CaMKII regulation in information processing and storage

Coultrap, Steven J.; Bayer, K. Ulrich

doi:10.1016/j.tins.2012.05.003

Cited by 294 publications

(357 citation statements)

References 147 publications

(325 reference statements)

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“…The results of this study demonstrate that NO-induced CaMKII autonomy is a novel regulatory mechanism for an enzyme critically involved in mediating synaptic plasticity (1,(3)(4)(5) and ischemic/excitotoxic neuronal cell death (6, 7). Indeed, CaMKII inhibition protected also from neuronal cell death directly induced by NO donors.…”

Section: Discussionmentioning

confidence: 95%

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Nitric Oxide Induces Ca2+-independent Activity of the Ca2+/Calmodulin-dependent Protein Kinase II (CaMKII)

Coultrap

Bayer

2014

Journal of Biological Chemistry

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146

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Background: Ca 2ϩ -independent autonomous CaMKII activity and nitric oxide (NO) signaling regulate neuronal function and death. Results: NO generated autonomous CaMKII activity by Ca 2ϩ /CaM-dependent S-nitrosylation, and CaMKII inhibition protected from NO-induced neuronal cell death. Conclusion: NO-mediated regulation of CaMKII contributes to its pathological functions. Significance: S-Nitrosylation is a novel path to CaMKII autonomy that connects Ca 2ϩ -and NO signaling.

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Section: Discussionmentioning

confidence: 95%

“…Model of CaMKII structure and regulation. A, CaMKII forms 12meric holoenzymes via C-terminal association domains, with the kinase domains radiating outward (1,2). Each kinase subunit is activated separately by direct binding of Ca 2ϩ /CaM, which can also induce intra-holoenzyme inter-subunit Thr-286 autophosphorylation (9).…”

Section: Methodsmentioning

confidence: 99%

Nitric Oxide Induces Ca2+-independent Activity of the Ca2+/Calmodulin-dependent Protein Kinase II (CaMKII)

Coultrap

Bayer

2014

Journal of Biological Chemistry

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146

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“…Not much is known about the biochemical requirements for Thr305/ 306 autophosphorylation or its prevention. It has been shown that Thr305/306 autophosphorylation requires Ca/CaM binding to CaMKII and subsequent dissociation (31). A possible, but not experimentally tested, scenario is that repeated 100-Hz PF bursts provide the calcium influx required for Ca/CaM binding to CaMKII, but that during the pauses between the bursts, which last almost 1 s, CaM dissociates from CaMKII, allowing inhibitory phosphorylation to take place.…”

Section: Discussionmentioning

confidence: 99%

“…CaMKII promotes LTD by suppressing the activity of protein phosphatase 2A through negative regulation of phosphodiesterase 1 and subsequent disinhibition of a cGMP/protein kinase G pathway (30). Negative regulation of CaMKII by Thr305/ 306 autophosphorylation requires prior calcium/calmodulin-mediated activation of CaMKII and subsequent calmodulin dissociation (31). Moreover, it has been shown that Thr305/306 phosphorylation, triggered by 10-Hz priming, reduces hippocampal LTP (32), whereas genetic manipulation of the Thr305/306 phosphorylation site lowers the LTP threshold and prevents priming (27,32).…”

Section: Significancementioning

confidence: 99%

Calcium threshold shift enables frequency-independent control of plasticity by an instructive signal

Piochon

Titley

Simmons

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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At glutamatergic synapses, both long-term potentiation (LTP) and long-term depression (LTD) can be induced at the same synaptic activation frequency. Instructive signals determine whether LTP or LTD is induced, by modulating local calcium transients. Synapses maintain the ability to potentiate or depress over a wide frequency range, but it remains unknown how calcium-controlled plasticity operates when frequency variations alone cause differences in calcium amplitudes. We addressed this problem at cerebellar parallel fiber-Purkinje cell synapses, which can undergo LTD or LTP in response to 1-Hz and 100-Hz stimulation. We observed that high-frequency activation elicits larger spine calcium transients than low-frequency stimulation under all stimulus conditions, but, regardless of activation frequency, climbing fiber (CF) coactivation provides an instructive signal that further enhances calcium transients and promotes LTD. At both frequencies, buffering calcium prevents LTD induction and LTP results instead, identifying the enhanced calcium signal amplitude as the critical parameter contributed by the instructive CF signal. These observations show that it is not absolute calcium amplitudes that determine whether LTD or LTP is evoked but, instead, the LTD threshold slides, thus preserving the requirement for relatively larger calcium transients for LTD than for LTP induction at any given stimulus frequency. Cerebellar LTD depends on the activation of calcium/ calmodulin-dependent kinase II (CaMKII). Using genetically modified (TT305/6VA and T305D) mice, we identified α-CaMKII inhibition upon autophosphorylation at Thr305/306 as a molecular event underlying the threshold shift. This mechanism enables frequencyindependent plasticity control by the instructive CF signal based on relative, not absolute, calcium thresholds.S ynaptic activation frequency is an important factor in the induction of long-term potentiation (LTP) and long-term depression (LTD). For example, it has been shown at Schaffer collateral-CA1 pyramidal cell synapses that application of 900 pulses at 1-3 Hz causes LTD, whereas the same number of pulses applied at 50 Hz causes LTP (1). However, LTP and LTD can also be induced at the same stimulus frequency. This phenomenon has been demonstrated at hippocampal, neocortical, and cerebellar synapses, where potentiation and depression mechanisms operate over a wide range of activation frequencies (2-7). In the neocortex and hippocampus, the level of postsynaptic depolarization determines whether LTP or LTD results from stimulation at a given frequency (2, 5). These voltage-dependent thresholds for LTP and LTD induction reflect thresholds in calcium signal amplitudes (3,4,(8)(9)(10)(11)) that, when maintained for sufficiently long time periods (12), control synaptic plasticity in concert with distinct calcium sensors that are restricted to local microenvironments (13,14).At cerebellar parallel fiber (PF)-Purkinje cell synapses, both LTP and LTD can be induced using 1-Hz and 100-Hz PF stimulation protocols, ...

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“…The most important of the latter is α-CaMKII (33)(34)(35)(36). An important source of [Ca 2+ ] i are the long-acting voltage-dependent calcium channels (L-VDCCs), which have been proposed to play some role in memory processes (37)(38)(39)(40).…”

mentioning

confidence: 99%

Memory reconsolidation and its maintenance depend on L-voltage-dependent calcium channels and CaMKII functions regulating protein turnover in the hippocampus

Silva

Cardoso

Bonini

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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Immediate postretrieval bilateral blockade of long-acting voltagedependent calcium channels (L-VDCCs), but not of glutamatergic NMDA receptors, in the dorsal CA1 region of the hippocampus hinders retention of long-term spatial memory in the Morris water maze. Immediate postretrieval bilateral inhibition of calcium/calmodulindependent protein kinase (CaMK) II in dorsal CA1 does not affect retention of this task 24 h later but does hinder it 5 d later. These two distinct amnesic effects are abolished if protein degradation by proteasomes is inhibited concomitantly. These results indicate that spatial memory reconsolidation depends on the functionality of L-VDCC in dorsal CA1, that maintenance of subsequent reconsolidated memory trace depends on CaMKII, and these results also suggest that the role played by both L-VDCC and CaMKII is to promote the retrieval-dependent, synaptically localized enhancement of protein synthesis necessary to counteract a retrieval-dependent, synaptic-localized enhancement of protein degradation, which has been described as underlying the characteristic labilization of the memory trace triggered by retrieval. Thus, conceivably, L-VDCC and CaMKII would enhance activity-dependent localized protein renewal, which may account for the improvement of the long-term efficiency of the synapses responsible for the maintenance of reactivated long-term spatial memory.

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CaMKII regulation in information processing and storage

Cited by 294 publications

References 147 publications

Nitric Oxide Induces Ca2+-independent Activity of the Ca2+/Calmodulin-dependent Protein Kinase II (CaMKII)

Nitric Oxide Induces Ca2+-independent Activity of the Ca2+/Calmodulin-dependent Protein Kinase II (CaMKII)

Calcium threshold shift enables frequency-independent control of plasticity by an instructive signal

Memory reconsolidation and its maintenance depend on L-voltage-dependent calcium channels and CaMKII functions regulating protein turnover in the hippocampus

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