In:
The Journal of Neuroscience, Society for Neuroscience, Vol. 26, No. 13 ( 2006-03-29), p. 3496-3504
Abstract:
Neurotrophins have been shown to play a critical role in activity-dependent synaptic plasticity such as long-term potentiation (LTP) in the hippocampus. Although the role of brain-derived neurotrophic factor (BDNF) and its tyrosine kinase receptor [tyrosine receptor kinase B (TrkB)] is well documented, it still remains unresolved whether presynaptic or postsynaptic activation of TrkB is involved in the induction of LTP. To address this question, we locally and specifically interfered with a downstream target of the TrkB receptor, phospholipase Cγ (PLCγ). We prevented PLCγ signaling by overexpression of the PLCγ pleckstrin homology (PH) domain with a Sindbis virus vector. The isolated PH domain has an inhibitory effect and thereby blocks endogenous PLCγ signaling and consequently also IP 3 production. Surprisingly, concurrent presynaptic and postsynaptic blockade of PLCγ signaling was required to reduce LTP to levels comparable with those in TrkB and BDNF knock-out mice. Blockade of presynaptic or postsynaptic signaling alone did not result in a significant reduction of LTP.
Type of Medium:
Online Resource
ISSN:
0270-6474
,
1529-2401
DOI:
10.1523/JNEUROSCI.3792-05.2006
Language:
English
Publisher:
Society for Neuroscience
Publication Date:
2006
detail.hit.zdb_id:
1475274-8
SSG:
12
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