>I recently saw a poster at the Neuroscience meeting in Miami that
>suggested that NO could act presynaptically to reduce neurotransmitter
>release, however, the molecular mechanism was not clear. During ishemia,
>one of the major events is massive release of neurotransmitter. Perhaps NO
>could play a positive role in reducing ishemic damage by reducing
>neurotransmitter release. Just a thought.
This is interesting. Last summer there was an article in Neuron
reporting that NO led to a calcium-independent _increase_ in
transmitter release. This was
Meffert M.K., Premack B.A., Schulman H. (1994)
"Nitric oxide stimulates Ca2+-independent synaptic vesicle release"
Neuron 12:1235-1244.
The work was done with hippocampal synaptosomes. Vesicle release was
measured either indirectly by a decrease in fluorescence of the dye
FM1-43, or directly by an increase in extra-synaptosomal tritiated
glutamate.
Can you give any more details of the poster you saw? Who were the
authors?
Thanks
John
------------------------------------------------------------------------
John E. Anderson 904-448-6286 (phone)
9439 San Jose Boulevard #226 anderson at cshl.org (email)
Jacksonville, Florida 32257 jander at unf6.unf.edu (email)
