Postsynaptic phospholipase C activity is required for the induction of homosynaptic long-term depression in rat hippocampus
Section snippets
Acknowledgements
These data are from a thesis submitted in partial fulfillment of requirements for the degree of Doctor of Philosophy in the Sue Golding Graduate Division of Medical Sciences, Albert Einstein College of Medicine. We thank T. Opitz for helpful discussions. This research was supported by the Whitehall Foundation (P.K.S.) and NIH MSTP Training Grant #F31GM16379 (M.R.), and is dedicated to the memory of Lewis N. Stanton, Sr. and Vilma Maldonado.
References (22)
- et al.
Mechanisms underlying induction of homosynaptic long-term depression in area CA1 of the hippocampus
Neuron
(1992) - et al.
Postsynaptic levels of [Ca2+]i needed to trigger LTD and LTP
Neuron
(1996) - et al.
Two distinct forms of long-term depression coexist in CA1 hippocampal pyramidal cells
Neuron
(1997) - et al.
Metabotropic glutamate receptor mediated long-term depression in developing hippocampus
Neuropharmacology
(1997) - et al.
2-Amino-3-phosphonopropionic acid, an inhibitor of glutamate-stimulated phosphoinositide turnover, blocks induction of homosynaptic long-term depression, but not potentiation, in rat hippocampus
Neurosci. Lett.
(1991) - et al.
U73122 inhibits Ca2+ oscillations in response to cholecystokinin and carbachol but not to JMV-180 in rat pancreatic acinar cells
J. Biol Chem.
(1992) - et al.
Long-term depression in hippocampus
Annu. Rev. Neurosci.
(1996) - et al.
Selective inhibition of receptor-coupled phospholipase C-dependent processes in human platelets and polymorphonuclear neutrophils
J. Pharmacol. Exp. Ther.
(1990) - et al.
Postsynaptic induction and presynaptic expression of hippocampal long-term depression
Science
(1994) - et al.
Pharmacology and functions of metabotropic glutamate receptors
Annu. Rev. Pharmcol. Toxicol.
(1997)
Homosynaptic long-term depression in area CA1 of hippocampus and effects of N-methyl-d-aspartate blockade
Proc. Natl. Acad. Sci. USA
Cited by (37)
Role of postsynaptic inositol 1, 4, 5-trisphosphate receptors in depotentiation in guinea pig hippocampal CA1 neurons
2016, Brain ResearchCitation Excerpt :In hippocampal CA1 neurons, the homosynaptic LTD induced by LFS at 1 Hz requires NMDAR activation and an increase in the postsynaptic [Ca2+]i, the latter triggering the activation of Ca2+-dependent second messenger systems (Linden 1994), followed by calcium-independent signaling steps (Bear and Abraham, 1996), i.e. the increase in the postsynaptic [Ca2+]i, during 1 Hz LFS activates calcineurin, which dephosphorylates and inactivates inhibitor 1, allowing protein phosphatase 1 to act on CaMKII or AMPA receptor subunits (Lisman 1994; Mulkey et al. 1994; Barria et al.,1997; Lee et al. 2000). Group I mGluRs are positively coupled to PLC and their activation is reported to be required for induction of LTD in hippocampal CA1 neurons (Palmer et al. 1997; Reyes-Harde and Stanton 1998). Taufiq et al. (2005) showed that activation of IP3Rs, which occurs downstream of group I mGluRs and PLC in the signaling cascade, plays an important role in facilitating N-methyl-D-aspartate glutamate receptor (NMDAR)-dependent LTD in hippocampal CA1 neurons.
Phosphoinositide dynamics in the postsynaptic membrane compartment: Mechanisms and experimental approach
2015, European Journal of Cell BiologyCitation Excerpt :It is well established that NMDAR-induced LTD is mediated by Ca2+-dependent activation of the phosphatase calcineurin (reviewed in (Huang, 1998)). However, various lines of evidence indicate that activation of PLCβ downstream of GqPCRs (Reyes-Harde and Stanton, 1998; Choi et al., 2005) and/or of PLCδ downstream of NMDA receptors (Codazzi et al., 2006; Horne and Dell’Acqua, 2007) are also required for the induction of LTD at least under some experimental conditions. PLC activity was shown to result in dissociation of a complex containing AKAP79/150 and protein kinase A (PKA) from the PSD (Horne and Dell’Acqua, 2007), which may alter phosphorylation of AMPA receptors and other substrates and thereby promote internalization of the receptors (Lee et al., 1998, 2000, 2003).
Involvement of inositol-1,4,5-trisphosphate receptors in the bidirectional synaptic plasticity induced in hippocampal CA1 neurons by 1-10 Hz low-frequency stimulation
2010, NeuroscienceCitation Excerpt :Since co-activation of NMDARs and mGluRs (Fig. 4B, E) and activation of PKC (Fig. 5B, E) were both required for the LTP induced by LFS of 80 pulses at 10 Hz, it is possible that the activation of group 1 mGluRs enhances Ca2+ influx through NMDARs by activation of the PLC-PIP2-DAG-PKC pathway, leading to an increase in the post-synaptic [Ca2+]i and triggering the activation of Ca2+-dependent second messenger systems to produce LTP (Bliss and Collingridge, 1993; Lisman, 1994; Fujii et al., 2004). Group 1 mGluRs are positively coupled to PLC and their activation are reported to be required for the induction of LTD in hippocampal CA1 neurons (Palmer et al., 1997; Reyes-Harde and Stanton, 1998). Taufiq et al. (2005) showed that the activation of IP3Rs, which occurs downstream of group 1 mGluRs and PLC in the signalling cascade (Berridge, 1993; Mikoshiba, 1993), plays an important role in attenuating LTP and facilitating LTD in hippocampal CA1 neurons.
Phosphatidylinositol-linked novel D<inf>1</inf> dopamine receptor facilitates long-term depression in rat hippocampal CA1 synapses
2009, NeuropharmacologyCitation Excerpt :First, the effect of PLC inhibitor U73122 on SKF83959-facilitated LTD was investigated. Similar to a previous report (Reyes-Harde and Stanton, 1998), LFS–induced LTD was blocked by 10 μM U73122. Furthermore, pre-treatment with 10 μM U73122 prevented the LTD facilitation induced by SKF83959 (U73122: 93.88 ± 5.15% of pre-stimulation baseline; n = 7; p < 0.05 vs SKF83959 alone, Fig. 4A).
LTD - synaptic depression and memory storage
2007, Learning and Memory: A Comprehensive ReferenceSensitivity to MK-801 in phospholipase C-Β1 knockout mice reveals a specific NMDA receptor deficit
2009, International Journal of Neuropsychopharmacology