(Q48381268)

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Intracerebroventricular administration of quinolinic acid induces a selective decrease of inositol(1,4,5)-trisphosphate receptor in rat brain.

scientific article published in August 1998

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5 December 2019

Intracerebroventricular administration of quinolinic acid induces a selective decrease of inositol(1,4,5)-trisphosphate receptor in rat brain (English)

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5 December 2019

Lenka Dvořáková

5

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5 December 2019

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L S Haug

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5 December 2019

A C Ostvold

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5 December 2019

I Torgner

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5 December 2019

B Roberg

4

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5 December 2019

F St'astný

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5 December 2019

S I Walaas

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5 December 2019

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1 August 1998

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5 December 2019

Neurochemistry International

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5 December 2019

33

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5 December 2019

2

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5 December 2019

109-119

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5 December 2019

Characterization of the activation of glutaminase induced by N-methyl-D-aspartate and potassium in cerebellar granule cells.

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Chronic intrastriatal dialytic administration of quinolinic acid produces selective neural degeneration.

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Inositol trisphosphate and calcium signalling

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Bell-shaped calcium-response curves of Ins(1,4,5)P3- and calcium-gated channels from endoplasmic reticulum of cerebellum

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Short- and long-term consequences of intracranial injections of the excitotoxin, quinolinic acid, as evidenced by GFA immunohistochemistry of astrocytes.

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A study of the conditions and mechanism of the diphenylamine reaction for the colorimetric estimation of deoxyribonucleic acid

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N-methyl-d-aspartate increases cytoplasmic free calcium in mouse hippocampus

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Chapter 7 Glutamate receptor transmission and ischemic nerve cell damage:evidence for involvement of excitotoxic mechanisms

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Excitotoxin lesions in primates as a model for Huntington's disease: histopathologic and neurochemical characterization

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L-Glutamate dehydrogenase from bovine liver

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Phosphoinositide second messenger system is enriched in striosomes: immunohistochemical demonstration of inositol 1,4,5-trisphosphate receptors and phospholipase C beta and gamma in primate basal ganglia.

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Inositol 1, 4, 5-trisphosphate receptor-mediated Ca2+ signaling in the brain.

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Diminished [3H]inositol(1,4,5)P3 but not [3H]inositol(1,3,4,5)P4 binding in Alzheimer's disease brain.

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Remote astrocytic response as demonstrated by glial fibrillary acidic protein immunohistochemistry in the visual cortex of dorsal lateral geniculate nucleus lesioned rats

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Decreased inositol (1,4,5)-trisphosphate receptor levels in Alzheimer's disease cerebral cortex: selectivity of changes and possible correlation to pathological severity.

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Quinolinic acid-induced increases in calbindin D28k immunoreactivity in rat striatal neurons in vivo and in vitro mimic the pattern seen in Huntington's disease

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Modification of [3H]inositoltrisphosphate binding in kainic acid-lesioned and postischemic rat hippocampus.

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Mosaic distribution of phosphate-activated glutaminase-like immunoreactivity in the rat striatum

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Quinolinate neurotoxicity and glutamatergic structures.

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Cerebellar [3H]inositol 1,4,5-trisphosphate binding is markedly decreased in human olivopontocerebellar atrophy

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Altered glutamate binding following quinolinate lesions in developing rat brain.

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Purification and characterization of P400 protein, a glycoprotein characteristic of Purkinje cell, from mouse cerebellum

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Calcium-induced degradation of the inositol (1,4,5)-trisphosphate receptor/Ca(2+)-channel.

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Ataxia and epileptic seizures in mice lacking type 1 inositol 1,4,5-trisphosphate receptor.

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beta-Amyloid peptides destabilize calcium homeostasis and render human cortical neurons vulnerable to excitotoxicity

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Intraventricular kainic acid preferentially destroys hippocampal pyramidal cells

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Identifiers

10.1016/S0197-0186(98)00021-7

1 reference

Europe PubMed Central

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:9761455%20AND%20SRC:MED&resulttype=core&format=json

5 December 2019

1 reference

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5 December 2019

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