An electrophysiology quesiton
johnh at faraway.hgmp.mrc.ac.uk
Thu Feb 19 11:49:28 EST 2004
"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
> 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,
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+
> > > 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
> > > metabolites in HIV brain injured patients (which exhibit abnormal
> > > 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).
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