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[I striked through some passages that might be misleading, resp. where I have been misled.]

Is the following - very simplified - model biologically (or physically) plausible, explaining how spatiotemporal processing on dendrites works, especially how dendritic spikes and short-term potentiation modification of synaptic strength might work together? (I've read the wikipedia article on NMDA receptors but found it quite hard to digest. It's not a gentle introduction into the topic.)

Let the blue dots be two ligand- and voltage-dependent ion channels (eg. NMDA-gated channels) sitting on two synapses.

Let the green dot be a voltage-dependent ion channel that generates dendritic spikes.

Let the red dots be voltage-dependent ion channels that generate action potentials.

Without the green channel (generating dendritic spikes), two simultaneously synaptic inputs with depolarization V0 which sum up at the branching point of the dendrite would not suffice to generate an action potential:

enter image description here

But with it, two subsequent synaptic inputs (e.g. in two synchronous spike trains) would, because the postsynaptic response is stronger due to an additional voltage signal from the dendritic spikes.

enter image description here

At time t2 another synaptic input and the dendritic spikes arrive at the blue channels. The resulting depolarization V1 > V0 suffices to evoke an action potential.

enter image description here

Is this picture correct in principle? Do such processes actually occur? Or are the real processes quite different? (Of course, they will be much more complicated and superimposed with other processes.) At least some NMDA receptors (which are ligand- and voltage-gated) sit on synapses.

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    $\begingroup$ You need to refine your concept of a dendritic spike. Perhaps you also then need to read about spike-timing dependent plasticity, and just replace backpropagating action potentials with dendritic spikes. Also note that you started by asking about plasticity but your drawings try to explain action potential generation. I think this confusion means that you need to better understand how synapses work and how they change. $\endgroup$ – vkehayas Sep 20 '17 at 12:27
  • $\begingroup$ @vkehayas: I didn't want to talk and ask about long-term plasticity, but only about short-term, maybe even ultra short-term "plasticity", i.e. potentation. But maybe I am misusing the term "short-term potentation". I explicitly did not want to "model" long-term potentation, but understand the short-term influence of dendritic spikes. $\endgroup$ – Hans-Peter Stricker Sep 20 '17 at 12:41
  • $\begingroup$ What I wasn't aware of is the existence of extrasynaptic NMDA receptors. This changes my picture a lot: non-synaptic ligand-gated ion channels? (Never heard of before.) $\endgroup$ – Hans-Peter Stricker Sep 20 '17 at 12:42
  • $\begingroup$ What we usually refer to as short-term plasticity has to do with pre-synaptic mechanisms. You don't necessarily need extrasynaptic NMDARs -and people don't generally consider this as the mechanism- in order to explain dendritic spike generation and synaptic potentiation through dendritic spikes (see REFs in my first comment). Having said that, this may prove interesting to you. $\endgroup$ – vkehayas Sep 20 '17 at 13:03
  • $\begingroup$ FYI, I found your previous question perfectly valid and interesting (it has a lot to do with what I work on). It's just that it's demanding and will take me a while to answer. $\endgroup$ – vkehayas Sep 20 '17 at 13:04

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