NMDA Receptor Overstimulation Triggers a Prolonged Wave of Immediate Early Gene Expression: Relationship to Excitotoxicity

Shan, Yuan; Carlock, Leon; Walker, Paul D.

doi:10.1006/exnr.1997.6427

Cited by 34 publications

(21 citation statements)

References 88 publications

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“…In neurodegenerative diseases, physiologically affected processes, including survival and neurotransmission, need to be enhanced in order to achieve sustained symptomatic benefit. The lesion paradigm used in the present study shows similarities with HD, like cell death and the loss of phenotypic markers in the surviving neurons (present results; Beal et al, 1991;Araujo and Hilt, 1997;Perez-Navarro et al, 1999a, 1999b, although other genes are also regulated by intrastriatal QUIN injection (Hughes et al, 1996;Shan et al, 1997;Qin et al, 1999). It is interesting to point out that NRTN not only prevented the loss of striatopallidal neurons but also the decrease in the expression of their phenotypic markers (present results), suggesting a preservation of neuronal function.…”

Section: Discussionmentioning

confidence: 59%

Striatopallidal neurons are selectively protected by neurturin in an excitotoxic model of Huntington's disease

et al. 2002

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Excitotoxicity has been involved in the pathogenesis of several neurodegenerative disorders. Using intrastriatal quinolinic acid (QUIN) injection as an animal model of Huntington's disease, we attempt to identify the neurotransmitter phenotype of striatal projection neurons protected by neurturin (NRTN). Control or NRTN-secreting cell lines were grafted in the striatum before QUIN injection and striatal projection neurons were examined by retrograde Fluorogold labeling and in situ hybridization. Intrastriatal grafting of NRTN-secreting cell line selectively prevented the loss of striatopallidal neurons and also the decrease in the mRNA levels for their markers (glutamic acid decarboxylase 67 and preproenkephalin) induced by QUIN, without affecting striatonigral neurons. Thus, our findings show that NRTN is a selective neuroprotective factor for striatopallidal neurons, suggesting that it might be a candidate for the treatment of movement disorders in which this neuronal population is affected.

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Section: Discussionmentioning

confidence: 59%

Striatopallidal neurons are selectively protected by neurturin in an excitotoxic model of Huntington's disease

et al. 2002

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“…Although this observation is not consistent with a previous study (31) that reported an increase in nNOS in postmortem hippocampal region from BD patients, the difference may represent differences in the response between the different brain regions. Further, characterization of the BD frontal cortex revealed a significant increase in c-fos expression, a marker of excitotoxicity (24, 32, 33), suggesting the presence of excitotoxicity in BD.…”

Section: Discussionmentioning

confidence: 95%

Increased excitotoxicity and neuroinflammatory markers in postmortem frontal cortex from bipolar disorder patients

et al. 2009

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Reports of cognitive decline, symptom worsening and brain atrophy in bipolar disorder (BD) suggest that the disease progresses over time. The worsening neuropathology may involve excitotoxicity and neuroinflammation. We determined protein and mRNA levels of excitotoxicity and neuroinflammatory markers in postmortem frontal cortex from 10 BD patients and 10 age-matched controls. The brain tissue was matched for age, postmortem interval and pH. The results indicated statistically significant lower protein and mRNA levels of the N-methyl-Daspartate receptors, NR-1 and NR-3A, but significantly higher protein and mRNA levels of interleukin (IL)-1b, the IL-1 receptor (IL-1R), myeloid differentiation factor 88, nuclear factorkappa B subunits, and astroglial and microglial markers (glial fibrillary acidic protein, inducible nitric oxide synthase, c-fos and CD11b) in postmortem frontal cortex from BD compared with control subjects. There was no significant difference in mRNA levels of tumor necrosis factor alpha or neuronal nitric oxide synthase in the same region. These data show the presence of excitotoxicity and neuroinflammation in BD frontal cortex, with particular activation of the IL-R cascade. The changes may account for reported evidence of disease progression in BD and be a target for future therapy.

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“…This phenomenon was shown to be mediated by the alkaloid fraction of UR. When cultured hippocampal neurons are pretreated with the alkaloid fraction of UR, neuronal death and apoptotic associated genes including c-jun, bax, and p53 were attenuated (Shan et al, 1997;Lee et al, 2003). Our previous studies have suggested that UR can decrease KA-induced lipid peroxide levels in vitro and behavior symptoms such as wet dog shakes (WDS), paw tremor (PT), and facial myoclonia (FM).…”

Section: Discussionmentioning

confidence: 98%

Oral Uncaria rhynchophylla (UR) reduces kainic acid-induced epileptic seizures and neuronal death accompanied by attenuating glial cell proliferation and S100B proteins in rats

Lin

Hsieh

2011

Journal of Ethnopharmacology

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NMDA Receptor Overstimulation Triggers a Prolonged Wave of Immediate Early Gene Expression: Relationship to Excitotoxicity

Cited by 34 publications

References 88 publications

Striatopallidal neurons are selectively protected by neurturin in an excitotoxic model of Huntington's disease

Striatopallidal neurons are selectively protected by neurturin in an excitotoxic model of Huntington's disease

Increased excitotoxicity and neuroinflammatory markers in postmortem frontal cortex from bipolar disorder patients

Oral Uncaria rhynchophylla (UR) reduces kainic acid-induced epileptic seizures and neuronal death accompanied by attenuating glial cell proliferation and S100B proteins in rats

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