nm_fournier at ns.sympatico.ca
Sat Apr 3 14:09:24 EST 2004
> Why I ask is this, one of the theories of amphetamine action is that
> amphetamines cause vesicles to leak monoamines into the cytoplasm, and
> from there, the monoamine transporter reverses, just because of the
> change in equilibrium. If that theory was correct, resperine should also
> cause monoamine outflow, because it also increases cytoplasmic
> concentrations of monoamines.
I know of the theory that you are talking about regarding the action of
amphetamine. You probably know more about that literature then I do. One
of the problems I have had with this concept is that if the vesicles have
become "leaky", then the vesicle must already be primed and partially docked
at the release sites within the active zones. However, those vesicles not
docked would expel their content in the intracellular compartment and be
basically catabolized by intrinsic enzymatic activity. However, spontaneous
transmitter release has been observed and this concept of already primed
vesicles have also been experimentally verified, thus it might be possible
that amphetamine may interact with the probability of spontaneous
transmitter released from already primed vesicles.
But can't amphetamine also intefere with the reuptake mechanism of various
monoamines? Also doesn't amphetamine lack a hydroxyl group in its ring
structure and possesses a isopropylamine instead of ethylamine side chain?
I was under the assumption that these chemical differences from other
sympathomimetic amines allowed amphetamine not to be destroyed by enzymes
that normally affect noradrenaline? It's an interesting theory, I just
don't know of any evidence that reserpine can trigger transmitter release in
a manner that you have asked which would be similar to amphetamine. If you
find evidence please post a response on it.
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