On Wed, 11 Feb 2004 00:46:11 +0000 (UTC) r norman rsn_{at}_comcast.net wrote:

N.C. wrote:
...............
>>r n:
>>
>>>I still think that "information translation" is not a
proper way of looking
>at
>>the situation.
>>Light entering the eye causes genes to be expressed in specific cells. There
>>are a lot of intermediate steps, but there is a demonstrable
>chain-and-effect
>>events that can be described linking stimulus to response. It is not
>necessary
>>to talk in terms of information generation, merely in terms of "event A
>causes
>>event B causes event C causes event D causes... causes eventZ. Light in a
>rod
>>or cone cell is translated into electrical potential, but that involves  a
>whole
>>series of intermediate steps. Changes in electrical potential in rod and cone
>>cells in the retina cause release of synaptic transmitter onto melatonin
>>secreting cells in the pineal, but that involves a whole series of
>intermediate
>>steps. Synaptic transmitter binding to receptors on melatonin secreting
>cells
>>in the pineal activate genes in the cell nucleus, but that involves a whole
>>series of intermediate steps.
>>
>>The problem is one of cell physiology, not of information translation.<
>>

>>If I got it right, you argue that the fact that "a whole series of
>intermediate
>>steps" are involved in the signal cascade from the external stimulus to
>genes,
>>this fact per se, excludes the possibility of any information being
>transmitted
>>via the cascade. Without the necessary explanation, this idea seems hardly
>>defensible to me.
>>
>>Applying the same criterium to the process of gene expression, which also
>>involves many "intermediate steps", would lead us to the
conclusion that no
>>genetic information is transmitted from genes to proteins, which is no less
>>difficult to defend.
>>
>>You correctly describe those pathways as chains of events where "event A
>causes
>>event B causes event C causes event D causes....causes event
Z." where the
>>effect of each element on the downstream element (secretion of hypothalamic
>>TRH, e.g. stimulates the  pituitary TSH, stimulates thyroid hormone, etc.)
>is
>>determined by stereochemical and thermodynamical properties of the
>interacting
>>molecules and of the environment. 
>>
>>What takes place in the case of melatonin synthesis is different in an
>>essential respect. The external stimulus per se is neutral to any known
>pathway
>>in metazoans, it can't activate any specific gene. In order that it serve as
>a
>>cue, the input on the stimulus must first be processed in the retinal
>neurons
>>(a computational process), which codes it in the form of a specific pattern
>of
>>electrical signals. But the "electrically coded" stimulus
is nothing less
>than
>>information on the stimulus. It is different from the stimulus itself in the
>>same way that my name identifies me but is not identical with me. 
>>
>>The information generated by processing the stimulus is not determined by
>the
>>stimulus itself but by computational properties in which the stimulus is
>>processed. That information is not stimulus-dependent but
>processing-dependent.
>>
>>
>>The information contained in the electrical code is still
"unintelligible"
>to
>>genes in the meaning that it can't activate the signal transduction pathway
>for
>>expression of melatonin genes. It must be further processed in the described
>>complex neural circuit, which ultimately transforms it in a chemical signal
>>that can activate that signal transduction pathway in all the
"intermediate
>>steps" you talk of. This ultimate chemical form that makes possible  the
>>expression of melatonin genes, is different from the stimulus itself; it is
>>information on that stimulus that is generated (not preexisting) in the
>neural
>>circuits. No melatonin genes can be expressed without this information. 
>>
>>This processing of stimuli in the CNS is necessary not only for external
>>stimuli, but for most of the internal stimuli, since because of the
>blood-brain
>>barrier most of the chemical signals (protein hormones, growth factors and
>>other secreted proteins) have no access to the CNS. It makes it possible for
>>them than in response to the same internal stimuli to activate genes that
>are
>>not expressed in other types of cells.
>
>We seem to be talking at such cross purposes that we cannot understand
>each other.  I find your discussion of the requirement for information
>processing (as in your final paragraph) to be essentially
>incomprehesible.
>
>I do not understand why you are making a simple situation very
>complicated.  If you chill me for a substantial period of time, my
>thyroid gland secretes thyroxin.  That process may also be associated
>with the transcription of genes coding for proteins in the thyroxin
>synthesis pathway.  If you shine light into my eyes, it affects the
>way that my pineal gland secretes melatonin.  That process may also be
>associated with the transcription of genes coding for proteins in the
>melatonin synthesis pathway.  There is no conceptual difference.
>There is absolutely NOTHING in the nervous system that codes for
>"thyroxin" or for "melatonin" or for
"transcribe this particular gene"
>or anything at all like that.  All that happens is that a chemical
>binds to a receptor in the membrane of the thyroid or pineal gland
>cell and makes that cell "do its thing". That
"thing" may involve gene
>transcription, or maybe not.  Whatever, the stimulus simply "doesn't
>care" what the target cell does with the signal.  The signal, in fact,
>doesn't carry any information other than "I have a message for you".
>It is completely up to the target cell to "know" how to respond.

>

Let me try once again to show you the "conceptual" difference between the
classical way of gene expression and the expression of genes in neural tissues?
In the classical mode of gene expression, the effect of the stimulus is
determined by stereochemical and thermodynamical properties of the stimulus and
the respective pathway. Unlike that, the activation/inactivation of genes in
the CNS does not depend on the stereochemical and thermodynamical properties of
the stimulus but on the computational properties of the neural circuit that
processes the stimulus: in response to the same external stimulus ( with the
same stereochemical and thermodynamical properties) the CNS is able to
manipulatively and adaptively activate different genes (examples bound). This
does not happen anywhere else in the body. It is the  processing of the
stimulus in neural circuits that makes possible "manipulative"
activation in
the CNS of genes (such as melatonin and thyroxin you mention) that can't be
activated in other types of cells. 

You say that "All that happens is that a chemical binds to a receptor in the
membrane of the thyroid or pineal gland cell and makes the cell "do its
thing"". Unfortunately, this is neither "all" nor the
essential that happens.
In both examples you see just the proximal link in a long cascade, ignoring the
series of signals  and especially the "essential" processing of
those stimuli
(chill and darkness) in neural circuits, without which neither thyroxin nor
melatonin is produced. You know better than me that chill applied to thyroid
won't make it synthesize thyroxin (only hypothalamic TRH will, which in turn is
synthesized according to signals generated computationally by processing of the
stimulus in neural circuits in other parts of the brain). The same I have
explained for melatonin synthesis. 

What makes unique the thyroid in producing thyroxin and pineal in producing
melatonin is the INFORMATION (computationally generated in neural circuits)
they receive on the external stimulus (not the stimulus itself). Deprived of
this INFORMATION generated in neural circuits, no other type of cell in the
animal body is capable of synthesizing those chemicals.

Is this manipulative (processing-dependent) activation/inactivation of genes in
the CNS requiring information ON THE STIMULUS "essentially different both in
the  the mechanism that makes it possible and the outcome?
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