Abstract:
:Considerable evidence suggests that an N-methyl-D-aspartate (NMDA) receptor plays a crucial role in memory and cognitive function. To identify the role of this receptor in higher functions of the brain, we delivered antisense oligonucleotides against an NMDA-NR1 subunit (NR1) to the hippocampus in rats using the HVJ-liposome-mediated gene-transfer method. NR1 hippocampal knockdown was performed by the focal injection of the NR1 antisense-HVJ-liposome complex into the bilateral hippocampus. The blocking effect of NR1-antisense on the expression of NR1 was confirmed by Western blot analysis. Spatial memory was tested by a water maze task, and sensorimotor gating was examined by prepulse inhibition (PPI). Western blot analysis demonstrated that the NR1-antisense treatment specifically provided the down-regulation (about 30%) of NR1 protein levels in the hippocampus. The water maze task showed that the antisense treatment did not affect spatial memory, while the PPI test revealed that NR1 hippocampal knockdown caused a deficit in sensorimotor gating. We conclude that mild dysfunction of hippocampal NMDA receptor causes sensorimotor gating deficit and relatively intact in spatial memory.
journal_name
Neurosci Resjournal_title
Neuroscience researchauthors
Inada K,Ishigooka J,Anzai T,Suzuki E,Miyaoka H,Saji Mdoi
10.1016/s0168-0102(03)00012-9subject
Has Abstractpub_date
2003-04-01 00:00:00pages
473-81issue
4eissn
0168-0102issn
1872-8111pii
S0168010203000129journal_volume
45pub_type
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