TY - JOUR 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. SP - 3496 LP - 3504 DO - 10.1523/JNEUROSCI.3792-05.2006 VL - 26 IS - 13 AU - Annette Gärtner AU - Dorit G. Polnau AU - Volker Staiger AU - Carla Sciarretta AU - Liliana Minichiello AU - Hans Thoenen AU - Tobias Bonhoeffer AU - Martin Korte Y1 - 2006/03/29 UR - http://www.jneurosci.org/content/26/13/3496.abstract N2 - 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. ER -