[From Bjorn Simonsen (2005.06.23,11:00 EST)]
From Bill Powers (2005.06.22.0904 MDT)
What is there in the explanation up to this point that makes the
reference value change? Why doesn't a perceptual signal simply
change? I assume that all the facts you report are correct. But
what effect do the changes you report have on all the rest of the
brain? Why is an increase in stimulation of a receptor treated
as a good effect or a bad effect by the rest of the brain? Why
isn't it just treated as an increase? The result of an increase of
a signal will depend on what the reference level for that signal
is, and how the associated control system is organized. Why
isn't the sudden change caused by the nicotine simply treated
as a disturbance, and corrected?
Your questions put me on a test. I am sorry I will use so many words, but I
cannot do it in another way.
What is there in the explanation up to this point that makes the reference
value change?
Dendrites act as receiving stations for incoming signals from other neurons.
If the signals are strong and/or sustained, they will be conducted along
the branch of the dendrite down to the cell body.
If the new net difference in voltage is large enough within the target cell,
it causes the sodium channels to open. Then a potential signal is generated.
An action potential is always the same size, typically some 90 millivolts.
( [From Bruce Abbott (2004.12.21.1800 EST)] and other places.
Because an action potential cannot be made bigger, the neuron will instead
generate more and more action potentials. The frequency will increase.
Conclusion: The frequency in the addresser neuron releases an amount
acetylcholine in the synapse. On the outside of the target neuron there
are special proteins called receptors. When the transmitter (acetylcholine)
meet the receptor it is formed a new chemical molecule of the two. This
molecule opens the channels for sodium or alternatively one of the other
ions. The entry or exit of any of these ions will be reflected in a
transient change in potential difference in the target cell. This signal
goes to the cell body.
A certain frequency in the addresser neuron results in a certain frequency
in the axon in the receiver neuron.
And Now. .... Then you start smoking for the first time. After 10 seconds
the nicotine reaches the brain. Nicotine (a supplement to acetylcholine)
works as a transmitter (acetylcholine) on _one_ type of receptors. The
stimulation of the receptor becomes far greater than would normally be the
case for acetylcholine itself.
Conclusion Conclusion: With nicotine in the brain some receiver neurons will
excite a higher frequency. The reference value somewhere changes.
Why doesn't a perceptual signal simply change?
Of course the perceptual signal changes. When the reference value is
increased, we wish something more. If the reference value is reduces, we
wish something less. Our actions also changes.
I assume that all the facts you report are correct. But what effect do the
changes you report have on
all the rest of the brain?
My "facts" come from one of us: [From Bruce Abbott (2004.12.21.1800 EST)].
and http://bio.winona.edu/berg/ANIMTNS/actpot.htm and m.m.
Nicotine actually works on one type of receptors, the type that is reserved
for acetylcholine. It doesn't work on the whole Brain. But the actual
receiver neurons) are organized with other neurons. And they will or may
respond to the change.
Why is an increase in stimulation of a receptor treated as a
good effect or a bad effect by the rest of the brain?
I don't know. It depends how the receiver neuron (above) is organized. But I
can imagine (this is just a thought and I will appreciate your comment) that
a reduced stimulation will result in too low (or a near zero reference)
references here and there. And this will result in reorganization.
Why isn't it just treated as an increase?
It is. And you presented your thoughts about the consequence of increased
perceptual signal or reference signal in [From Bill Powers (2005.06.17.0651
MDT)].
The result of an increase of a signal will depend on what the
reference level for that signal is, and how the associated
control system is organized.
Yes of course. It is not easy to forecast where the hare jumps.
Why isn't the sudden change caused by the nicotine simply treated
as a disturbance, and corrected?
It is. All perceptual signals coming from one level is a disturbance in the
input function at a higher level. And it the perceptual signals are
corrected when you take a new cigarette. I liked this last answer. 
You could make a similar presentation for the effects of any
stimulus on any part of the nervous system. But there is nothing
in such a description to predict how the whole system will act
when such a change happens.
Yes I agree. But maybe I mis-understand you. Of course nobody could tell how
the system would act the first time a person (the first person who smoked
tobacco) lighted a cigarette.
To make a prediction, you have to know what all the control
systems are, what their parameters and reference settings
are, and how they relate to the other control systems in the
same brain. The chemistry of neurotransmitters
is never going to explain that.
I absolutely agree. I also agree with your last sentence. But I have not
used the word prediction. I will not use the word prediction when we talk
about nicotine, medicine or other chemicals. I think chemicals have an
effect, but the effect is dependent on parameters, reference settings and
organization.
I think many doctors also think so about chemicals/medicines, but they don't
know anything about PCT.
The reference value in a loop is changed.
Why do you say that? How do you know the nicotine isn't
affecting a perceptual signal, or the way a comparator works,
or an output signal?
There are many loops and many reference signals. Of course I could say that
nicotine affects a perceptual signal. But a copy of that perceptual signal
goes to a higher level, and to a higher level. There the effect is a changed
error and a changed output signal. And an output signal at one level may
become a reference signal at a lower level. Am I wrong when I think a change
in a perceptual signal also may become a change in a reference signal?
Therefore I just wrote "The reference value in a loop is changed".
How do you know it isn't changing the gain of the system without
any direct effect on signal amplitude?
I don't know. But I thought the gain is a result of different
physical/biological circumstances. (I hope to mail another mail about gain
in my economic model).
I am neither sure what to say when you talk about signal amplitudes. Of
course I have seen the scope of a heart machine watching a dying person. But
I can't explain the amplitude if it is correct that: "An action potential is
always the same size, typically some 90 millivolts. ( [From Bruce Abbott
(2004.12.21.1800 EST)]. Because an action potential cannot be made bigger,
the neuron will instead generate more and more action potentials. The
frequency will increase."
I have thoughts about the amplitude on the scope of a heart machine. But the
amplitude there isn't comparable with what happen in a loop. I think the
machine plug is in contact with many neurons and the more neurons it is in
contact with, the higher amplitude. When a person is dying all the neurons
don't stop functioning at the same millisecond.
Because an action potential cannot be made bigger, the neuron will instead
generate more and more action potentials. The frequency will increase."
You see the problem. The chemical details tell us nothing about what
the brain is DOING, or how its parts are connected to each other.
Yes I see problems, and I agree that chemical details tell us nothing about
_what_ the brain is doing. But I think chemical details tell us something
about _how_ the brain is doing in the organization it has.
Of course chemical details doesn't tell us how parts are connected, but I
think chemical details tell us how the connected parts work.
I liked this answer. I feel more sure myself. What can you do with that?
bjorn