Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
6283862 | Neuroscience Letters | 2012 | 5 Pages |
Effect of (+)-epi-clausenamide and (â)-epi-clausenamide on synaptic transmission in CA1 region of hippocampal slice was compared in this study. (+)-epi-Clausenamide showed more potency than (â)-clausenamide on either induction or maintenance of long term potentiation (LTP). Effect of (+)-epi-clausenamide on potentiating basic synaptic transmission was also superior to (â)-clausenamide. However, (â)-epi-clausenamide showed only slight effects on synaptic transmission, suggesting that the effect of (+)-epi-clausenamide and (â)-epi-clausenamide on synaptic transmission depended on their chirality. Calcium influx was not involved in (+)-epi-clausenamide facilitating synaptic transmission in this study. (+)-epi-Clausenamide might promote glutamate release through the activation of Synapsin I(Ser9) to activate the downstream effectors which play a key role in synaptic plasticity. Elucidating the mechanism of each optical isomer of clausenamide by electrophysiological methods provided basis for therapeutic strategies for neurological disorders.
⺠(+)-epi-clausenamide potentiated synaptic transmission in a dose dependent manner. ⺠Calcium influx was not involved in (+)-epi-clausenamide facilitating synaptic transmission. ⺠Excitatory transmitter release might play key roles in the mechanism.