From: jbates@encore.com (John W. Bates)
Subject: Re: Spoken Like a True ProLifer
Organization: Encore Computer Corporation
Date: Thu, 21 Jan 1993 07:50:10 GMT
	<1993Jan15.082321.13848@organpipe.uug.arizona.edu>


In article <1993Jan15.082321.13848@organpipe.uug.arizona.edu> sfm@manduca.neurobio.arizona.edu (Stephen Matheson) writes:
> From article <JBATES.93Jan13141408@pinocchio.encore.com>,
> by jbates@encore.com (John W. Bates):
>> In article <1993Jan13.025950.8555@mnemosyne.cs.du.edu>
>> mcochran@nyx.cs.du.edu (Mark A. Cochran) writes:
>>>In article <JBATES.93Jan12132814@pinocchio.encore.com>
>>>jbates@encore.com (John W. Bates) writes:

> [It was interesting, but I deleted it.  So sue me.]

>> The human brain is composed of myelinated and unmyelinated
>> portions.  I know that Steve doesn't want to compare demyelinated
>> humans to unmyelinated fetuses,

> Do you understand why?  Do you agree that the difference is
> significant?  I have said that a demyelinated fiber is often
> *incapable* of conducting impulses due to the suddenly-exposed
> inexcitable membrane of the internodes.  An unmylinated fiber is a
> long tube of excitable membrane.  Our comparison will be of slow
> conduction to no conduction.  With that in mind,...

Oopsie. Well, just forget about it all...

No, seriously, I'd thought that your objection was to another point
entirely. I dealt with that imaginary point quite well, I thought.

So, I've been digging around in my texts and found something interesting.
From the only strictly neuro book I own: ([] comments are mine)
	"As would be expected, one of the consequences of extensive
	demyelination is conduction block. [See, just goes to show
	ya, I should look it up before I open my big mouth...] However,
	mammalian axons that have been demyelinated chronically with
	diptheria toxin can develop continuous conduction through a
	demyelinated region, implying that after demyelination 
	voltage-sensitive sodium channels appear in the exposed
	axon membrane." _From Neuron to Brain_, Kuffler, Nicholls,
	& Martin, page 183

The same reference also mentions one J.M. Ritchie, who has examined
the axon membrane by loosening the myelin sheathing. Now, at this
point, I've entirely lost track of the terminology and shall go
whimper in the corner, while someone else can determine the relevance
of this citation.

Here's another question: do the internodal regions develop before or
after myelination occurs? If before, then one *can* compare demyelinated
humans to unmyelinated fetuses, at least on an axon to axon level.

> OK.  We've got a cognitive scientist, a neurobiologist, and a
> physician (right, Mark?) here.  We should be able to make some
> progress.  I'll start with Kandel & Schwartz, _Principles of Neural
> Science_, 2nd ed., p. 475.  "...for instance, the combination of
> proprioceptive sensory loss and signs of upper motor neuron disease
> together with evidence of either cerebellar dysfunction -- ataxia,
> tremor of the arms, disorders of eye movement (nystagmus),
> difficulty in speaking (dysarthria) -- or a history or signs of
> optic neuritis.  In addition to signs of disorder elsewhere in the
> nervous system..."

> Not very helpful in our quest for cognitive dysfunction.  Anyone
> else?

Well, assuming that my citation above has no relevance, looking at
cognitive dysfunction in demyelinated patients won't give us any 
help except for revealing which functions would require myelinated
axons. Just out of curiousity, what are the additional signs of 
disorder elsewhere?

>> If my hypothesis is correct (that the cognitive abilities of adult
>> humans are dependent upon synchronized activities within the
>> brain), then cognition (in the commonly accepted fashion) is
>> dependent upon myelin. Testable hypothesis, and I'll try to find
>> evidence to back it up. Now, this implies that an unmyelinated
>> fetus is either not cognitive, or is cognitive in some radically
>> different fashion.

> Your hypothesis also requires the assumption that myelin is
> necessary for synchronized activity.

That's a very reasonable assumption, if and only if a synchronized
activity occurs involving both myelinated and unmyelinated portions.
I've been trying to find references to such processes, but I've been
unsuccessful thus far. Mostly 'cause I can't get to the library until
next week. My own references tend to gloss over descriptions of the
physical aspects of any one section of the brain, and describe the
serial aspects instead.

[The rest is deleted. I think that I'll be addressing the points
 raised there in a few more responses.]

John