jamie morken wrote in message <36CA03C2.61769D6D at uvic.ca>...
>Richard Norman wrote...
>>And then the excitability of the neuron can be plastic,
>>so that threshold might vary.
>>Once a second messenger signalling mechanism
>>cuts loose and starts to phosphorylate all sorts of
>>cell proteins, and possibly starts activating gene
>>control mechanisms, there is no telling how, how
>>much, or for how long, the cell is likely to change.
>>Is there another way that the neurons firing voltage can
>change besides your above example? Will the neuron
>fire differently if the firing voltage is reached in one
>case and surpassed in another case?
Probably variability in threshold is less significant than
that in synaptic efficacy, I just threw it in as another
complicating factor. How hard you cross threshold
is probably not one of the factors. Except that how
hard you cross threshold will certainly influence when
the cell is going to fire next! Another major problem
you should realize is that, in some cells, the action
potential back fires from the axon hillock into the soma
and that, too, influences charge distribution in the
post-synaptic that remains from earlier synapses.
>>synapses alter the membrane conductance, and
>>therefore influence the current loops that carry the
>>potential from the site of the synapse to the spike
>>initiation zone. Even an excitatory synapse "short
>circuits" the membrane and reduces the effect of
>>more distant excitation.
>>Can you explain how/why the synapses short circuit
>the membranes? I assume an excitory synapse would
>want as little short circuiting of the membrane as possible,
>so as to carry as much voltage to the spike initiation zone
>as possible. Does an inhibitory synapse release chemicals that
>purposely short circuit the membrane? Or is there a different
>method inhibitory neurons use to reduce neuron firing, such as
>sending a negative voltage towards the spike initiation zone?
The opening of a synaptic ion channel is necessarily a high
conductance/low resistance pathway across the membrane.
This is the "short circuit". The effect of this conductance change
is the same whether the synapse is excitatory or inhibitory.
Excitatory synapses don't "want" to to anything, they just increase
the probability that the post-synaptic cell fires and if the
contribution of their synaptic current exceeds the "short-circuiting"
effect of their synaptic impedance change, they will accomplish
If the synaptic impedance change is isolated from the dendritic cable,
perhaps by enclosing the synapse in a dendritic spike, for example,
that effect can be reduced. Inhibitory synapses whose reversal
potential is close to resting potential can be said to rely on the
circuit" effect as their major role. This leads to the notion that
at the base of a dendrite substantially reduces the effect of all
on that dendrite, without necessarily influencing the contribution of
Other major problems in doing simplified threshold calculations to
"real" neurones -- many cells form local circuits that function
without action potentials, perhaps microcircuits within the dendrites
else as entire neurons that function without making action potentials.
The roundworm Caenorhabditis elegans doesn't even seem to produce
the sodium channels necessary for the action potential! And then
there may be "dendritic hot spots" that produce at least partial