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2013-04-18 - Colloque/Présentation - communication orale - Anglais - 1 page(s)

Villers Agnès , Lucchesi Walter, Giese K.P., Ris Laurence , "L-LTP can be induced in CA1 pyramidal cells in the absence of alpha-CaMKII autophosphorylation" in 1st European Neuroscience Conference by Doctoral Students, Bordeaux, France, 2013

  • Codes CREF : Neurophysiologie (DI3224)
  • Unités de recherche UMONS : Neurosciences (M119)
  • Instituts UMONS : Institut des Biosciences (Biosciences)

Abstract(s) :

(Anglais) Encoding of memories relies on modifications in the strength of the synapses connecting the different cells within a neuronal network. Within this framework, long-term potentiation (LTP) is a lasting increase in synaptic strength induced by high-frequency stimulation (HFS) of the related presynaptic fibers. In the CA1 region of mice hippocampal slices, long-lasting long-term potentiation (L-LTP) can be induced by a strong tetanic stimulation or by forskolin and IBMX application, two drugs which increase cAMP concentration. We have studied T286A missense mutant mice lacking autophosphorylation at threonine 286 of the alpha-isoform of calcium/calmodulin-dependent kinase II (alpha-CaMKII), a major protein of glutamatergic synapses in the forebrain. It has been demonstrated that T286A mutants have fully blocked NMDA receptor-dependent synaptic strengthening at hippocampal CA1 synapses. However, we show here that long-lasting LTP can be recorded in CA1 synapses of T286A mutant mice. (1) NMDA receptor-independent L-LTP could be induced but specificity of synaptic plasticity was lost. We used either a fifteen minutes application of forskolin and IBMX or allowed the slices to recover in submersion, after dissection, before applying 4 trains of HFS in interface to trigger L-LTP. In this case, the potentiation was not limited to synapses having undergone HFS. We observed a slow-onset L-LTP in a second pathway stimulated at 0.017 Hz. (2) When rapamycin, a drug known for targeting the mTOR pathway, was continuously applied, starting from the recovery period, a pathway-specific L-LTP could be induced by 4 trains of HFS. This priming effect of rapamycin probably arose from modifications of NMDA receptors, as NMDA input-output curves were significantly increased following a 2-hour drug perfusion. From these results, we suggest that autophosphorylation of alpha-CaMKII, in close relationship with NMDA receptors, is needed to tag the stimulated synapses, allowing specificity of the synaptic plasticity process, but is not required for an unspecific whole cell plasticity process.