RT Journal Article
SR Electronic
T1 Hippocampal Long-Term Potentiation Is Supported by Presynaptic and Postsynaptic Tyrosine Receptor Kinase B-Mediated Phospholipase Cγ Signaling
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 3496
OP 3504
DO 10.1523/JNEUROSCI.3792-05.2006
VO 26
IS 13
A1 Annette Gärtner
A1 Dorit G. Polnau
A1 Volker Staiger
A1 Carla Sciarretta
A1 Liliana Minichiello
A1 Hans Thoenen
A1 Tobias Bonhoeffer
A1 Martin Korte
YR 2006
UL http://www.jneurosci.org/content/26/13/3496.abstract
AB 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 IP3 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.