Changes in neural cell adhesion molecule mRNA expression and protein level in the CA1 region of the hippocampus during long term potentiation induction and maintenance / 生理学报

It has been demonstrated that neural cell adhesion molecule (NCAM) is critical for the induction and maintenance of long term potentiation (LTP) in the CA1 region of rat hippocampus. In the present study, we investigated the changes in NCAM mRNA expression and NCAM protein level after the induction of LTP in vitro using the techniques of in situ hybridization and Western blot. The results showed that the number of NCAM mRNA positive labelled neurons significantly increased (76.6+/-11.5 neurons) 10 min after tetanus when the slope of fEPSP markedly increased. The level of NCAM protein also increased significantly (7.190+/-0.64 arbitrary unit/50 microg protein) 10 min after tetanus. The number of NCAM mRNA positive labelled neurons no longer changed (73.3+/-14.0) 1 h after tetanus, however, the NCAM protein level (9.031+/-0.71) at 1 h after tetanus was higher than that at 10 min after tetanus. Moreover, the NMDA receptor inhibitor AP-5, which blocked LTP, prevented the increase in NCAM mRNA expression and NCAM protein level. The results demonstrate that NCAM mRNA expression maintains a high level, whereas NCAM protein changes from a low level to a high level during induction and maintenance of LTP.

Relationship between hippocampal long term potentiation induction and activity of 26S proteasome / 生理学报

The present study examined the changes in 26S proteasome activity and the signal molecule mechanism regulating 26S proteasome activity in long term potentiation (LTP) in rat hippocampal slices. The results are as follows: 26S proteasome activity was 190+/-14.3 cpm/(100 microg.2 h) before tetanus, a significant increase in 26S proteasome activity (273+/-18.3 cpm/(100 microg.2 h) was found 10 min after tetanus, when the slope of fEPSP was markedly increased. Interestingly, 26S proteasome activity returned to baseline level (210+/-12.8 cpm/(100 microg.2 h) 60 min after tetanus. Moreover, the N-methyl-D-aspartate (NMDA) receptor inhibitor AP-5, which blocked LTP, prevented the increase in the 26S proteasome activity. The results suggest that NMDA receptors contribute to the transient increase in 26S proteasome activity during induction of LTP in the hippocampal CA1 region.