IUBio

a thinking brain

ray scanlon rscanlon at nycap.rr.com
Mon Jun 28 12:18:21 EST 2004


Learning:

Learning is not fundamentally part of the process of thinking,
although thinking presupposes learning. If the thalamic reticular
nucleus were active in the brain as constructed by the DNA, it is
difficult to image anything of interest happening. When we talk about
thinking, we subconsciously posit a brain that has been up against the
environment and has learned a few things.

Before we consider what in learning is germane to the design of a
thinking brain, we should point out what is not. The research on
learning by psychologists is almost wholly irrelevant. What is
behavior except the expression of a motor program through the
motoneurons? Our interest is in the motor program as it passes through
the thalamus. At this level, all motor programs are the same. They are
just motor programs. They all have their origin in a pattern
generator. We think of pattern generators in groups. For instance,
reaching, grasping, and punching form a group that we distinguish from
kicking. However, future research may locate all of these pattern
generators in one small region, in which case we might want to group
them together on anatomical grounds. Who can say? It is not important.

It is widely held that there are two basic types of memory, long term
and short term. It is also held (but not so widely) that long term
memory involves structural change in the neuron and that short term
does not. Both are involved in thinking

Many candidates for structural change are advanced. The most popular
ones involve the synapse. The area of the synapse can be increased or
new synapses formed. The post-synaptic density can be increased. The
pre-synaptic potential or propensity for releasing neurotransmitter
can be increased. There seems no end to possibilities.

To those interested in thinking, these many choices have little
meaning. The brain can learn and that is enough.

With learning comes forgetting. And forgetting may be just as
important. New synapses can be formed, but old ones can be sloughed.
The brain is alive and interacting with the environment. At the same
time, we must always remember that the basic architecture of the
brain, as laid down by the DNA, is unalterable. The nuclei remain
unaltered, but smaller regions may be reorganized.

There are endless schemes, of course, for explaining how one learns to
avoid fire and other dangerous things, but we will choose one that
appeals on grounds of simplicity.

Learning to avoid the bad and approach the good are two sides of the
same coin. We will assume that upon disaster a neurohormone is
released—call it the A neurohormone. Upon a success, a different
neurohormone is released—call it the B neurohormone.

The A neurohormone strengthens recently exercised excitatory synapses
in the thalamic reticular nucleus and also (possibly) inhibitory
synapses in the central pattern generator that initiated the action.
Note that excitatory synapses in the thalamic reticular nucleus
include not only the motor program but also sensory input from the
environment.

If the same bad situation arises again, the motor program will tend
not to be activated, and if it is activated it will tend to be stopped
at the ventral anterior-ventral lateral complex. Bad things are
avoided.

Exactly the reverse happens with the B neurohormone. Recently
exercised inhibitory synapses in the thalamic reticular nucleus and
also (possibly) excitatory neurhormones in the central pattern
generator that initiated the action.

If the same good situation arises again, the motor program will tend
to be activated and will be passed through the ventral
anterior-ventral lateral complex. Good things are approached.

This fandango with the A and B neurohormones is enough to get us
through life.

A neurohormone is a hormone produced by or acting on the nervous
system, compared to hormones produced by the endocrine system.

The brain could have been organized as a mass of equipotential
neurons. It wasn't. One wonders why. A possible explanation is to
restrict the activity of neurohormones. Releasing a neurohormone in
the thalamic reticular nucleus, as an instance, would tend to
concentrate the hormonal activity where it would do the most good. If,
of course, the goal of the neurohormone is to reach neurons in the
thalamic reticular nucleus.

In the last analysis, we are always reduced to the principle of
survival. That which survived, survived. A brain composed of nuclei
did survive.

When one reaches for a cup of coffee, a hierarchy of neurons is
activated. A reaching pattern controller is activated. It fires a
reaching pattern initiator. The reaching pattern initiator releases a
reaching pattern generator that, in turn, sets off the motoneurons. We
reach.

We speak of these as units, but in the mammalian brain they are
populations of neurons, not individual neurons. To return to the cup
of coffee, does the reaching pattern controller consist of fifty or
five hundred neurons? It is certainly a relatively small number, but
not too small. It is important to remember that the reaching pattern
controller, initiator, generator, is set up by the DNA, not by
experience. Experience modifies the pattern generator and the thalamic
reticular nucleus, as we have set out above.

In one sense, of course, all the neurons are working all the time, but
some are more equal than others. On the one hand, we see the original
neural net as it exists in the most primitive animals. Excitation
flows back and forth through the neural net. At one glance, all are
equal. But there are cusps. The excitation does become concentrated at
points. Evolution has caused these cusps to reside in nuclei—that's
about all there is to it.

ray



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