Further investigation indicates that vesicle release intensity is a 4th
power function of the Ca++ concentration at the synapse. Hence the 50%
reduction in intensity seen in short-term habituation corresponds to a
concentration decrease of about 10-15%. If we assume short-term
habituation reflects a decrease in the Ca++ concentration, rather than a
decrease in the number of available vesicles (see below for rationale),
then the question comes up--suppose the synapse is potentiated. How much
does that decrease the Ca++ concentration? If the voltage-dependent Ca++
channels on the postsynaptic side remove as much Ca++ as the channels on
the presynaptic side, this implies that the short term increase in
sensitivity on the postsynaptic side has to more than make up for the 75%
reduction in intensity predicted by the power law for a 30% reduction in
Ca++ concentration.
BTW, the reason I would expect the mechanism to be Ca++ concentration
decrease rather than decrease in transmitter/vesicles is that per Sir John
Eccles the process of transmitter release appears to have evolved a
quantization mechanism that appears to me (contra Sir John's
interpretation in Eccles, 1993, 'Evolution of Complexity of the brain with
the Emergence of Consciousness,' in Rethinking Neural Networks, K.
Pribram, ed., INNS Press, 1993) to have the function of ensuring that the
number of vesicles released over all the synapses connecting the two
neurons remains approximately constant, despite variation in number of
vesicles available. Eccles points out that the mechanism of release
appears to limit the number of vesicles released to zero or one, despite
the normal availability of 40-60 in the synaptic bouton. Since habituation
takes place after a very small number of nerve impulses, the depletion of
transmitter during habituation is at most a few percent.
Cheers,
Cheers,
--
Harry Erwin
Internet: erwin at trwacs.fp.trw.comherwin at cs.gmu.edu
Working on Freeman nets....
