea to a simple test.
“It was just on a lark,” said Dr. Sisodia. “We had no idea how it would turn out.”
“He and his colleagues gave antibiotics to mice prone to develop a version of Alzheimer’s disease, in order to kill off much of the gut bacteria in the mice. Later, when the scientists inspected the animals’ brains, they found far fewer of the protein clumps linked to dementia.
“Just a little disruption of the microbiome was enough to produce this effect. Young mice given antibiotics for a week had fewer clumps in their brains when they grew old, too.
“I never imagined it would be such a striking result,” Dr. Sisodia said. “For someone with a background in molecular biology and neuroscience, this is like going into outer space.”
“Following a string of similar experiments, he now suspects that just a few species in the gut — perhaps even one — influence the course of Alzheimer’s disease, perhaps by releasing chemical that alters how immune cells work in the brain.
“He hasn’t found those microbes, let alone that chemical. But “there’s something’s in there,” he said. “And we have to figure out what it is.”
Read Carl Zimmer’s full article at The New York Times: Germs in Your Gut are Talking to Your Brain. Scientists Want to Know What They’re Saying.