A CaMKII inhibitor, KN-62, facilitates DHPG-induced LTD in the CA1 region of the hippocampus

Schnabel, Rebecca; Palmer, Mary J.; Kilpatrick, Ian C.; Collingridge, Graham L.

doi:10.1016/s0028-3908(98)00229-9

Cited by 34 publications

(31 citation statements)

References 14 publications

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“…The present findings showing a lack of effect of PKC inhibition, as reported previously (Schnabel et al, 1999a;Rush et al, 2002), suggests that DHPG-LTD is not mediated by the classically described mGluR/PLC/PKC intracellular pathway. To confirm this, we tested whether PLC inhibition blocks DHPG-stimulated protein synthesis.…”

Section: Regional Regulation Of Dhpg-induced Protein Synthesissupporting

confidence: 86%

Calcium/Calmodulin-Dependent Protein Kinase II Mediates Group I Metabotropic Glutamate Receptor-Dependent Protein Synthesis and Long-Term Depression in Rat Hippocampus

Mockett¹,

Guévremont²,

Wutte³

et al. 2011

J. Neurosci.

117

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Activation of Group I metabotropic glutamate receptors (mGluRs) in rat hippocampus induces a form of long-term depression (LTD) that is dependent on protein synthesis. However, the intracellular mechanisms leading to the initiation of protein synthesis and expression of LTD after mGluR activation are only partially understood. We investigated the role of several pathways linked to mGluR activation, translation initiation, and induction of LTD. We found that Group I mGluR-dependent protein synthesis and associated LTD, as induced by the agonist (RS)-3,5-dihydrophenylglycine (DHPG) or paired-pulse synaptic stimulation, was dependent on activation of calcium/

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Section: Regional Regulation Of Dhpg-induced Protein Synthesissupporting

confidence: 86%

Calcium/Calmodulin-Dependent Protein Kinase II Mediates Group I Metabotropic Glutamate Receptor-Dependent Protein Synthesis and Long-Term Depression in Rat Hippocampus

Mockett¹,

Guévremont²,

Wutte³

et al. 2011

J. Neurosci.

117

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“…There is considerable evidence that CaMKII as well as MAPKs are critical for the induction of persistent LTP as well as LTD (Malinow et al, 1988(Malinow et al, , 1989Stevens et al, 1994;Mayford et al, 1995;Stanton and Gage, 1996;English and Sweatt, 1997;Bortolotto and Collingridge, 1998;Schnabel et al, 1999;Winder et al, 1999;Lee et al, 2000;Dudek and Fields, 2001;Giovannini et al, 2001;Komiyama et al, 2002;Miller et al, 2002;Kelleher et al, 2004a;Sweatt, 2004). In a first set of experiments, we have reproduced these findings to show that our preparations functionally resemble that of others.…”

Section: Inhibition Of Camkii or Mapks On Ltp And Ltdsupporting

confidence: 62%

Identification of Compartment- and Process-Specific Molecules Required for “Synaptic Tagging” during Long-Term Potentiation and Long-Term Depression in Hippocampal CA1

Sajikumar

Navakkode

Frey³

2007

J. Neurosci.

188

230

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Protein synthesis-dependent forms of hippocampal long-term potentiation (late LTP) and long-term depression (late LTD) are prominent cellular mechanisms underlying memory formation. Recent data support the hypothesis that neurons store relevant information in dendritic functional compartments during late LTP and late LTD rather than in single synapses. It has been suggested that processes of "synaptic tagging" are restricted to such functional compartments. Here, we show that in addition to apical CA1 dendrites, synaptic tagging also takes place within basal CA1 dendritic compartments after LTP induction. We present data that tagging in the basal dendrites is restricted to these compartments. Plasticity-related proteins, partially nonspecific to the locally induced process, are synthesized in dendritic compartments and then captured by local, process-specific synaptic tags. We support these findings in two ways: (1) late LTP/LTD, locally induced in apical or basal (late LTP) dendrites of hippocampal CA1 neurons, does not spread to the basal or apical compartment, respectively; (2) the specificity of the synaptic plasticity event is achieved by the activation of process-and compartmentspecific synaptic tag molecules. We have identified calcium/calmodulin-dependent protein kinase II as the first LTP-specific and extracellular signal-regulated kinase 1/2 as LTD-specific tag molecules in apical dendritic CA1 compartments, whereas either protein kinase A or protein kinase M mediates LTP-specific tags in basal dendrites.

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“…In contrast to the mechanisms of NMDA receptor-dependent LTD, which are fairly well established, the mechanisms of induction and the site of expression of mGluR-dependent LTD are still a matter of some considerable debate. Current studies have reported that the induction of mGluR-dependent LTD does not require extracellular Ca 2ϩ (6), Ca 2ϩ release from intracellular stores (7), activation of Ca 2ϩ /calmodulin-dependent protein kinase II (8), protein kinase A or protein kinase C (7,9), or serine/ threonine protein phosphatases (9). However, this form of LTD requires activation of G q -type G proteins (10), a local translation of dendritic mRNA (5,11), a long-lasting loss of postsynaptic AMPA receptors (12,13), and activation of protein tyrosine phosphatases (14).…”

mentioning

confidence: 99%

Rap1-induced p38 Mitogen-activated Protein Kinase Activation Facilitates AMPA Receptor Trafficking via the GDI·Rab5 Complex

Huang

You

et al. 2004

Journal of Biological Chemistry

166

198

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Recent evidence has emphasized the importance of p38 mitogen-activated protein kinase (MAPK) in the induction of metabotropic glutamate receptor (mGluR)-dependent long term depression (LTD) at hippocampal CA3-CA1 synapses. However, the cascade responsible of mGluR to activate p38 MAPK and the signaling pathway immediately downstream from it to induce synaptic depression is poorly understood. Here, we show that transient activation of group I mGluR with the selective agonist (S)-3,5-dihydroxyphenylglycine (DHPG) activates p38 MAPK through G protein ␤␥-subunit, small GTPase Rap1, and MAPK kinase 3/6 (MKK3/6), thus resulting in mGluR5-dependent LTD. Furthermore, our data clearly show that an accelerating AMPA receptor endocytosis by stimulating the formation of guanyl nucleotide dissociation inhibitor-Rab5 complex is a potential downstream processing of p38 MAPK activation to mediate DHPG-LTD. These results suggest an important role for Rap1-MKK3/6-p38 MAPK pathway in the induction of mGluR-dependent LTD by directly coupling to receptor trafficking machineries to facilitate the loss of synaptic AMPA receptors.Long term depression (LTD) 1 is a persistent activity-dependent decrease of synaptic efficacy that together with the converse process, long term potentiation, has been considered to be crucial for information storage in the brain (1, 2). In the hippocampus, LTD is divided into three categories: homosynaptic, heterosynaptic, and associative LTD (3). The bestcharacterized form of homosynaptic LTD is induced in the CA1 region of the hippocampus by prolonged low frequency synaptic stimulation via a NMDA receptor-dependent rise in postsynaptic [Ca 2ϩ ] i and the activation of serine/threonine protein phosphatases (4). Recent work has shown that mechanistically distinct type of LTD can be induced in the CA1 region by other types of synaptic stimulation or brief pharmacological treatments. For example, a prolonged period of paired-pulse stimulation or a direct application of the selective group I mGluR agonists, such as DHPG, can induce a robust mGluR-dependent form of LTD that is independent of NMDA receptor activation (5). In contrast to the mechanisms of NMDA receptor-dependent LTD, which are fairly well established, the mechanisms of induction and the site of expression of mGluR-dependent LTD are still a matter of some considerable debate. Current studies have reported that the induction of mGluR-dependent LTD does not require extracellular Ca 2ϩ (6), Ca 2ϩ release from intracellular stores (7), activation of Ca 2ϩ /calmodulin-dependent protein kinase II (8), protein kinase A or protein kinase C (7, 9), or serine/ threonine protein phosphatases (9). However, this form of LTD requires activation of G q -type G proteins (10), a local translation of dendritic mRNA (5, 11), a long-lasting loss of postsynaptic AMPA receptors (12, 13), and activation of protein tyrosine phosphatases (14). In addition, more recent studies suggest that p38 MAPK signaling also serves as a signal mediator in the induction of mGluR-depende...

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A CaMKII inhibitor, KN-62, facilitates DHPG-induced LTD in the CA1 region of the hippocampus

Cited by 34 publications

References 14 publications

Calcium/Calmodulin-Dependent Protein Kinase II Mediates Group I Metabotropic Glutamate Receptor-Dependent Protein Synthesis and Long-Term Depression in Rat Hippocampus

Calcium/Calmodulin-Dependent Protein Kinase II Mediates Group I Metabotropic Glutamate Receptor-Dependent Protein Synthesis and Long-Term Depression in Rat Hippocampus

Identification of Compartment- and Process-Specific Molecules Required for “Synaptic Tagging” during Long-Term Potentiation and Long-Term Depression in Hippocampal CA1

Rap1-induced p38 Mitogen-activated Protein Kinase Activation Facilitates AMPA Receptor Trafficking via the GDI·Rab5 Complex

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