ArticleBrain research2007
Stimulation of the cAMP pathway protects cultured cerebellar granule neurons against alcohol-induced cell death by activating the neuronal nitric oxide synthase (nNOS) gene.
Article in Brain research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 36 citations in OpenAlex.
- Exacerbating effects of single-dose acute ethanol exposure on neuroinflammation and amelioration by GPR110 (ADGRF1) activation.Journal of neuroinflammation · 2023Article
- Purkinje cell-specific deletion of CREB worsens alcohol-induced cerebellar neuronal losses and motor deficits.Alcohol (Fayetteville, N.Y.) · 2022Article
- Neurotoxic Potential of Deoxynivalenol in Murine Brain Cell Lines and Primary Hippocampal Cultures.Toxins · 2022Article
- Early Intervention of Gastrodin Improved Motor Learning in Diabetic Rats Through Ameliorating Vascular Dysfunction.Neurochemical research · 2020Article
- Regional Patterns of Alcohol-Induced Neuronal Loss Depend on Genetics: Implications for Fetal Alcohol Spectrum Disorder.Alcoholism, clinical and experimental research · 2018Article
- Cyclic nucleotide phosphodiesterases: potential therapeutic targets for alcohol use disorder.Psychopharmacology · 2018Review
- Developmental Alcohol Exposure Impairs Activity-Dependent S-Nitrosylation of NDEL1 for Neuronal Maturation.Cerebral cortex (New York, N.Y. : 1991) · 2017Article
- Peroxynitrite is Involved in the Apoptotic Death of Cultured Cerebellar Granule Neurons Induced by Staurosporine, but not by Potassium Deprivation.Neurochemical research · 2016Article
- The neuronal nitric oxide synthase (nNOS) gene and neuroprotection against alcohol toxicity.Cellular and molecular neurobiology · 2015Review
- Genetic absence of nNOS worsens fetal alcohol effects in mice. I: behavioral deficits.Alcoholism, clinical and experimental research · 2015Article
- Genetic absence of nNOS worsens fetal alcohol effects in mice. II: microencephaly and neuronal losses.Alcoholism, clinical and experimental research · 2015Article
- Importance of genetics in fetal alcohol effects: null mutation of the nNOS gene worsens alcohol-induced cerebellar neuronal losses and behavioral deficits.Neurotoxicology · 2015Article
- Fetal stress and programming of hypoxic/ischemic-sensitive phenotype in the neonatal brain: mechanisms and possible interventions.Progress in neurobiology · 2012Review
- Role of nitric oxide in cerebellar development and function: focus on granule neurons.Cerebellum (London, England) · 2012Review
- Increased neuronal nitric oxide synthase dimerisation is involved in rat and human pancreatic beta cell hyperactivity in obesity.Diabetologia · 2011Article
- Phosphodiesterase type 4 inhibition does not restore ocular dominance plasticity in a ferret model of fetal alcohol spectrum disorders.Alcoholism, clinical and experimental research · 2010Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Neuronal loss is a key component of fetal alcohol syndrome pathophysiology. Therefore, identification of molecules and signaling pathways that ameliorate alcohol-induced neuronal death is important. We have previously reported that neuronal nitric oxide synthase (nNOS) can protect developing cerebellar granule neurons (CGN) against alcohol-induced death both in vitro and in vivo. However, the upstream signal controlling nNOS expression in CGN is unknown. Activated cAMP response element binding protein (CREB) has been strongly linked to the survival of multiple cell types, including CGN. Furthermore, the promoter of the nNOS gene contains two cAMP response elements (CRE). Using cultures of CGN, we tested the hypothesis that cAMP mediates nNOS activation and the protective effect of nNOS against alcohol-induced cell death. Forskolin, an activator of the cAMP pathway, stimulated expression of a reporter gene under the control of the nNOS promoter, and this stimulation was substantially reduced when the two CREs were mutated. Forskolin increased nNOS mRNA levels several fold, increased production of nitric oxide, and abolished alcohol's toxic effect in wild type CGN. Furthermore, forskolin's protective effect was substantially reduced in CGN cultures genetically deficient for nNOS (from nNOS-/- mice). Delivery of nNOS cDNA using a replication-deficient adenoviral vector into nNOS-/- CGN abolished alcohol-induced neuronal death. In addition, overexpression of nNOS in wild type CGN ameliorated alcohol-induced cell death. These results indicate that the neuroprotective effect of the cAMP pathway is mediated, in part, by the pathway's downstream target, the nNOS gene.
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