Brain surface

[Matthew Kirkcaldie]

In article <u24op0her5t9ss5tblv8kgei6nr7df5q0b at 4ax.com>,
 r norman <rsn_ at _comcast.net> wrote:

> The traditional mediators of increased local circulation include
> "metabolites" like decreased pO2, increased pCO2,  increased
> extracellular [K+] and adenosine. Any number of cellular metabolic
> processes produce the first two: nerve activity resulting in increased
> Na/K pump activity is certainly a leading candidate.  The same nerve
> activity will also increase K+.  These factors would readily diffuse
> over distances up to 1 mm.  The pO2 and pCO2 changes would readily
> cross glial cells, probably a pH change could also, although the
> astrocytes may shield arterioles from K+ changes.  However, you could
> easily imagine that whatever metabolic effect controls arteriolar
> dilation would be something that the astrocytes were adapted to pass
> through rather than shield.
> 
> Using up ATP most definitely does mean a change in the metabolic rate
> of the cells -- the oxygen consumption -- since brain ATP is
> essentially produced completely by aerobic metabolism.  Even if the
> energy is derived from local stores, you still need oxygen and that
> means blood flow.

These things are true in principle, of course, but are you really saying 
that the picomoles of K+ crossing the neural membrane during an AP are 
going to make a detectable dint in the millimolar K+ extracellular 
concentration a millimetre away?  I'm not pretending superior knowledge 
here, I'd be stupid to, but that really surprises me.

      Matthew.