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Recent News and Articles on the Keywords: newborn neurons + newborn + neurons  Related to the article below (Last Update: 7/1/2008)

Adult Stem Cells Reprogrammed In Their Natural Environment
Science Daily (press release) -
Under normal conditions, the majority of newborn cells differentiated into neurons. When he introduced the Ascl1, which had previously been shown to be ...
Photo by Einat Adar
ScienceBlogs - Jun 6, 2008
He and his colleagues showed that the survival of newborn neurons in the forebrain of the adult zebra finch (Taeniopygia guttata) was significantly affected ...
Stem cells show promise in treating fatal children?s disease
Fresh News, India - Jun 7, 2008
Myelin coats long sections, known as axons, of brain cells called neurons, without which electrical signalling between neurons becomes sluggish and muddied, ...
First stem cell trials might start in OC
OCRegister, CA - Jun 25, 2008
Affecting fewer than 1000 infants per year in the United States, the genetic disease causes motor neurons to degenerate, leaving the baby unable to control ...
How the Mind Works: Revelations
The New York Review of Books - Jun 5, 2008
The brain is of course tremendously complex: a bundle of some hundred billion neurons, or nerve cells, each sharing as many as ten thousand connections with ...
Investigating the complexity of respiratory patterns during the ...
7thSpace Interactive (press release), NY - Jun 20, 2008
... exhibit lower complexity, suggesting that a synchronized homogeneous group of neurons in the central respiratory network are active during these events. ...
Human Stem Cells Show Promise Against Fatal Children's Diseases
Science Daily (press release) - Jun 4, 2008
Myelin coats long sections, known as axons, of brain cells called neurons, and without it, the electrical signaling between neurons becomes sluggish and ...
Respiratory Control in Neonatal Rats Exposed to Prenatal Cigarette ...
RedOrbit, TX - Jun 3, 2008
Point: medullary pacemaker neurons are essential for both eupnea and gasping in mammals vs. medullary pacemaker neurons are essential for gasping, ...
Stem Cells Stop Mouse Shivers Cold, Could Thwart Rare ...
Scientific American - Jun 5, 2008
The problems are caused by disruptions in nerve cell (neuron), communication triggered by a lack of myelin, which, in normal nerve cells, ...
Natus Medical raises FY and Q2 revenue guidance
SmallCapInvestor - Jun 5, 2008
Neuron diagnostic and newborn care products manufacturer Natus Medical Inc. (Nasdaq:BABY) this morning raised its full year and second quarter 2008 revenue ...BABY
Source: Google News

Enriched Odor Exposure Increases the Number of Newborn Neurons in the Adult Olfactory Bulb and … -
C Rochefort, G Gheusi, JD Vincent, PM Lledo - Journal of Neuroscience, 2002 - neuroscience.org
... 2689. Enriched Odor Exposure Increases the Number of Newborn Neurons in the
Adult Olfactory Bulb and Improves Odor Memory. Christelle ...

Epidermal growth factor and fibroblast growth factor-2 have different effects on neural progenitors … -
HG Kuhn, J Winkler, G Kempermann, LJ Thal, FH Gage - J Neurosci, 1997 - Soc Neuroscience
... EGF, on the other hand, reduced the total number of newborn neurons reaching the
olfactory bulb and substantially enhanced the generation of astrocytes in the ...

… of cAMP Signaling Facilitates the Morphological Maturation of Newborn Neurons in Adult Hippocampus -
T Fujioka, A Fujioka, RS Duman - Journal of Neuroscience, 2004 - neuroscience.org
... Development/Plasticity/Repair Activation of cAMP Signaling Facilitates the
Morphological Maturation of Newborn Neurons in Adult Hippocampus. ...

GABAergic Signaling to Newborn Neurons in Dentate Gyrus -
LO Wadiche, DA Bromberg, ASL Bensen, GL Westbrook - Journal of Neurophysiology, 2005 - Am Physiological Soc
... REPORT. GABAergic Signaling to Newborn Neurons in Dentate Gyrus. ... sIPSCs in newborn
neurons decayed more slowly than sIPSCs in neighboring mature granule cells. ...

… causes abnormalities in glutamate transporters and death of astroglia and neurons in newborn -
LJ Martin, AM Brambrink, C Lehmann, C Portera- … - Ann Neurol, 1997 - ncbi.nlm.nih.gov
Ann Neurol. 1997 Sep;42(3):335-48. Hypoxia-ischemia causes abnormalities in glutamate
transporters and death of astroglia and neurons in newborn striatum. ...

Functional integration of adult-born neurons -
M Carlen, RM Cassidy, H Brismar, GA Smith, LW … - Curr Biol, 2002 - current-biology.com
... Previous studies have shown that newborn neurons in the adult dentate gyrus, upon
maturation, extend appropriate axonal processes to the CA3 subregion of the ...

GABA regulates synaptic integration of newly generated neurons in the adult brain -
S Ge, ELK Goh, KA Sailor, Y Kitabatake, G Ming, H … - Nature, 2006 - pubmedcentral.nih.gov
... GABA, the major inhibitory neurotransmitter in the adult brain, initially exerts
an excitatory action on newborn neurons due to their high cytoplasmic chloride ...

Neonatal and Adult Neurogenesis Provide Two Distinct Populations of Newborn Neurons to the Mouse … -
M Lemasson, A Saghatelyan, JC Olivo-Marin, PM … - Journal of Neuroscience, 2005 - Soc Neuroscience
... Development/Plasticity/Repair Neonatal and Adult Neurogenesis Provide Two Distinct
Populations of Newborn Neurons to the Mouse Olfactory Bulb. ...

Neuropeptide expression by newborn and adult rat sensory neurons in culture: effects of nerve growth … -
PK Mulderry - Neuroscience, 1994 - ncbi.nlm.nih.gov
... They also stimulated vasoactive intestinal polypeptide expression in newborn rat
neurons in the presence of nerve growth factor but not to such high levels as ...

… K+ channels during anoxia: major differences between rat (newborn and adult) and turtle neurons -
C Jiang, Y Xia, GG Haddad - The Journal of Physiology, 1992 - Physiological Soc
... RESEARCH PAPERS. Role of ATP-sensitive K+ channels during anoxia: major
differences between rat (newborn and adult) and turtle neurons. ...

Source: Google Scholar
 

Newborn Neurons Like to Hang with the In-Crowd

Like any new kid on the block that tries to fit in, newborn brain cells need to find their place within the existing network of neurons. The newcomers jump right into the fray and preferentially reach out to mature brain cells that are already well connected within the established circuitry, report scientists at the Salk Institute for Biological Studies in the online edition of Nature Neuroscience.

At first, they gingerly sniff out pre-existing connections between brain cells but as the new neurons mature over time they get emboldened and muscle out the old guys. “Adding new neurons could be a very problematic process if newborn cells would make connections all over the place,” explains Fred H. Gage, Ph.D., a professor in the Gene Expression Laboratory and the Vi and John Adler Chair for Research on Age-Related Neurodegenerative Diseases. “But if they are only replacing already existing connections there is less chance of error,” he adds.

Article continues below and (thank you)

 

Newborn neurons send out tiny dendritic protrusions (shown in green) that seek out pre-synaptic areas -- the sending terminals of nerve cells (shown in purple) -- that are already well connected within the established circuitry (shown in red). Middle: Over time, the tip of the dendritic protrusions thickens, strengthening the connection between young and old. Top: As the young neuron matures, it monopolizes the synaptic connection site.

Top: Newborn neurons send out tiny dendritic protrusions (shown in green) that seek out pre-synaptic areas -- the sending terminals of nerve cells (shown in purple) -- that are already well connected within the established circuitry (shown in red). Middle: Over time, the tip of the dendritic protrusions thickens, strengthening the connection between young and old. Top: As the young neuron matures, it monopolizes the synaptic connection site.

 

Neurons make contact via specialized structures called synapses. As a signal traveling along a nerve branch arrives at the pre-synaptic area, it releases a chemical signal. The signaling molecules travel across the synapse and induce a signal on the neighboring, receiving nerve fiber or dendrite. A typical neuron sports about 7,000 synapses through which it stays in touch with roughly 1,000 other cells. But just how young neurons make their presence known and hook up with already well-connected elders has been unclear.

“If you have hopes that one day neuronal stem cells can replace damaged neurons in neurodegenerative diseases such as Alzheimer’s or Parkinson’s disease you have to ensure that these cells make proper connections, form functional synapses and integrate into the rest of the brain,” says postdoctoral fellow Nicolas Toni, Ph.D., who headed the current study.

To figure out how the newcomers do it, the Salk researchers injected a virus carrying the gene for green fluorescent protein into the hippocampus, a brain region harboring neural stem cells that give rise to new neurons. Newly born neurons infected with virus were marked by a fluorescent dye enabling the researchers to follow their fate over time as they tried to get accepted into the existing circuitry.

 

With the help of a whole arsenal of high-tech imaging technology and the electron tomography expertise of Mark. H. Ellisman, Ph.D., a professor at the National Center for Microscopy and Imaging Research at the University of California, San Diego, Toni then zoomed in at a nanometer scale and watched how the young and the old got acquainted.

He observed that between three and four weeks after injection of the virus newborn neurons sent out dendritic filopodia—tiny feelers that probe the environment. “When we analyzed them in three dimensions, the tip of the filopodia was preferentially associated with synapses already connected to other neurons,” explains Toni.

However, as the new neurons matured, the tiny tips filled out and started to monopolize the synaptic connections. “That’s what we believe is the crux of the study: the survival of new neurons may depend on the ability to compete out the older existing neurons,” says Gage. Earlier studies had shown that if young neurons fail to receive signals from other brain cells they wither and die. By connecting to functional synapses, the newborn neurons ensure that they are not reaching out to deadbeats.

The Gage lab previously identified a subunit of the NMDA receptor, a protein complex that transduces signals sent by neighboring cells, as the newborn neurons’ life-saving equipment. The NMDA receptor is activated by the neurotransmitter glutamate, a chemical released by neurons in order to transmit information to neighboring cells. Whenever the receptor picks up a glutamate signal it is stimulated and relays the signal. For young neurons that signal means survival.

As a matter of fact, only about half of all newly born neurons manage to successfully integrate into the existing network of brain cells, at least in mice living in bare standard cages. Providing the mice with a stimulating, enriched environment—large cages filled with running wheels, colored tunnels and playmates—boost the number of neurons that manage to hook up with the existing network to 80 percent, reinforcing the observation that using one’s brain cells is the best way to optimize brain function throughout one’s lifetime.

Also contributing to the study where postdoctoral researchers E. Matthew Teng, Ph.D., James B. Aimone, Ph.D., Chunmei Zhao, Ph.D., Antonella Consiglio, Ph.D., staff scientist Henriette van Praag, Ph.D., all at the Salk Institute, and postdoctoral fellows Eric A. Bushong , Maryann E. Martone, Ph.D., and Mark H. Ellisman at the National Center for Microscopy and Imaging Research at the University of California, San Diego.

The Salk Institute for Biological Studies in La Jolla, California is an independent nonprofit organization dedicated to fundamental discoveries in the life sciences, the improvement of human health, and the training of future generations of researchers. Jonas Salk, M.D., whose polio vaccine all but eradicated the crippling disease poliomyelitis in 1955, opened the Institute in 1965 with a gift of land from the City of San Diego and the financial support of the March of Dimes.

 
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Transcript: "How Alzheimer's Affects Neurons in the Brain"

Narrator: The human brain employs a complex mix of chemical and electrical processes allowing us to speak, move, see, think, and remember. To do this, the brain operates a vast communications network made up of billions of nerve cells called neurons. Within this network, chemical messages - or neurotransmitters pass in fractions of a second from one neuron to another. An electrical charge travels to the end of the neuron resulting in the release of messages along countless pathways. Alzheimer's disease disrupts this intricate signaling system. Mostly to blame are two abnormal structures in the brain -- amyloid plaques and neurofibrillary tangles. Plaques are made of beta amyloid, a toxic molecule that comes from a normal protein. Something causes enzymes to snip this protein. The beta amyloid fragments can clump together into damaging plaques. Tangles form following changes in the protein tau. Normally, tau stabilizes the internal support structure of neurons, but in Alzheimer's disease changes cause threads of tau to become entangled, killing the neuron by damaging critical parts of its transport system. As Alzheimer's disease progresses, more and more neurons die. The brain shrinks. Memory is lost. Today's research tells us a great deal about the development of plaques and tangles, ultimately allowing us to unravel the secrets behind Alzheimer's disease. With new understanding, we look forward to better ways to treat and perhaps even to prevent this devastating disease.

What is ALS

Amyotrophic lateral sclerosis (ALS), often referred to as "Lou Gehrig's disease," is a progressive neurodegenerative disease that affects nerve cells in the brain and the spinal cord. Motor neurons reach from the brain to the spinal cord and from the spinal cord to the muscles throughout the body. The progressive degeneration of the motor neurons in ALS eventually lead to their death. When the motor neurons die, the ability of the brain to initiate and control muscle movement is lost. With voluntary muscle action progressively affected, patients in the later stages of the disease may become totally paralyzed. Yet, through it all, for the vast majority of people, their minds remain unaffected.

A-myo-trophic comes from the Greek language. "A" means no or negative. "Myo" refers to muscle, and "Trophic" means nourishment---"No muscle nourishment." When a muscle has no nourishment, it "atrophies" or wastes away. "Lateral" identifies the areas in a person's spinal cord where portions of the nerve cells that signal and control the muscles are located. As this area degenerates it leads to scarring or hardening ("sclerosis") in the region.

As motor neurons degenerate, they can no longer send impulses to the muscle fibers that normally result in muscle movement. Early symptoms of ALS often include increasing muscle weakness, especially involving the arms and legs, speech, swallowing or breathing. When muscles no longer receive the messages from the motor neurons that they require to function, the muscles begin to atrophy (become smaller). Limbs begin to look "thinner" as muscle tissue atrophies.

Nerves

What Types of Nerves Make Your Body Work Properly?

(from Living with ALS, Manual 1: What's It All About?)

       The body has many kinds of nerves. There are those involved in the process of thinking, memory, and of detecting sensations (such as hot/cold, sharp/dull), and others for vision, hearing, and other bodily functions. The nerves that are affected when you have ALS are the motor neurons that provide voluntary movements and muscle power. Examples of voluntary movements are your making the effort to reach for the phone or step off a curb; these actions are controlled by the muscles in the arms and legs.

       The heart and the digestive system are also made of muscle but a different kind, and their movements are not under voluntary control. When your heart beats or a meal is digested, it all happens automatically. Therefore, the heart and digestive system are not involved in ALS. Breathing also may seem to be involuntary. Remember, though, while you cannot stop your heart, you can hold your breath - so be aware that ALS may eventually have an impact on breathing.

 

Although the cause of ALS is not completely understood, the recent years have brought a wealth of new scientific understanding regarding the physiology of this disease.

While there is not a cure or treatment today that halts or reverses ALS, there is one FDA approved drug, Rilutek®, that modestly slows the progression of ALS as well as several other drugs in clinical trials that hold promise.

Importantly, there are significant devise and therapies that can manage the symptoms of ALS that help people maintain as much independence as possible and prolong survival.  It is important to remember that ALS is a quite variable disease; no two people will have the same journey or experiences.  There are medically documented cases of people in whom ALS ‘burns out,’ stops progressing or progresses at a very slow rate.  No matter what your individual course or situation may be, The ALS Association and your medical team are here to help.

To learn more about the personal stories of people who are living fully, click here. As one man put it, “I’ve made ALS part of my life, not my whole life.”   

 

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