Scientists used to believe that the brain stopped making new brain cells past a certain age. But that believe changed in the late 1990’s as a result of several studies which were performed on mice at the Salk Institute.
After conducting maze tests, neuroscientist Fred H. Gage and his colleagues examined brain samples collected from mice. What they found challenged long standing believes held about neurogenesis, or the creation of new neurons.
To their astonishment, they discovered that the mice were creating new neurons. Their brains were regenerating themselves.
All of the mice showed evidence of neurogenesis but the brains of the athletic mice showed even more.
These mice, the ones that scampered on running wheels, were producing two to three times as many new neurons as the mice that didn’t exercise.
The difference between the mice who performed well on the maze tests and those that floundered was exercise.
That’s great for the mice, but what about humans?
To find out if neurogensis occurred in adult humans, Gage and his colleagues obtained brain tissue from deceased cancer patients who had donated their bodies to research. While still living, these people were injected with the same type of compound used on Gage’s mice to detect new neuron growth. When Gage dyed their brain samples, he saw new neurons. Like in the mice study, they found evidence of neurogenesis – the growth of new brain cells.
From the mice study, it appears that those who exercise produce even more new brain cells than those who don’t. Several studies on humans seem to suggest the same thing.
Studies performed at both the University of Illinois at Urbana- Champaign and Columbia University in New York City have shown that exercise benefits brain function. The test subjects were given aerobic exercises such as walking for at least one hour three times a week. After 6 months they showed significant improvements in memory as measured by a word-recall test. Using fMRI scans they also showed increases in blood flow to the hippocampus (part of the brain associated with memory and learning). Scientists suspect that the blood pumping into that part of the brain was helping to produce fresh neurons.
Dr. Patricia A. Boyle and her colleagues of Rush Alzheimer’s Disease Center in Chicago found that the greater a person’s muscle strength, the lower their likelihood of being diagnosed with Alzheimer’s. The same was true for the loss of mental function that often precedes full-blown Alzheimer’s.
Neuroscientist Gage, by the way, exercises just about every day, as do most colleagues in his field. As Scott Small a neurologist at Columbia explains,
I constantly get asked at cocktail parties what someone can do to protect their mental functioning. I tell them, ‘Put down that glass and go for a run.
So if you want to grow some new brain cells and improve your brain function, go get some exercise!
Source: How to Make New Brain Cells and Improve Brain Function | Online Brain Games Blog
A new study has found evidence that a section of our neurons, called the dendrites, aren’t the passive receivers we’ve always assumed them to be.
Instead, researchers have found that dendrites generate up to 10 times more electrical pulse spikes than parts of our brain cells called the soma, which until now were thought to be the main area to produce these electrical signals.
If verified, the study could change our understanding of neurons, and how the various parts of the human brain work together.
“Knowing [dendrites] are much more active than the soma fundamentally changes the nature of our understanding of how the brain computes information,” said one of the team, Mayank Mehta, from the University of California, Los Angeles (UCLA).
“It may pave the way for understanding and treating neurological disorders, and for developing brain-like computers.”
Dendrites are long, branch-like structures that make up over 90 percent of our neuronal tissue. They’re connected to the soma, which is the part of the neuron that surrounds the nucleus.
Here’s a illustration to show the different sections:
According to traditional thinking, somas generate the electrical pulses, also known as ‘spikes’, that brain cells use to communicate with each other.
Until recently, scientists generally assumed that these somatic spikes activated the dendrites, which then passively passed the currents onto other neurons’ somas – but this had never been directly tested.
Although recent studies of human brain slices had shown that dendrites could generate spikes, it wasn’t known if this happened naturally, and it hadn’t been shown in a live animal model.
As the team explains in a press release:
“It was neither clear that this could happen during natural behaviour, nor how often. Measuring dendrites’ electrical activity during natural behaviour has long been a challenge because they’re so delicate.
In studies with laboratory rats, scientists have found that placing electrodes in the dendrites themselves while the animals were moving actually killed those cells.”
Obviously, this wasn’t an ideal situation, so the UCLA scientists placed the electrodes near the dendrites in rats, instead of on them.
They were able to measure the dendrites’ activity for four days,while the rats performed activities such as moving through a maze.
What’s interesting is that the researchers found many more spikes in dendrites than somas – five times more whilen the rats were sleeping, and up to 10 times more while they were exploring.
This is very different to the established understanding, and could show that our brains have much more ‘computational’ power than we thought.
“A fundamental belief in neuroscience has been that neurons are digital devices. They either generate a spike or not. These results show that the dendrites do not behave purely like a digital device,” said Mehta.
“Dendrites do generate digital, all-or-none spikes, but they also show large analogue fluctuations that are not all or none. This is a major departure from what neuroscientists have believed for about 60 years.”
So how much more processing power do we suddenly have in our brains?
Mehta explains that because dendrites are nearly 100 times larger in volume than somas, the large number of dendritic spikes means we could have over 100 times the processing capacity than we thought.
That’s a pretty big stretch, and more research will be needed before we can confirm exactly how much processing power our brain actually has.
It’s also important to note that this study has only been investigated in rats – we’d still need to investigate if the dendrites are behaving similarly in our own brains as they are in the animal models before we can start confirming any such numbers.
But these findings are an impressive step for the neurological field – and it may one day lead to better ways to treat neurological disorders, and even the basis behind how we learn.
“Our findings indicate that learning may take place when the input neuron is active at the same time that a dendrite is active – and it could be that different parts of dendrites will be active at different times, which would suggest a lot more flexibility in how learning can occur within a single neuron,” said one of the team, Jason Moore.
The research has been published in Science.
Source: New study suggests our understanding of brain cells is flawed, and here’s why – ScienceAlert
Restorative neuroscience, the study to identify means to replace damaged neurons and recover permanently lost mental or physical abilities, is a rapidly advancing scientific field considering our progressively aging society. Redirecting immature neurons that reside in specific brain areas towards the sites of brain damage is an appealing strategy for the therapy of acute brain injury or stroke. A collaborative effort between the Center for Brain Research of Medical University of Vienna and the National Brain Research Program of Hungary/Semmelweis University in Budapest revealed that some mature neurons are able to reconfigure their local microenvironment such that it becomes conducive for adult-born immature neurons to extensively migrate. Thus, a molecular principle emerges that can allow researchers to best mobilize resident cellular reserves in the adult brain and guide immature neurons to the sites of brain damage.
The adult brain has limited capacity of self-repair
In the aging Western society, acute brain damage and chronic neurodegenerative conditions (e.g. Alzheimer’s and Parkinson’s diseases) are amongst the most debilitating diseases affecting hundreds of millions of people world-wide. Nerve cells are particularly sensitive to microenvironmental insults and their loss clearly manifests as neurological deficit. Since the innate ability of the adult human brain to regenerate is very poor and confined to its few specialized regions, a key question in present-day neurobiology is how to establish efficient strategies that can replace lost neurons, guide competent cells to the sites of injury and facilitate their functional integration to regain lost functionality. “Cell replacement therapy” thus offers frontline opportunities to design potent therapeutic interventions.
Neurons drive neurons: a new concept integrating brain activity with repair
Only two regions of the postnatal mammalian brain are known to retain their intrinsic potential to allow the generation of new neurons throughout life: the olfactory system decoding smell and the hippocampus acting as a key hub for memory encoding and storage. In humans, the generation of new neurons in the olfactory system rapidly ceases during early childhood. “Which are the processes that disallow this innate regenerative process in the human brain and how can dormant progenitors be reinstated to produce new neurons and guide those towards brain areas that require repair?” is a central yet unresolved question for brain repair strategies.
For neuronal migration, the widely-accepted concept is that support cells called astroglia are of primary importance to promote the movement of adult-born neurons through chemical signals and physical interactions. The new study involving researchers from the Department of Molecular Neurosciences of the Center for Brain Research goes well beyond these known frontiers through the discovery that the migration of new-born neurons requires resident, differentiated nerve cells to “clear their path” by digesting away some of the glue that fills the space between nerve cells. This process is dependent on the activity of resident neurons, thus suggesting the integration of the ancient developmental process of active cell movement with the integrative capacity and activity patterns of the brain. “By realizing that differentiated neurons are critical operators in this process we finally lay our hands on an “on switch” which we can use to produce a molecular landing strip for migrating neuroblasts to home in at areas of critical need” says Alán Alpár, senior author of the study.
Opportunities for restorative neuroscience
Tibor Harkany, Professor of Molecular Neurosciences at the Medical University of Vienna goes one step further “We mapped the entire molecular machinery used by differentiated neurons to make way for their migrating adult-born replacements. This clearly offers a pharmacological concept to reroute neurons in sufficient quantities for neurorepair once damage occurs. Even though distances can be considerably long, we are confident that molecular means exist to tackle these challenges”.
Brain activity defines therapeutic success?
The realization that differentiated neurons hold the key to directional cell migration is of enormous significance since they are wired into the brain circuitry, receive information from not only adjacent but also far-away regions and are activated by these specific connections at precisely given times. Consequently, migration controlled by the newly described specific neuronal subset can be aligned with brain activity, or conversely, with inactivity as evoked by neuronal loss during brain diseases. “To identify the physiological stimuli and stressors, which activate these guide-neurons will herald a new and exciting opportunity for regenerative neuroscience” adds Tomas Hökfelt, Guest Professor at the Center for Brain Research.
Like many other studies at the Department of Molecular Neurosciences, the European Research Council (ERC) and the European Molecular Biology Organisation (EMBO) frontier research programs funded this project. Alán Alpár’s work is supported by the National Brain Research Program of the Hungarian Academy of Sciences.
Source: Study offers novel principle to reroute neurons for brain repair
FEBRUARY 3, 2017
Summary: Researchers report adult neurogenesis not only helps increase the number of cells in a neural network, it also promotes plasticity in the existing network. Additionally, they have identified the role the Bax gene plays in synaptic pruning.
Source: University of Alabama at Birmingham.
One goal in neurobiology is to understand how the flow of electrical signals through brain circuits gives rise to perception, action, thought, learning and memories.
Linda Overstreet-Wadiche, Ph.D., and Jacques Wadiche, Ph.D., both associate professors in the University of Alabama at Birmingham Department of Neurobiology, have published their latest contribution in this effort, focused on a part of the brain that helps form memories — the dentate gyrus of the hippocampus.
The dentate gyrus is one of just two areas in the brain where new neurons are continuously formed in adults. When a new granule cell neuron is made in the dentate gyrus, it needs to get ‘wired in,’ by forming synapses, or connections, in order to contribute to circuit function. Dentate granule cells are part of a circuit that receive electrical signals from the entorhinal cortex, a cortical brain region that processes sensory and spatial input from other areas of the brain. By combining this sensory and spatial information, the dentate gyrus can generate a unique memory of an experience.
Overstreet-Wadiche and UAB colleagues posed a basic question: Since the number of neurons in the dentate gyrus increases by neurogenesis while the number of neurons in the cortex remains the same, does the brain create additional synapses from the cortical neurons to the new granule cells, or do some cortical neurons transfer their connections from mature granule cells to the new granule cells?
Their answer, garnered through a series of electrophysiology, dendritic spine density and immunohistochemistry experiments with mice that were genetically altered to produce either more new neurons or kill off newborn neurons, supports the second model — some of the cortical neurons transfer their connections from mature granule cells to the new granule cells.
This opens the door to look at how this redistribution of synapses between the old and new neurons helps the dentate gyrus function. And it opens up tantalizing questions. Does this redistribution disrupt existing memories? How does this redistribution relate to the beneficial effects of exercise, which is a natural way to increase neurogenesis?
“Over the last 10 years there has been evidence supporting a redistribution of synapses between old and new neurons, possibly by a competitive process that the new cells tend to ‘win,’” Overstreet-Wadiche said. “Our findings are important because they directly demonstrate that, in order for new cells to win connections, the old cells lose connections. So, the process of adult neurogenesis not only adds new cells to the network, it promotes plasticity of the existing network.”
The study opens the door to look at how this redistribution of synapses between the old and new neurons helps the dentate gyrus function. NeuroscienceNews.com image is for illustrative purposes only.
“It will be interesting to explore how neurogenesis-induced plasticity contributes to the function of this brain region,” she continued. “Neurogenesis is typically associated with improved acquisition of new information, but some studies have also suggested that neurogenesis promotes ‘forgetting’ of existing memories.”
The researchers also unexpectedly found that the Bax gene, known for its role in apoptosis, appears to also play a role in synaptic pruning in the dentate gyrus.
“There is mounting evidence that the cellular machinery that controls cell death also controls the strength and number of synaptic connections,” Overstreet-Wadiche said. “The appropriate balance of synapses strengthening and weakening, collectively termed synaptic plasticity, is critical for appropriate brain function. Hence, understanding how synaptic pruning occurs may shed light on neurodevelopmental disorders and on neurodegenerative diseases in which a synaptic pruning gone awry may contribute to pathological synapse loss.”
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
All of the work was performed in the Department of Neurobiology at UAB. In addition to Overstreet-Wadiche and Wadiche, co-authors of the paper, “Adult born neurons modify excitatory synaptic transmission to existing neurons,” published in eLife, are Elena W. Adlaf, Ryan J. Vaden, Anastasia J. Niver, Allison F. Manuel, Vincent C. Onyilo, Matheus T. Araujo, Cristina V. Dieni, Hai T. Vo and Gwendalyn D. King.
Much of the data came from the doctoral thesis research of Adlaf, a former UAB Neuroscience graduate student who is now a postdoctoral fellow at Duke University.
Funding: Funding for this research came from Civitan International Emerging Scholars awards, and National Institutes of Health awards or grants NS098553, NS064025, NS065920 and NS047466.
Source: Jeff Hansen – University of Alabama at Birmingham
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Full open access research for “Adult-born neurons modify excitatory synaptic transmission to existing neurons” by Elena W Adlaf, Ryan J Vaden, Anastasia J Niver, Allison F Manuel, Vincent C Onyilo, Matheus T Araujo, Cristina V Dieni, Hai T Vo, Gwendalyn D King, Jacques I Wadiche, and Linda Overstreet-Wadiche in eLife. Published online January 30 2017 doi:10.7554/eLife.19886
Did You Know How Loud Balloons Can Be?
Adult-born neurons are continually produced in the dentate gyrus but it is unclear whether synaptic integration of new neurons affects the pre-existing circuit. Here we investigated how manipulating neurogenesis in adult mice alters excitatory synaptic transmission to mature dentate neurons. Enhancing neurogenesis by conditional deletion of the pro-apoptotic gene Bax in stem cells reduced excitatory postsynaptic currents (EPSCs) and spine density in mature neurons, whereas genetic ablation of neurogenesis increased EPSCs in mature neurons. Unexpectedly, we found that Bax deletion in developing and mature dentate neurons increased EPSCs and prevented neurogenesis-induced synaptic suppression. Together these results show that neurogenesis modifies synaptic transmission to mature neurons in a manner consistent with a redistribution of pre-existing synapses to newly integrating neurons and that a non-apoptotic function of the Bax signaling pathway contributes to ongoing synaptic refinement within the dentate circuit.
“Adult-born neurons modify excitatory synaptic transmission to existing neurons” by Elena W Adlaf, Ryan J Vaden, Anastasia J Niver, Allison F Manuel, Vincent C Onyilo, Matheus T Araujo, Cristina V Dieni, Hai T Vo, Gwendalyn D King, Jacques I Wadiche, and Linda Overstreet-Wadiche in eLife. Published online January 30 2017 doi:10.7554/eLife.19886
Source: Brain Plasticity: How Adult Born Neurons Get Wired – Neuroscience News