Abstract
Drebrin A (DA), an F-actin binding protein, is involved in spine morphogenesis. We have recently demonstrated that knock down (KD) of DA expression attenuates synaptic clustering of PSD-95, and decrease the number of dendritic protrusions in developing hippocampal neurons. Furthermore, in-vivo experiments indicate that DA-KD in the rat hippocampus impairs pre-pulse inhibition. These data suggest that DA plays a role in the regulatory mechanism of glutamate receptor activity in addition to that of spine shapes. To investigate the effect of DA-KD on glutamate receptor activities in vitro, 12-DIV hippocampal neurons were treated with antisense oligonucleotide specific to DA (AOD) and reverse AOD (ROD). Then at 14 DIV, NMDA and AMPA currents in mock-treated, AOD-treated, and ROD-treated neurons were measured using whole cell patch-clamp technique. We applied glutamate (1, 10, 30, 100 and 300 μM) in the presence of 50 μM AP5, and NMDA (1, 10, 30, 100 and 1000 μM) in the presence of 20 μM CNQX. The AMPA currents seemed larger in AOD-treated neurons than mock-treated and ROD-treated neurons. There were no clear differences in the NMDA currents between AOD-treated and ROD-treated neurons. The data suggest that drebrin A is involved in the regulatory mechanism of glutamate receptor activities. [J Physiol Sci. 2006;56 Suppl:S87]
