The control of glutamate receptor delivery to the synapse is a mechanism that is critical for defining synaptic strength and potential of plasticity. To date, it remains unclear whether synaptic activation history controls receptor trafficking at the synapse. Rabaptin-5 is known to be participated in end some function with rab5. We previously reported that over expression of rabaptin-5 promotes GluA1 surface delivery and rabaptin-5 is down-regulated by substantial synaptic activity. These data indicate that rabaptin-5 is a key mediator for metaplasticity.
Rabaptin-5 is ubiquitously expressed and has multiple spliced variants. To further characterize the role of rabaptin-5, we examined these expression in central nervous system. We confirm at least two transcripts, rabaptin-5 and rabaptin-4. Although rabaptin-4 is a splice variant lacking rab5 binding domain, this spliced variant did not show activity dependent decrease, which are observed in the case of rabaptin-5. This would support activity independent AMPA receptor trafficking via rabaptin-4. These results indicate that these spliced variants can mediate receptor traffickings via activity dependent and/or independent manner.
A part of this work was supported by KAKENHI (20500304)