Geon Short Term Potentiation
May Result from Tubulin Inhibition of NMDA Receptors
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Abstract

The synaptic potentiation induced by tetanic stimulations includes not only the well-known long-term potentiation (a sustained phase), but also a transient phase referred to as short-term potentiation (STP). The mechanism of STP remains elusive. This paper shows that STP could originate from microtubule invasion into spines, resulting in the inhibition of NR2B-containing NMDA receptors by tubulin and CRMP2 (Paper 15). The Tubulin Inhibition Hypothesis leads to the following experimentally testable predictions:

  1. The major cargoes transported by the dynamic microtubules into spines could be tubulin and CRMP2.
  2. Phosphorylation of Serine 1166 in NR2B (also known as GluN2B), or pseudophosphorylation by mutating this residue to glutamate, may prevent tubulin binding to NR2B, thereby suppressing STP.
  3. Tubulin could also bind to NR2D (GluN2D), as STP is also sensitive to the NR2D-selective antagonist UBP145.

 

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