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SNAP‐25 in hippocampal CA1 region is involved in memory consolidation
Author(s) -
Hou Qiuling,
Gao Xiang,
Zhang Xuehan,
Kong Lingwei,
Wang Xinming,
Bian Wei,
Tu Yanyang,
Jin Meilei,
Zhao Guoping,
Li Baoming,
Jing Naihe,
Yu Lei
Publication year - 2004
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2004.03600.x
Subject(s) - long term potentiation , neuroscience , memory consolidation , hippocampal formation , hippocampus , inhibitory postsynaptic potential , neural facilitation , neurotransmission , synaptic plasticity , biology , psychology , excitatory postsynaptic potential , receptor , biochemistry
As a synaptosomal protein, SNAP‐25 plays a role in a number of neuronal functions including axonal growth, dendrite formation, fusion of synaptic vesicles with membrane and the expression of long‐term potentiation (LTP) in the hippocampus. Using a learning/memory behavior screening, we identified SNAP‐25 as one of the differentially expressed genes in the hippocampus upon behavioral training. The inhibition of SNAP‐25 with intracerebroventricular antisense oligonucleotide caused a deficit in long‐ but not short‐term memory for step‐down inhibitory avoidance. Intra‐CA1 infusion of the SNAP‐25 antisense oligonucleotide impaired long‐term contextual fear memory and spatial memory and interfered with the LTP of synaptic transmission in the CA1 region. The inhibitory effect on LTP was not mediated by a pre‐synaptic mechanism because paired pulse facilitation of synaptic transmission was not affected after administration of the antisense oligonucleotide. Together, the results suggest that SNAP‐25 in the CA1 region is involved in memory consolidation.