Behavioural analysis and susceptibility to CNS injury of four inbred strains of mice

Royle, Stephen; Collins, Fiona C; Rupniak, H. T.; Barnes, Julie C.; Anderson, Richard B.

doi:10.1016/s0006-8993(98)01122-6

Cited by 106 publications

(66 citation statements)

References 48 publications

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“…NeuN immunoreactivity in the CA3 subregion was not decreased in either wild-type or galectin-1 knockout mice (Figure 4b-e and j), indicating no apparent neuronal loss in the CA3 subregion. The mouse 129 strain used in this experiment is known to respond mildly to kainate as compared with other mouse strains, 22 and this may be the reason why we did not observe a loss of pyramidal cells in CA3. The extent of gliosis in the CA3 subregion was assessed by GFAP immunoreactivity, and we found that, after kainate administration, the GFAP index in Figure 3 Isolated primary astrocytes express and secrete galectin-1 in vitro.…”

Section: Resultsmentioning

confidence: 78%

Galectin-1 promotes basal and kainate-induced proliferation of neural progenitors in the dentate gyrus of adult mouse hippocampus

et al. 2008

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We examined the expression of galectin-1, an endogenous lectin with one carbohydrate-binding domain, in the adult mouse hippocampus after systemic kainate administration. We found that the expression of galectin-1 was remarkably increased in activated astrocytes of the CA3 subregion and dentate gyrus of the hippocampus, and in nestin-positive neural progenitors in the dentate gyrus. Quantitative reverse transcription PCR (RT-PCR) analysis revealed that the galectin-1 mRNA level in hippocampus began to increase 1 day after kainate administration and that a 13-fold increase was attained within 3 days. Western blotting analysis confirmed that the level of galectin-1 protein increased to more than three-fold a week after the exposure. We showed that isolated astrocytes express and secrete galectin-1. To clarify the significance of the increased expression of galectin-1 in hippocampus, we compared the levels of hippocampal cell proliferation in galectin-1 knockout and wild-type mice after saline or kainate administration. The number of 5-bromo-2 0 -deoxyuridine (BrdU)-positive cells detected in the subgranular zone (SGZ) of galectin-1 knockout mice decreased to 62% with saline, and to 52% with kainate, as compared with the number seen in the wild-type mice. Most of the BrdU-positive cells in SGZ expressed doublecortin and neuron-specific nuclear protein, indicating that they are immature neurons. We therefore concluded that galectin-1 promotes basal and kainateinduced proliferation of neural progenitors in the hippocampus.

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Section: Resultsmentioning

confidence: 78%

Galectin-1 promotes basal and kainate-induced proliferation of neural progenitors in the dentate gyrus of adult mouse hippocampus

et al. 2008

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“…To assess HuRs involvement in KAinduced neuronal dysfunction, we treated control (Elavl1 fl/fl and CamKIICre − Elavl fl/fl ) and CN-KO mice with two systemic doses of KA (20 and 30 mg/kg). These doses were previously reported to induce a mild excitotoxic response in the genetic background of our mutations (C57BL/6), 19,20 which is partially resistant to KA challenges. Following KA administration, mice were initially scored for the extent of epileptic seizures occurring within the first 3 h. In control mice, seizure-rating scores increased by 10 min, peaked between 20 and 30 min and gradually subsided thereafter.…”

Section: Elavl1mentioning

confidence: 84%

“…15 Experiments involving the administration of KA (intraperitoneal; K0250; Sigma, St. Louis, MO, USA) were supervised by Fleming's Veterinarian. Seizure severity was quantified via a 5-pointed rating scale 20 that included the frequency, latency and duration of shakes, convulsions, tonic-clonic seizures and death by two observers (OP and DLK). Surviving mice returned to their cages 3 h after the cessation of seizure activity or killed for histology.…”

Section: Methodsmentioning

confidence: 99%

Neuroprotection requires the functions of the RNA-binding protein HuR

et al. 2014

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Alterations in the functions of neuronal RNA-binding proteins (RBPs) can contribute to neurodegenerative diseases. However, neurons also express a set of widely distributed RBPs that may have developed specialized functions. Here, we show that the ubiquitous member of the otherwise neuronal Elavl/Hu family of RNA-binding proteins, Elavl1/HuR, has a neuroprotective role. Mice engineered to lack exclusively HuR in the hippocampal neurons of the central nervous system (CNS), maintain physiologic levels of neuronal Elavls and develop a partially diminished seizure response following strong glutamatergic excitation; however, they display an exacerbated neurodegenerative response subsequent to the initial excitotoxic event. This response was phenocopied in hippocampal cells devoid of ionotropic glutamate receptors in which the loss of HuR results in enhanced mitochondrial dysfunction, oxidative damage and programmed necrosis solely after glutamate challenge. The molecular dissection of HuR and nElavl mRNA targets revealed the existence of a HuR-restricted posttranscriptional regulon that failed in HuR-deficient neurons and is involved in cellular energetics and oxidation defense. Thus, HuR acts as a specialized controller of oxidative metabolism in neurons to confer protection from neurodegeneration.

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“…Although C57BL/6 mice are known to be less susceptible to kainate-induced seizures 82,83 and seizureinduced damage, 84 Morrison and collegues 79 demonstrated significant neuronal damage in the CA3 and CA1 subregions of the hippocampus in p53 wild-type mice (129/SvEv6C57BL/6 background) despite the genetic contribution from the C57BL/6 strain. Others have also reported significant induction of neuronal damage in the CA3 and CA1 subregions of the hippocampus in C57BL/6 mice in response to kainate-induced seizures.…”

Section: The Relationship Between P53 Expression and Neuronal Cell Deathmentioning

confidence: 99%

The role of p53 in neuronal cell death

2000

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The p53 tumor suppressor gene is a sequence-specific transcription factor that activates the expression of genes engaged in promoting growth arrest or cell death in response to genotoxic stress. A possible role for p53-related modulation of neuronal viability has been suggested by the finding that p53 expression is elevated in damaged neurons in acute models of injury such as ischemia and epilepsy and in brain tissue samples derived from patients with chronic neurodegenerative diseases. Moreover, the absence of p53 has been shown to protect neurons from a wide variety of acute toxic insults. Signal transduction pathways associated with p53-induced cell death are being unraveled and suggest that intervention may prove fruitful in maintaining neuronal viability and restoring function following cytopathic insults.

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Behavioural analysis and susceptibility to CNS injury of four inbred strains of mice

Cited by 106 publications

References 48 publications

Galectin-1 promotes basal and kainate-induced proliferation of neural progenitors in the dentate gyrus of adult mouse hippocampus

Galectin-1 promotes basal and kainate-induced proliferation of neural progenitors in the dentate gyrus of adult mouse hippocampus

Neuroprotection requires the functions of the RNA-binding protein HuR

The role of p53 in neuronal cell death

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