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I assume, that the signal that forces a synaptic receptor/ion channel complex to change its behaviour (i.e. strengthening in the course of upregulation) must be the combination of the state of the complex ("occupied" or "open" or any other state except the ground or rest state) and an extraordinarily high membrane potential at the complex (caused by a retrograded action potential).

The not-ground state indicates that the presynaptic neuron recently has fired, the potential indicates that the postsynaptic neuron recently has fired. According to the rule "fire together, wire together", both conditions must be fulfilled for Hebb-like strengthening to occur.

I assume further that the membrane potential that triggers the upregulation of the complex must be significantly higher than the typical post-synaptic potential generated by the synapse, otherwise activation of the synapse alone would suffice for strengthening to occur, which violates Hebb's rule.

Is this way of thinking essentially correct? Or is strengthening triggered by other signals than the ones mentioned above?

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  • $\begingroup$ Are you looking for an explanation of the biology, or something else? It sort of seems like you are trying to derive biology from logic rather than logically understanding biology; that's a good way to generate hypotheses but might not be the best approach for understanding what is already known about biology. $\endgroup$
    – Bryan Krause ♦
    Commented Sep 8, 2017 at 20:20
  • $\begingroup$ Not from logic, but from what I can imagine: How can a receptor be upregulated but only shortly after (or while it is "active") and shortly after its neuron has created an action potential? (The first it "knows" by its own state, the latter it "knows" from the membrane voltage at its location. So my imagination goes. Both together result in the physical process of upregulation.) But of course, I am looking for an explanation of the biology. $\endgroup$
    – Hans-Peter Stricker
    Commented Sep 11, 2017 at 10:31

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The dynamics of Hebbian or associative synaptic plasticity are thought to be governed primarily through the function of the NMDA glutamate receptor. The short answer is that you are basically right on all counts.

Figure of the NMDA receptor present the nervous system.
Figure of the NMDA receptor present the nervous system.
By Blanca Piedrafita [CC BY-SA 1.0 or CC BY-SA 2.5], via Wikimedia Commons

The NMDA receptor is a non-selective cation ionotropic receptor. The reversal potential of the NMDA receptor is around 0 mV, in contrast to the resting membrane potential of a 'typical' excitatory neuron which is around -70 mV. This means that a pretty strong stimulus is required in order for the NMDA receptor to be activated. Whereas some current can pass through the channel upon binding of its preferred ligands (glutamate or glycine), the pore is normally blocked by a magnesium ion. This mechanism confers some degree of voltage-dependent regulation of ion flow through the channel. When a strong stimulus raises the membrane potential at sufficient levels the magnesium block is lifted, allowing more current to pass through. The slow kinetics of the NMDA receptor allow the temporal integration of incoming signals. This makes the NMDA receptor function as a coincidence detector or AND gate. There are many more known details about the mechanisms involved but the above should suffice to answer your specific question.

Further reading: https://en.wikipedia.org/wiki/NMDA_receptor

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  • $\begingroup$ At first glance I am not quite sure, if your answer covers (subjectively) the details of my question, but I am confident and will have a closer look. Thanks anyway! $\endgroup$
    – Hans-Peter Stricker
    Commented Sep 8, 2017 at 20:06
  • $\begingroup$ If you feel that you need more info, let me know and I will update my answer. $\endgroup$
    – vkehayas
    Commented Sep 8, 2017 at 20:16
  • $\begingroup$ Thanks for the offer, but it will take some time to formulate my concerns. Let me first digest your answer. $\endgroup$
    – Hans-Peter Stricker
    Commented Sep 8, 2017 at 20:35

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