Geon Short Term Potentiation:
Translocation of CABT into Spines



The synaptic potentiation induced by tetanic stimulations includes not only the well-known long-term potentiation (a sustained phase), but also a transient decaying 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, transporting the CABT complex (a CRMP2 monomer and a tubulin heterodimer) to block GluN2B-containing NMDA receptors (NMDARs). The CABT Hypothesis is supported by the following findings:

  1. Microtubule invasion into spines takes minutes. This time course is approximately the same as STP.
  2. Tetanic stimulation is known to cause spine enlargement as early as 2 minutes, in line with the finding that overexpression of CRMP2 results in an increase of mushroom-shape spines.
  3. STP can be abolished by Ro 25-6981, which selectively inhibits GluN2B-NMDARs.
  4. STP can be abolished by 3-isobutyl-1-methylxanthine (IBMX), which is an inhibitor of phosphodiesterase (an enzyme that degrades cAMP). The cAMP/PKA signaling pathway plays a pivotal role in the regulation of the CABT-GluN2B binding (Paper 24).


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