Neuroscience 2005 Abstract
| Presentation Number: | 996.5 |
|---|---|
| Abstract Title: | SAP102 mutant mice show selective learning and memory deficits. |
| Authors: |
Stanford, L. E.*1
; Cuthbert, P. C.1
; Ainge, J. A.
; Cooke, H. J.1
; Green, M.1
; Komiyama, N. H.1
; Grant, S. G. N.1
1Wellcome Trust Sanger Inst., Hinxton, Cambs, United Kingdom |
| Primary Theme and Topics |
Cognition and Behavior - Animal Cognition and Behavior -- Cognitive learning and memory systems |
| Session: |
996. Cognitive Learning and Memory Systems: Gene Regulation and Knock-Outs II Poster |
| Presentation Time: | Wednesday, November 16, 2005 1:00 PM-2:00 PM |
| Location: | Washington Convention Center - Hall A-C, Board # KK33 |
| Keywords: | WATER MAZE, BEHAVIOR, MAP KINASE, NMDA RECEPTOR |
Synapse-Associated Protein 102 (SAP102/Dlg3) and PSD-95/SAP90/Dlg4 belong to the Membrane-Associated Guanylate Kinase (MAGUK) family. They contain protein-protein interaction domains & bind directly to NMDA receptors (NMDAR). PSD-95 mutants are profoundly disturbed in cell signalling, LTP & spatial behaviour (Migaud et al, 1998). Mutations in the human SAP102/Dlg3 gene result in X-linked mental retardation (Tarpey et al, 2005). To examine the role of SAP102 in vivo, mice were created with a targeted knockout mutation (Cuthbert et al, SfN 2005). Here we report the behavioral characterisation of these mice in a battery designed to assess aspects of learning & memory (L&M). During acquisition of the water maze task (5d), the mutants had similar escape latencies to controls, but were swimming faster over longer distances but no differences in 2 probe tests. During reversal training (5d), no differences in escapes to the new platform were seen, but in daily probe trials, the mutants took longer than controls to remember the platform location (6 vs 1d). No further differences were seen in probe trials up to 8 weeks later. In a T-maze, mutants made the same number of alternations as controls, but were slower in completing the task. Also, mutants failed to habituate or dis-habituate to an odor whereas the controls found the task easy. The L&M differences were not motoric, as similar grip-strength and fixed-speed rotorod performance at 4 or 32 rpm was seen. At 16 rpm, mutants were slightly worse but performance improved. The L&M differences were not due to anxiety either, as the mutants only moved less in the elevated plus maze. Moreover, performance in an open field was similar to controls but again, the mutants moved less than controls. These data suggest the learning deficits in SAP102 mutants are suitable for modelling the human deficits. Together with PSD-95 mutants, these data support the model that the signalling complex associated with the NMDAR is important for L&M in mice & humans.
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2005 Neuroscience Meeting Planner. Washington, DC: Society for Neuroscience, 2005. Online.
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