Ca2+ and synaptic plasticity

Cavazzini, Michele; Bliss, T. V. P.; Emptage, Nigel J.

doi:10.1016/j.ceca.2005.06.013

Cited by 67 publications

(45 citation statements)

References 163 publications

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“…Between the control and NGF-treated neurons, a statistically significant difference in the SD of the [Ca 2+ ] i fluctuations was detected only in group 4 neurons (P<0.05 by t-test). of neurons has important roles not only in transmitter release, but also in gene expression, the regulation of membrane excitability and cell survival [7,8,36]. This is also the case in DRG neurons.…”

Section: +mentioning

confidence: 93%

Chronic Treatment with NGF Induces Spontaneous Fluctuations of Intracellular Ca2+ in Icilin-Sensitive Dorsal Root Ganglion Neurons of the Rat

Kayano

Naoki

Moriya

et al. 2010

The Journal of Veterinary Medical Science

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ABSTRACT. Adult rat dorsal root ganglion (DRG) neurons cultured in the presence of 100 ng/ml NGF show spontaneous action potentials and fluctuations in their cytosolic Ca 2+ concentrations ([Ca 2+ ] i ). In the present study, the Ca 2+ sources of the [Ca 2+ ] i fluctuations and the types of neurons whose excitability was affected by NGF were examined. In the subpopulation of NGF-treated neurons, obvious fluctuations of [ Peripheral nerve injury frequently results in neuropathic pain, e.g., hyperalgesia and allodynia. Since neuropathic pain is poorly responsive to general analgesic therapy, it is difficult to improve quality of life in patients affected by neuropathic pain. Experimental peripheral nerve injury in animals induces neuropathic symptoms [6,11,20,33,37,38]. Abnormal spontaneous electrical firing has been observed in the sensory neurons of animals whose nerves were injured artificially [12,18], and this abnormal firing is considered to result in neuropathic pain. Nerve growth factor (NGF) has been reported to induce hyperalgesia in rats [24]. Such action of NGF is not restricted to the peripheral tissues, but is also seen in the CNS [16,25]. Recently, we reported that rat DRG neurons cultured in the presence of NGF showed spontaneous action potentials [21] and spontaneous rises and falls in the intracellular Ca Among DRG neurons, A-and C-neurons are generally considered to be involved in nociception. It is widely accepted that NGF plays roles in cell survival, apoptosis, differentiation, the growth of axons/dendrites and the expression of various proteins through two types of receptors. DRG neurons require NGF for their survival and differentiation at an immature stage, but not after maturation [29,31].Indeed, NGF seems to be associated with various disorders of DRG neurons rather than with the maintenance of normal functions in adult animals [9,29]. For example, the intrathecal administration of NGF in adult rats has been reported to result in hyperalgesia [24]. The NGF concentration in the DRG of neuropathic pain model rats has been reported to increase [17,34], and this increased NGF is considered to be one of the mediators contributing to the pathogenesis of peripheral neuropathy [29]. We previously reported that cultured DRG neurons responding to the TRPV1 agonist capsaicin were affected by NGF, became hyperexcitable and showed spontaneous rises and falls in [Ca 2+ ] i [30]. It has been reported that in some DRG neurons, one type of coldsensing TRP, TRPA1, but not the other type of cold-sensing TRP, TRPM8, is expressed together with the hot-sensing TRP, TRPV1, in the same neurons; it was suggested that such neurons can be expected to have physiological roles not simply as thermo sensors, but also as nociceptors [5,22,28,35]. Based on these reports, we wondered 1) whether or not NGF acts on the cold-sensing DRG neurons and thus makes them hyperexcitable, and 2) if so, whether or not there is a correlation between the activity of these TRPs and the spontaneous electrical activity and [Ca ...

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Section: +mentioning

confidence: 93%

Chronic Treatment with NGF Induces Spontaneous Fluctuations of Intracellular Ca2+ in Icilin-Sensitive Dorsal Root Ganglion Neurons of the Rat

Kayano

Naoki

Moriya

et al. 2010

The Journal of Veterinary Medical Science

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“…The fact that a subliminal duration of isometric contraction was sufficient to reverse the polarity of cTBS300-induced effects under the influence of a subliminal dose of NDP suggests that Ca 2ϩ dynamics are involved not only in regulating the polarity changes of naive synapses exposed to a plasticity-inducing stimulation protocol (as indicated above) but also are involved in the physiological events induced by isometric contractions. Ca 2ϩ dynamics are regulated by several mechanisms, which include-apart from L-VGCC-ligand-gated channels and release from intracellular Ca 2ϩ stores (Cavazzini et al, 2005). It is not a priori clear which of these mechanisms predominates.…”

Section: Regulation Of Activation-induced Motor Cortical Metaplasticimentioning

confidence: 99%

L-Type Voltage-Gated Ca²⁺Channels: A Single Molecular Switch for Long-Term Potentiation/Long-Term Depression-Like Plasticity and Activity-Dependent Metaplasticity in Humans

Wankerl¹,

Weise²,

Gentner³

et al. 2010

J. Neurosci.

104

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“…During action potentials, extracellular Ca 2ϩ enters postsynaptic dendritic and spine compartments largely through NMDA receptors and L-type VGCC (41,42). Furthermore, the influx of Ca 2ϩ into postsynaptic compartments regulates many biochemical signaling pathways that are involved in controlling synaptic strength (43).…”

Section: Action Potential Blockade and Up-regulation Produce Rapid Anmentioning

confidence: 99%

Regulation of the Proteasome by Neuronal Activity and Calcium/Calmodulin-dependent Protein Kinase II

Djakovic

Schwarz

Baryłko

et al. 2009

Journal of Biological Chemistry

209

213

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Protein degradation via the ubiquitin proteasome system has been shown to regulate changes in synaptic strength that underlie multiple forms of synaptic plasticity. It is plausible, therefore, that the ubiquitin proteasome system is itself regulated by synaptic activity. By utilizing live-cell imaging strategies we report the rapid and dynamic regulation of the proteasome in hippocampal neurons by synaptic activity. We find that the blockade of action potentials (APs) with tetrodotoxin inhibited the activity of the proteasome, whereas the up-regulation of APs with bicuculline dramatically increased the activity of the proteasome. In addition, the regulation of the proteasome is dependent upon external calcium entry in part through N-methyl-D-aspartate receptors and L-type voltage-gated calcium channels and requires the activity of calcium/calmodulindependent protein kinase II (CaMKII). Using in vitro and in vivo assays we find that CaMKII stimulates proteasome activity and directly phosphorylates Rpt6, a subunit of the 19 S (PA700) subcomplex of the 26 S proteasome. Our data provide a novel mechanism whereby CaMKII may regulate the proteasome in neurons to facilitate remodeling of synaptic connections through protein degradation.

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Ca2+ and synaptic plasticity

Cited by 67 publications

References 163 publications

Chronic Treatment with NGF Induces Spontaneous Fluctuations of Intracellular Ca2+ in Icilin-Sensitive Dorsal Root Ganglion Neurons of the Rat

Chronic Treatment with NGF Induces Spontaneous Fluctuations of Intracellular Ca2+ in Icilin-Sensitive Dorsal Root Ganglion Neurons of the Rat

L-Type Voltage-Gated Ca²⁺Channels: A Single Molecular Switch for Long-Term Potentiation/Long-Term Depression-Like Plasticity and Activity-Dependent Metaplasticity in Humans

Regulation of the Proteasome by Neuronal Activity and Calcium/Calmodulin-dependent Protein Kinase II

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Ca2+ and synaptic plasticity

Cited by 67 publications

References 163 publications

Chronic Treatment with NGF Induces Spontaneous Fluctuations of Intracellular Ca2+ in Icilin-Sensitive Dorsal Root Ganglion Neurons of the Rat

Chronic Treatment with NGF Induces Spontaneous Fluctuations of Intracellular Ca2+ in Icilin-Sensitive Dorsal Root Ganglion Neurons of the Rat

L-Type Voltage-Gated Ca2+Channels: A Single Molecular Switch for Long-Term Potentiation/Long-Term Depression-Like Plasticity and Activity-Dependent Metaplasticity in Humans

Regulation of the Proteasome by Neuronal Activity and Calcium/Calmodulin-dependent Protein Kinase II

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L-Type Voltage-Gated Ca²⁺Channels: A Single Molecular Switch for Long-Term Potentiation/Long-Term Depression-Like Plasticity and Activity-Dependent Metaplasticity in Humans