As you
read the words on this page, you are utilizing thousands of
the 100 billion (more or less) nerve cells that make up your
brain. The electrical firings and chemical messages running
between these cells, called neurons, are what produce our
thoughts, feelings and interactions with the world around
us.
One hundred
billion neurons may seem like a lot of nerve cells, but is
actually only about 20% of the number we originally start
with. The number of nerve cells in our brain peaks prenatally
and then they start to prune themselves out, one by one, through
childhood. By the time we enter adolescence, our brain has
chosen the final select neurons it will keep throughout our
adult life. The decision is based on which cells we use and
which we do not. The cells we do not use are pruned away leaving
more room to add branches, or dendrites, to the nerve cells
that we do use. New branches are added as the brain receives
and processes any new information.
How does
the brain actually "prune" the garden? The answer lies in
a number of chemicals and their actions and reactions. The
chief pruner is probably an enzyme named Calpain. Calpain
has the ability to self-destruct a cell. Technically this
is known as autolysis ("auto" meaning self, and "lysis" meaning
to destroy).
Calpain
is produced in the nerve cells when there is a heavy calcium
ion concentration in their surrounding environment. Reduced
blood flow can cause this high calcium ion build up between
and within cells (for you biology enthusiasts, the calcium
comes from the mitochondria and the ER as well as an influx
from outside the cell). In other words, high activity in a
brain region calls for heavy blood flow to service the cells,
low activity requires little blood flow. Therefore, the less-used
areas, with their limited blood flow activity, tend to build
up calcium ions. This build-up triggers the secretion of the
enzyme Calpain, which causes the nerve cell to self -destruct.
New growth,
on the other hand, comes in the dendrite development, or branching
of well-used neurons. This branching is caused from chemicals
known as Neurotrophins. Neurotrophins are a group of proteins
which are responsible for the growth and development of neurons.
As you may suspect, we use a lot of neurotrophins during childhood
as the brain has massive growth and development. But we continue
to use neurotrophins all of our lives, especially in the hippocampus
area, the brain region responsible for new learning and new
memory formation.
There
are many neurotrophins at work in the brain. The first one
discovered is known as NGF (nerve growth factor). Others,
discovered since, have equally self-explanatory names as brain
derived neurotrophic factor (bFGF), and glial cell-line derived
neurotropic factor (GDNF). These neurotrophins work by attaching
themselves to receptor sites on nerve cells and causing the
cell membrane to change shape, grow and branch.
Because
most growth hormones throughout the body are especially active
during sleep, it is thought that the majority of neurotrophic
work is also done during sleep, especially the non-REM cycles
of sleep. The work of Marcos Frank and Michael Stryker, at
UC San Francisco, caught the education world by surprise in
2001 with their startling research showing the tremendous
amount of branching and subsequent learning that took place
during sleep. While most of the science community historically
considered that the REM, or dreaming cycle of sleep was the
time when most wiring took place, Stryker's work and the research
following that study continue to show that it is actually
the non-REM cycles that help hard wire in the information
learned the previous day.
From a
practical standpoint, sleep research continues to show the
importance of sleep to the learning brain. Students MUST get
sufficient sleep following the learning of new information
if we want that information stored in a long-term, complex
network of neuron branches.
The research
on brain wiring and the biology behind it continues to be
a fascinating topic. It gives hope to people with stroke damage,
Alzheimer's and other neurological problems, as well as providing
a better understanding for those of us who parent and teach
young brains.
Remember
to learn something new today. . . then sleep on it.
References:
Bax, et al. (1997). Structure, 5,
1275-1285.
Birkbeck, et al. 1991. Nature 354: 411-414.
Bothwell, M. & Rev, A. (1995). Neuroscience. 18, 223-253.
Cunningham, L. et al. (1994). Brain Research, 658, 219-231.
Date, I. et al. (1996). Neurosurgery, 84, 1006-1012.
DiStefano, P. et al (1992). Neuron, 8, 983-993.
Frank, M. & Stryker, M. 2001, April 26. Neuron.
Gage, F. et al. (1988). Neurology. 269, 147-155.
Kang, H., et al. (1997). Neurotrophins and time: different
roles for TrkB signaling in hippocampal long-term potentiation,,
Neuron, 19, 653-664.
Kang, H. & Schuman, E.M. (1996). A requirement for local
protein synthesis in neurotrophin-induced synaptic plasticity,
Science, 273, 1402-1406.
Lindholm D, et al. (1997). Neurotrophins and cerebellar development.
Perspectives on Developmental Neurobiology. 5(1):83-94.
Lindsay, R. et al. (1994). Neuroscience. 17, 182-190.
Paschen W. & Doutheil J. (1999). Disturbances of the functioning
of endoplasmic reticulum: A key mechanism underlying neuronal
cell injury? Journal of Cerebral Blood Flow & Metabolism.
19(1):1-18.
Schweizer F. et al., (1998). Regulation of neurotransmitter
release kinetics by NSF. Science. 279(5354):1203-1206.
Thoenen, H. (1995). Neurotrophins and neuronal plasticity.
Science 270: 593-598.