Neurotoxic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin in cerebellar granule cells

Kim, Sun‐Young; Yang, Jae‐Ho

doi:10.1038/emm.2005.8

Cited by 45 publications

(38 citation statements)

References 26 publications

(30 reference statements)

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“…Kim and Yang [127] have examined the neurotoxic effects of TCDD in cerebellar granule cells. TCDD-induced dosedependent increases in protein kinase C (PKC) activity, ROS production, and intracellular calcium concentration effects were shown to be AHR dependent.…”

Section: Oxidative Stress and Neurotoxicitymentioning

confidence: 99%

Dioxin‐Activated AHR: Toxic Responses and the Induction of Oxidative Stress

Stohs

Hassoun

2011

The AH Receptor in Biology and Toxicology

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Section: Oxidative Stress and Neurotoxicitymentioning

confidence: 99%

Dioxin‐Activated AHR: Toxic Responses and the Induction of Oxidative Stress

Stohs

Hassoun

2011

The AH Receptor in Biology and Toxicology

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“…Toxicological and epidemiological studies revealed that exposure to environmental AhR ligands are associated with delayed development of brain sexual dimorphism, social behavior, learning ability, and neuropsychiatric disorders in both animal models and humans (Ikeda et al 2005;Nishijo et al 2007;Piedrafita et al 2008;Patandin et al 1999;Goetz et al 1994). Although AhR-mediated neurotoxicity has been demonstrated in various experimental systems (Kim and Yang 2005;Akahoshi et al 2006;Lin et al 2008), information were limited to its up-regulation of CYP1A1 and oxidative stress. The extent to which AhR participates in neuronal survival and plasticity remains poorly understood.…”

mentioning

confidence: 99%

Knockdown of the aryl hydrocarbon receptor attenuates excitotoxicity and enhances NMDA‐induced BDNF expression in cortical neurons

Lin

Chen

Chou

et al. 2009

Journal of Neurochemistry

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NMDA receptors play dual and opposing roles in neuronal survival by mediating the activity‐dependent neurotrophic signaling and excitotoxic cell death via synaptic and extrasynaptic receptors, respectively. In this study, we demonstrate that the aryl hydrocarbon receptor (AhR), also known as the dioxin receptor, is involved in the expression and the opposing activities of NMDA receptors. In primary cultured cortical neurons, we found that NMDA excitotoxicity is significantly enhanced by an AhR agonist 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin, and AhR knockdown with small interfering RNA significantly reduces NMDA excitotoxicity. AhR knockdown also significantly reduces NMDA‐increases intracellular calcium concentration, NMDA receptor expression and surface presentation, and moderately decreases the NMDA receptor‐mediated spontaneous as well as miniature excitatory post‐synaptic currents. However, AhR knockdown significantly enhances the bath NMDA application– but not synaptic NMDA receptor‐induced brain‐derived neurotrophic factor (BDNF) gene expression, and activating AhR reduces the bath NMDA‐induced BDNF expression. Furthermore, AhR knockdown reveals the calcium dependency of NMDA‐induced BDNF expression and the binding activity of cAMP‐responsive element binding protein (CREB) and its calcium‐dependent coactivator CREB binding protein (CBP) to the BDNF promoter upon NMDA treatment. Together, our results suggest that AhR opposingly regulates NMDA receptor‐mediated excitotoxicity and neurotrophism possibly by differentially regulating the expression of synaptic and extrasynaptic NMDA receptors.

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“…It was shown that administration of vitamin E reduced the secretion of reactive oxygen species (ROS) induced by TCDD; at the same time it showed the protective properties of the brain structures. 34,35 A significant increase in tumor necrosis factor alpha (TNF-α) in mice treated with TCDD was also noted. In turn, the increase in the level of TNF-α is responsible for lethargy and anorexia.…”

Section: Introductionmentioning

confidence: 99%

The protective action of tocopherol and acetylsalicylic acid on the behavior of rats treated with dioxins

Rosińczuk¹,

Dymarek²,

Całkosiński³

2018

Adv Clin Exp Med

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Background. Dioxins contribute to neurological disorders in humans and animals, causing also neurological disorders in offspring during prenatal and postnatal periods. These compounds significantly affect the development of the central nervous system (CNS) structures, which results in behavioral changes. Tocopherol (TCP) and acetylsalicylic acid (ASA) may provide protective measures to reduce the inflammatory effects in the CNS associated with free radicals generated by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), thus contributing to the reduction of the negative effects of dioxin.

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Neurotoxic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin in cerebellar granule cells

Cited by 45 publications

References 26 publications

Dioxin‐Activated AHR: Toxic Responses and the Induction of Oxidative Stress

Dioxin‐Activated AHR: Toxic Responses and the Induction of Oxidative Stress

Knockdown of the aryl hydrocarbon receptor attenuates excitotoxicity and enhances NMDA‐induced BDNF expression in cortical neurons

The protective action of tocopherol and acetylsalicylic acid on the behavior of rats treated with dioxins

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