LTP but not seizure is associated with up-regulation of AKAP-150.

Alexis Génin (1) , Pim J. French (2, 3) , Valérie Doyère (4) , Sabrina Davis (4) , Michael L. Errington (2) , M Maroun (4, 5) , S Stean (6) , T Truchet (2) , M Webber (7) , Gael Richter-Levin (5) , S Sanger (6) , Stephen P. Hunt (7) , Jacques Mallet (1) , Serge Laroche (4) , Timothy V. P. Bliss (2) , Vincent O'Connor (2)

1 CHU Pitié-Salpêtrière [AP-HP]
2 Division of Neurophysiology, National Institute for Medical Research
3 Netherlands Institute for Neuroscience
4 NAMC - Neurobiologie de l'apprentissage, de la mémoire et de la communication
5 Department of Psychology, University of Haifa
6 GlaxoSmithKline
7 Laboratory for Molecular Cell Biology and Cell Biology Unit, Department of Anatomy and Developmental Biology

We have used differential display to profile and compare the mRNAs expressed in the hippocampus of freely moving animals after the induction of long-term potentiation (LTP) at the perforant path-dentate gyrus synapse with control rats receiving low-frequency stimulation. We have combined this with in situ hybridization and have identified A-kinase anchoring protein of 150 kDa (AKAP-150) as a gene selectively up-regulated during the maintenance phase of LTP. AKAP-150 mRNA has a biphasic modulation in the dentate gyrus following the induction of LTP. The expression of AKAP-150 was 29% lower than stimulated controls 1 h after the induction of LTP. Its expression was enhanced 3 (50%), 6 (239%) and 12 h (210%) after induction, returning to control levels by 24 h postinduction. The NMDA receptor antagonist CPP blocked the tetanus-induced modulation of AKAP-150 expression. Interestingly, strong generalized stimulation produced by electroconvulsive shock did not increase the expression of AKAP-150. This implies that the AKAP-150 harbours a novel property of selective responsiveness to the stimulation patterns that trigger NMDA-dependent LTP in vivo. Its selective up-regulation during LTP and its identified functions as a scaffold for protein kinase A, protein kinase C, calmodulin, calcineurin and ionotropic glutamate receptors suggest that AKAP-150 encodes is an important effector protein in the expression of late LTP.

Domaines: Neurobiologie; Psychologie et comportements; Sciences cognitives

Alexis Génin, Pim J. French, Valérie Doyère, Sabrina Davis, Michael L. Errington, et al.. LTP but not seizure is associated with up-regulation of AKAP-150.. Supplement .. to the European journal of neuroscience., 2003, 17 (2), pp.331-40. ⟨10.1046/j.1460-9568.2003.02462.x⟩. ⟨hal-01468132⟩