Richard M Wagers wrote:
>kkollins at pop3.concentric.net wrote:
>> > jimmyd at cc.gatech.edu wrote:
> > > * If neurons get all their energy from glucose, then what is the purpose of
> > > oxygen in the brain?
> > The same purpose it serves in an automobile engine.
>> (this is over-simplified, but..) It is necessary to maintain normal metabolic
> activity. Oxygen acts as a mitochondrial electron acceptor. Glucose is the
> substrate. Also necessary, are adequeate numbers of mitochondria to produce the
> energy.Without sufficient oxygen (or the ability to produce energy from it), anerobic
> metabolism commences and its end products may be fatal to the cell.
I was thinking of the cytochrome transport system, which yields by far the greatest
portion of new ATP. The anerobic components are normal stuff, but of course they can't
carry on for more than ~ 4 minutes.
> [text removed]
>> > > * What happens if a neuron is heavily stimulated with messages from its
> > > dendrites, but there is not enough energy in the local bloodstream to increase
> > > the firing rate very much?
>> > kkollins wrote:
> > If this condition occurred, neural activations states would tend to become random
> > to the degree that it did, and the nervous system's information-processing
> > capacities would be decreased accordingly. But the evolutionary engineer has
> > handled this very circumstance nicely, and as any such condition shows itself,
> > system reconfiguration mechanisms are activated, and the nervous system guides the
> > effector activations of its host organism so that the organism will "move away
> > from" what has become a noxious environmental circumstance.
>> IMHO, if the rate of firing of presynaptic pools exceeds the metabolic rate/capacity
> of the postsynaptic pool, we have very characteristic, predictable changes (not
> random). If these pools lack sufficient fuel and intracellular machinery to produce
> ATP without anaerobic metabolic activities, they suffer (one example) failure of
> ATP-dependent functions such as ionic pumping. This allows a build-up of Na+ in the
> cell, or a shift towards the sodium equilibrium potential, and off we go. The same
> fate also finds the neuron which suffers too little stimulation.
We disagree, fundamentally. And kainate studies (excitotoxicity in gereral), studies must
be reckoned with. Additionally, the manifestation of any particular behavior, regardless
of behavioral modality (walking, writing, typing, language, "thought", etc.) requires
that the activation that will, in fact drive the "effectors" so that the particular
behavior is, in fact manifested, be relatively more excited than all other activation, or
the behavior will not be manifested... either some other behavior will be manifested, or
no discernable behavior will be manifested.
The neural architecture incorporates elegant system configuration mechanisms which take
care of all of this... (the neruaxis is not entirely reticulated as you imply) and the
only thing that these mechanisms key upon is the topologically-distributed ratios of
excitation to inhibition that are occuring within the system as a whole... with respect
to such, "overactivated neruons" would really muck things up. It's as I described in my
> Because of the reticular and integrated nature of the neuraxis, decreased (or, loss
> of) function of one pathway or neuronal pool will surely affect another. (i.e.
> spreading depression, or transneuronal degeneration).
> The human nervous system is sensory based
Sensori-motor-based, including the internal "motor" dynamics which underlie "thought"...
everything within nervous systems is a seeking of "balance" between the "sensory" and
"motor" activation "states"... eliminate the "motor" stuff and the sensory stuff runs
wild... no convergence occurs. This is, in fact, what occurs, briefly, during the
> and the ability to transduce environmental information into action potentials dictates
> the state of integration of central
> neuronal structures. Our ability to perceive our environment, to experience our
> world, is dictated by the frequency of activation of peripheral receptors, and the
> subsequent increased probability of summation of central post-synaptic pools.
Yes, but one must carry the geometry rigorously through such, or it's meaningless.
> *Attempting to be professionally _polite_ and accurate,
More accuracy, please. I've not time for the rest.. ken collins