An electrophysiology quesiton

k p Collins kpaulc at [----------]earthlink.net
Thu Feb 19 15:01:15 EST 2004


Hi John,

"John H." <johnh at faraway.> wrote in message
news:4034e856 at dnews.tpgi.com.au...
>
> "NMF" <nm_fournier at ns.sympatico.ca> wrote in message
> news:nmsYb.4941$d34.758000 at news20.bellglobal.com...
> > Dear Ken,
> >
> >
> > I still don't agree with you on that entirely.  Perhaps we can agree to
> > disagree.  But astrocytes are extremely responsive to calcium.  Perhaps
I
> > should have been more clear in my previous response.   I am not
dismissing
> > K+ role in regulating glia transmission.  But for evoking the necessary
> > changes in synaptic efficacy that would underlie the theories you
suggest
> in
> > my opinion it is highly dependent upon calcium activity.
>
> That's not an opinion:
>
> Glia 1999 Oct;28(1):1-12
> Glucocorticoids-potent modulators of astrocytic calcium signaling.
>
> Simard M, Couldwell WT, Zhang W, Song H, Liu S, Cotrina ML, Goldman S,
> Nedergaard M.
>
> The Journal of Neuroscience, March 1, 2000, 20(5):1767-1779
> A Fundamental Role for the Nitric Oxide-G-Kinase Signaling Pathway in
> Mediating Intercellular Ca2+ Waves in Glia
> Nicholas J. Willmott, Kay Wong, and Anthony J. Strong
>
> Glia are not exclusively permeable to K+

A better way to say what I said about glia
and K+ ions is that K+ is the only ion species
that goes-right-through them.

This's why the glial tuning of 'memory' can
be really profound. It really has the K+
concentration, upon which action potentials
are dependent, in its grasp.

CA++ is a 2nd messenger all over the place.

There has to be a mechanism that acts to
set glial K+ distribution, CA++ is probably
involved, but there's probably other stuff too,
because the glial K+ control that's =hypoth-
esized= in NDT has to be 3-D-variable.

The refs you've cited are all new-to-me
stuff, but, if I were still able to read in
Neuroscience, I'd jump-on-them with
respect to the hypothesis I've been dis-
cussing.

The "waves" are just artifactual thresholding
dynamics within the globally-integrated
TD E/I-minimization dynamics.

[This "it's-only-continuous-thresholding-
dynamics stuff =really= needs to be grasped
by Neuroscience. The thresholding dynamics
are just portions of larger, continuous, energy-
flow that happen to be easily distinguishible
because there's a directionality-change in-
herent. But they're =not= what's important.
What's important is the =overall= tuning
of energy-flow inherent in convergence. With
respect to this overal stuff, the 'waves' are
=just= artifacts of the way that convergence
procedes, via overshoot-detection that 'closes-
the-door' to energy-flow in the direction in
which it's over-shot convergence. It's all
=just= TD E/I-minimization, but, at this ionic
'level', it's the opening and closing of the 'door'
with respect to ionic-conductance directionality
that constitute "excitation" and "inhibition", res-
pectively.]

Anyway K+ permeability is special, in glia,
because it flows-right-through glia.

[Although the 2nd ref you cite, above, is
with respect to =intercellular= Ca++ stuff,
is it a Ca++ flowing, or a cell-to-cell sig-
nalling? If it's a flowing, NDT's position
would have to be reworked, but if it's a
signalling, then that's already predicted
in NDT's position [NDT didn't address
particular signalling mechanisms, just said
they had to be in-there to tune K+ per-
meability.]

Gee, I feel some of the old 'juice' getting
worked-up. Thought it'd all 'drained' :-]

So, Thank You, John, for posting these
refs.

I'm not going to follow-up. [I think it's
because my trailer is so 'cramped'. I
need to spread the refs I work with
out on the floor, hang them on the walls,
stack them in trays, etc. And I've zero
space in which to do any of that.] But
Encourage others to do so.

Cheers, ken [k. p. collins]

> > >
> > > > Two recent studies may be of interest to
> > > > you.  One study showed that activation of working memory networks
was
> > > > significantly correlated with the extent of  glial cell activation
> and
> > > > metabolites in HIV brain injured patients (which exhibit abnormal
> glial
> > > > inflammatory effects).  They hypothesized that the increased glial
> > > > processing is associated with a decrease in neuronal processing.
>
> Via iNOS activity generating NO inhibiting the electron tranport chain. NO
> rapidly diffuses. NO via il1(p38 or NFkb?, Ca2+ will increase NO, but
don't
> know if via iNOS (bad), or nNOS(good).
>
>
> John H.
>
>





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