(Q44868458)

English

Status epilepticus results in an N-methyl-D-aspartate receptor-dependent inhibition of Ca2+/calmodulin-dependent kinase II activity in the rat.

scientific article published in January 2000

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scholarly article

1 reference

Europe PubMed Central

7 December 2017

Status epilepticus results in an N-methyl-D-aspartate receptor-dependent inhibition of Ca2+/calmodulin-dependent kinase II activity in the rat. (English)

1 reference

Europe PubMed Central

7 December 2017

status epilepticus

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author name string

Kochan LD

1

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Europe PubMed Central

7 December 2017

Churn SB

2

1 reference

Europe PubMed Central

7 December 2017

Omojokun O

3

1 reference

Europe PubMed Central

7 December 2017

Rice A

4

1 reference

Europe PubMed Central

7 December 2017

DeLorenzo RJ

5

1 reference

Europe PubMed Central

7 December 2017

language of work or name

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publication date

1 January 2000

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Europe PubMed Central

7 December 2017

1 reference

Europe PubMed Central

7 December 2017

95

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Europe PubMed Central

7 December 2017

3

1 reference

Europe PubMed Central

7 December 2017

735-743

1 reference

Europe PubMed Central

7 December 2017

Effects of intracellular calcium on GABAA receptors in mouse cortical neurons

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Convulsive disorders: status epilepticus

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A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding

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Decreased calmodulin kinase activity after status epilepticus.

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Kindling induced changes in calmodulin kinase II immunoreactivity.

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Long-lasting decreases of type II calmodulin kinase expression in kindled rat brains

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Protein phosphorylation and neuronal function

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Ca2+- and calmodulin-stimulated endogenous phosphorylation of neurotubulin

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Multifunctional calcium and calmodulin-dependent kinase II in neuronal function and disease

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Exposure of hippocampal slices to magnesium-free medium produces epileptiform activity and simultaneously decreases calcium and calmodulin-dependent protein kinase II activity

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Modulation of GABAergic receptor binding by activation of calcium and calmodulin-dependent kinase II membrane phosphorylation

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Global forebrain ischemia results in decreased immunoreactivity of calcium/calmodulin-dependent protein kinase II

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Excitotoxic activation of the NMDA receptor results in inhibition of calcium/calmodulin kinase II activity in cultured hippocampal neurons.

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Ischemic brain injury selectively alters ATP binding of calcium and calmodulin-dependent protein kinase II.

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Temperature modulation of ischemic neuronal death and inhibition of calcium/calmodulin-dependent protein kinase II in gerbils

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Global forebrain ischemia induces a posttranslational modification of multifunctional calcium- and calmodulin-dependent kinase II

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MK-801 blocks NMDA receptor-mediated synaptic transmission and long term potentiation in rat hippocampal slices

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Frequency-dependent N-methyl-D-aspartate receptor-mediated synaptic transmission in rat hippocampus

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Calcium dependent neurotransmitter release and protein phosphorylation in synaptic vesicles

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A prospective, population-based epidemiologic study of status epilepticus in Richmond, Virginia

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Regional distribution of type II Ca2+/calmodulin-dependent protein kinase in rat brain

1 reference

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Kindling induces a long-lasting change in the activity of a hippocampal membrane calmodulin-dependent protein kinase system.

1 reference

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Calcium . calmodulin-dependent protein kinase II and calcium . phospholipid-dependent protein kinase activities in rat tissues assayed with a synthetic peptide

1 reference

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Frequency-dependent involvement of NMDA receptors in the hippocampus: a novel synaptic mechanism.

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Stimulatory effects of protein kinase C and calmodulin kinase II on N-methyl-D-aspartate receptor/channels in the postsynaptic density of rat brain.

1 reference

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Ca2+/calmodulin-dependent protein kinase II and protein kinase C phosphorylate a synthetic peptide corresponding to a sequence that is specific for the gamma 2L subunit of the GABAA receptor

1 reference

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An essential role for postsynaptic calmodulin and protein kinase activity in long-term potentiation.

1 reference

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Inhibition of postsynaptic PKC or CaMKII blocks induction but not expression of LTP

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Phosphorylation and regulation of glutamate receptors by calcium/calmodulin-dependent protein kinase II.

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Circuit mechanisms of seizures in the pilocarpine model of chronic epilepsy: cell loss and mossy fiber sprouting.

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Loss of type II calcium/calmodulin-dependent kinase activity correlates with stages of development of electrographic seizures in status epilepticus in rat

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Modification of seizure activity by electrical stimulation. 3. Mechanisms.

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Modulation of calcium-mediated inactivation of ionic currents by Ca2+/calmodulin-dependent protein kinase II.

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Multifunctional Ca2+/calmodulin-dependent protein kinase: domain structure and regulation

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CREB: a Ca(2+)-regulated transcription factor phosphorylated by calmodulin-dependent kinases

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Calcium and ischemic brain damage

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Spontaneous calcium transients regulate neuronal plasticity in developing neurons

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Phosphorylation of AMPA-type glutamate receptors by calcium/calmodulin-dependent protein kinase II and protein kinase C in cultured hippocampal neurons.

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Generalized convulsive status epilepticus in the adult

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Association of calcium/calmodulin-dependent kinase with cytoskeletal preparations: phosphorylation of tubulin, neurofilament, and microtubule-associated proteins.

1 reference

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Alpha-subunit of calcium/calmodulin-dependent protein kinase II enhances gamma-aminobutyric acid and inhibitory synaptic responses of rat neurons in vitro

1 reference

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Pathophysiological mechanisms of brain damage from status epilepticus

1 reference

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Ca2+, calmodulin-dependent regulation of microtubule formation via phosphorylation of microtubule-associated protein 2, tau factor, and tubulin, and comparison with the cyclic AMP-dependent phosphorylation.

1 reference

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7 January 2021

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Identifiers

10.1016/S0306-4522(99)00462-5

1 reference

Europe PubMed Central

7 December 2017

1 reference

Europe PubMed Central

7 December 2017

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