This note was posted on another forum and I thought it might be of interest. It
can help
underscore why hyper-localized training processes are misguided in their
fundamental
assumptions about where, how, what and why to train. The CNS is simply vastly
more
interconnected on multiply interconnected levels than previous linear
conceptions had
imagined. Of course the article is largely oriented to medication and medical
implications,
but it also indicates a horizon of possibilities about how the CNS actually
communicates
with itself -- and that might seem quite new to many.

And that can have profound implications for how neurofeedback training can be
done.


Contact: PD Dr. Dirk Dietrich
dirk.dietrich@...
49-228-287-19224
University of Bonn <http://www.uni-bonn.de>

Brain works more chaotically than previously thought
Information is not only transferred at synapses
This release is also available in German
<http://www.eurekalert.org/staticrel.php?view=ubonn02272007> .
The brain appears to process information more chaotically than has long been
assumed. This is demonstrated by a new study conducted by scientists at the
University of Bonn. The passing on of information from neuron to neuron does
not, they show, occur exclusively at the synapses, i.e. the junctions
between the nerve cell extensions. Rather, it seems that the neurons release
their chemical messengers along the entire length of these extensions and,
in this way, excite the neighbouring cells. The findings of the study are of
huge significance since they explode fundamental notions about the way our
brain works. Moreover, they might contribute to the development of new
medical drugs. The study is due to appear shortly in the prestigious
academic journals "Nature Neuroscience" and has already been posted online
(doi:10.1038/nn1850).
Until now everything seemed quite clear. Nerve cells receive their signals
by means of little "arms", known as dendrites. Dendrites pass on the
electrical impulses to the cell body, or soma, where they are processed. The
component responsible for "distributing" the result is the axon. Axons are
long cable-like projections of the cell along which the electrical signals
pass until they meet, at a synapse, the dendritic arm of another neuron. The
synapse presents an insurmountable barrier to the neuron's electrical
pulses. The brain overcomes this obstruction by means of an amazing signal
conversion: the synapse releases chemical messengers, known as
neurotransmitters, which diffuse to the dendrites. There, they dock onto
specific receptors and generate new electrical impulses. "It was previously
thought that neurotransmitters are only released at synapses," points out
Dr. Dirk Dietrich at Bonn University. "But our findings indicate that this
is not the case."
The messenger attracts insulating cells
Together with his colleagues Dr. Maria Kukley and Dr. Estibaliz
Capetillo-Zarate, Dietrich has conducted a careful examination of the "white
matter" in the brain of rats. This substance contains the "cable ducts"
linking the right and left halves of the brain. They consist essentially of
axons and ancillary cells. There are no dendrites or even synapses here. "So
it is not a place where we would expect to see the release of messengers,"
the neuroscientist explains.
Yet it is in the white matter that the scientists have made a remarkable
discovery. As soon as an electrical impulse runs through an axon cable, tiny
bubbles containing glutamate travel to the axon membrane and release their
content into the brain. Glutamate is one of the most important
neurotransmitters, being released when signal transmission occurs at
synapses. The researchers were able to demonstrate that certain cells in the
white matter react to glutamate: the precursor to what are known as
oligodendrocytes. Oligodendrocytes are the brain's "insulating cells". They
produce the myelin, a sort of fatty layer that surrounds the axons and
ensures rapid retransmission of signals. "It is likely that insulating cells
are guided by the glutamate to locate axons and envelope them in a layer of
myelin," says Dirk Dietrich.
As soon as the axons leave the white "cable duct" they enter the brain's
grey matter where they encounter their receptor dendrites. Here, the
information is passed on at the synapses to the receptor cells. "We think,
however, that on their way though the grey matter the axons probably release
glutamate at other points apart from the synapses," Dietrich speculates.
"Nerve cells and dendrites are closely packed together here. So the axon
could not only excite the actual receptor but also numerous other nerve
cells."
If this hypothesis is correct, the accepted scientific understanding of the
way neurons communicate, which has prevailed for over a hundred years, will
have to be revised. In 1897 Sir Charles Sherrington first put forward the
idea that chemical messengers are only released at "synapses", a term he
coined. According to the founder of modern neurophysiology this means that
nerve cells can only communicate with a small number of other nerve cells,
i.e. only with those with which they are connected via synapses. This
concept is the basis of the notion that neuronal information in the brain,
somewhat like electricity in a computer, only spreads directionally in the
brain, following specific ordered circuits.
Too much glutamate is the death of cells
There is, however, also an aspect to the research team's discovery that is
of considerable medical interest. It has long been known that in the event
of oxygen deficiency or a severe epileptic fit, large numbers of insulating
cells in the white matter are destroyed. The trigger for this damage is our
old friend, the neurotransmitter glutamate. "Nobody knew until now where the
glutamate actually comes from," says Dr. Dietrich. "Our results might open
the door to totally new therapeutic options." After all, drugs have already
been developed that prevent glutamate bubbles from discharging their load
into the brain. Indeed, Bonn's neuroscientists now know precisely which
receptors of the insulating cells are stimulated by the neurotransmitter ˆ
another starting point for developing new drugs.
Yet, why can glutamate sometimes be so dangerous? When an epileptic fit
occurs, the nerve cells "fire" very rapidly and fiercely. In this event so
many impulses run through the axons that large quantities of glutamate are
released all at once. "In these concentrations the neurotransmitter damages
the insulating cells," says Dietrich. "It's the dosage that makes it
harmful."