Journal
JOURNAL OF NEUROSCIENCE
Volume 26, Issue 13, Pages 3496-3504Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.3792-05.2006
Keywords
synaptic plasticity; hippocampus; long-term potentiation; neurotrophins; neurotrophin receptors; intracellular signaling
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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 C gamma(PLC gamma). We prevented PLC gamma signaling by overexpression of the PLC gamma pleckstrin homology (PH) domain with a Sindbis virus vector. The isolated PH domain has an inhibitory effect and thereby blocks endogenous PLC gamma signaling and consequently also IP3 production. Surprisingly, concurrent presynaptic and postsynaptic blockade of PLC gamma 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.
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