Brain surface

r norman rsn_ at _comcast.net
Wed Nov 17 22:25:02 EST 2004


On Thu, 18 Nov 2004 11:22:41 +1100, Matthew Kirkcaldie
<m.kirkcaldie at removethis.unsw.edu.au> wrote:

>In article <CNmdnVIaJq9AJwbcRVn-hw at giganews.com>,
> "MZ" <zarellam at removetwcny.rr.comspam> wrote:
>
>> > There's no proven
>> > causal chain between, say, a neuron firing more actively and a change in
>> > the amount of oxygenated blood flowing through the nearest capillary.
>> 
>> Neurovascular coupling has been demonstrated quite thoroughly by Grinvald's
>> group (among others), I believe.  I have Villringer and Dirnagl (1995)
>> written down.  May be time to review it.
>
>Yes, I forgot I was taking a shot at optical imaging as well!  As I 
>mentioned, this is not my area of expertise.  That article looks 
>interesting but isn't accessible at my institution, which is a shame.  
>Can you recommend any others?
>
>When I say "causal chain", I mean a chain of cellular events which start 
>with increased numbers of action potentials, and specify how that causes 
>vasodilatation. Is that elucidated?  What's the messenger that dilates 
>capillaries?  What secretes it?  Under what conditions is it secreted?
>
>> > 2. As far as I know, the mechanism by which blood flow is altered is not
>> > understood. It is likely to be strongly mediated by astrocytes, whose
>> > processes wrap brain capillaries in continuous sheaths, and hence would
>> > be controlled by glial cells, rather than neurons.  Hence it seems
>> > likely that the needs of glia are more relevant to fMRI than the
>> > activity of neurons directly.
>> 
>> I think it's been shown that action potential propagation and synaptic
>> transmission require the bulk of the ATP available and are therefore
>> responsible for the hemodynamic signal.
>
>Action potentials using up the bulk of ATP doesn't automatically mean 
>that they will cause a change in the blood flow, of course - it may 
>involve mobilisation of internal energy stores, etc. depending on the 
>type or duration of activity.
>
<snip>

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.







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