Permanently compromised NADPH-diaphorase activity within the osmotically activated supraoptic nucleus after in utero but not adult exposure to Aroclor 1254

Coburn, Cary G.; Watson-Siriboe, Abena; Hou, Borin; Cheetham, Chad C.; Gillard, Elizabeth R.; Lin, Lisa; León-Olea, Martha; Sánchez-Islas, Eduardo; Mucio-Ramírez, Samuel; Currás-Collazo, Margarita

doi:10.1016/j.neuro.2014.12.009

Cited by 10 publications

(11 citation statements)

References 88 publications

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“…The dosing and experimental paradigm used in this study match the experimental conditions in our previous reports (Coburn et al, 2015;Shah et al, 2011). Kodavanti et al (1998) where we showed that adult rats dosed orally with A1254 (30 mg/kg/day for 20 days), have brain tissue concentrations of 8.2-15.1 ppm or 20-50 μM.…”

Section: Perinatal Exposure To A1254 and De-71mentioning

confidence: 67%

“…In the PVN and SON hypothyroidism prevents osmotically-stimulated upregulation of transcripts for nitric oxide synthase (NOS), which is required for AVP functions (Ueta et al, 1995). Related to this our group has shown persistent reduction of NOS activity in the osmotically activated MNC system after similar developmental exposure to A1254 (Coburn et al, 2015;Leon-Olea et al, 2004;Mucio-Ramírez et al, 2008). Moreover, A1254 affects the expression of aquaporin 1 (AQP1) water channels (Tewari et al, 2009), which are regulated and linked to AVP V2 receptors and nitric oxide synthase (NOS) involved in water reabsorption (Klokkers et al, 2009;Swenson et al, 1997); deficiencies in the latter has been shown to impair water retention (Ma et al, 1998).…”

Section: Perinatal Exposure To A1254 and De-71 Disrupts Avp Responsesmentioning

confidence: 86%

“…We used this high dose and the same lot numbers of A1254 or DE-71 that were proven to produce neurotoxicity in previous studies Kodavanti and Ward, 2005). Delivery of toxicants via dietary snacks has consistently proven to be an effective method of oral exposure in our lab and others using different snacks or mixed in pellets (Coburn et al, 2015;Coburn et al, 2005;Rickert et al, 1978). A1254 at 30 mg/kg/day of exposure could reduce litter size (Brezner et al, 1984).…”

Section: Perinatal Exposure To A1254 and De-71mentioning

confidence: 99%

“…with either 3.5 M NaCl (Hyperosmotic solution) or 0.154 M NaCl (0.9% NaCl isotonic solution; Control) and animals were sacrificed 4-4.5 h later as described (Ludwig et al, 1994;Coburn et al, 2015). This manipulation has been shown to produce marked stimulation of somatodendritic AVP release (Coburn et al, 2015;Ludwig et al, 1994). Tail blood was collected before sacrifice and plasma osmolality was measured to confirm increased plasma osmolality in Hyper rats of 5.0% or greater.…”

Section: Acute Osmoregulatory Challengementioning

confidence: 99%

“…The effects of these organohalogens depend on factors such as dosage, sex, susceptibility of each organism, type of congener, duration of exposure, physiological activation, and life stage at which the organism is exposed (Faroon et al, 2001;McKinney and Waller, 1994;Viberg et al, 2006). PCBs and PBDEs produce neurotoxicity by disrupting protein kinase C (PKC) and perturbing intracellular calcium homeostasis, nitric oxide signaling, neurotransmitter release, synaptic plasticity, gene expression, oxidative stress, and energy metabolism in the brain (Coburn et al, 2008(Coburn et al, , 2015Kodavanti et al, 2011;Royland and Kodavanti, 2008;Tilson et al, 1998;Westerink, 2014;Wong et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

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Perinatal exposure to organohalogen pollutants decreases vasopressin content and its mRNA expression in magnocellular neuroendocrine cells activated by osmotic stress in adult rats

Mucio-Ramírez

Sánchez-Islas

Sánchez-Jaramillo

et al. 2017

Toxicology and Applied Pharmacology

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Polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDEs) are environmental pollutants that produce neurotoxicity and neuroendocrine disruption. They affect the vasopressinergic system but their disruptive mechanisms are not well understood. Our group reported that rats perinatally exposed to Aroclor-1254 (A1254) and DE-71 (commercial mixtures of PCBs and PBDEs) decrease somatodendritic vasopressin (AVP) release while increasing plasma AVP responses to osmotic activation, potentially emptying AVP reserves required for body-water balance. The aim of this research was to evaluate the effects of perinatal exposure to A1254 or DE-71 (30mgkg/day) on AVP transcription and protein content in the paraventricular and supraoptic hypothalamic nuclei, of male and female rats, by in situ hybridization and immunohistochemistry. cFOS mRNA expression was evaluated in order to determine neuroendocrine cells activation due to osmotic stimulation. Animal groups were: vehicle (control); exposed to either A1254 or DE-71; both, control and exposed, subjected to osmotic challenge. The results confirmed a physiological increase in AVP-immunoreactivity (AVP-IR) and gene expression in response to osmotic challenge as reported elsewhere. In contrast, the exposed groups did not show this response to osmotic activation, they showed significant reduction in AVP-IR neurons, and AVP mRNA expression as compared to the hyperosmotic controls. cFOS mRNA expression increased in A1254 dehydrated groups, suggesting that the AVP-IR decrease was not due to a lack of the response to the osmotic activation. Therefore, A1254 may interfere with the activation of AVP mRNA transcript levels and protein, causing a central dysfunction of vasopressinergic system.

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Section: Perinatal Exposure To A1254 and De-71mentioning

confidence: 67%

Section: Perinatal Exposure To A1254 and De-71 Disrupts Avp Responsesmentioning

confidence: 86%

Section: Perinatal Exposure To A1254 and De-71mentioning

confidence: 99%

Section: Acute Osmoregulatory Challengementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Perinatal exposure to organohalogen pollutants decreases vasopressin content and its mRNA expression in magnocellular neuroendocrine cells activated by osmotic stress in adult rats

Mucio-Ramírez

Sánchez-Islas

Sánchez-Jaramillo

et al. 2017

Toxicology and Applied Pharmacology

Self Cite

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Dirty Minds: How Endocrine Disrupting Chemicals (EDCs) and Other Pollutants Affect the Neuroendocrinology of Behavior and Emotions

Patisaul

2024

Neuroendocrinology of Behavior and Emotions

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Persistent autism-relevant behavioral phenotype and social neuropeptide alterations in female mice offspring induced by maternal transfer of PBDE congeners in the commercial mixture DE-71

et al. 2021

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Polybrominated diphenyl ethers (PBDEs) are ubiquitous persistent organic pollutants (POPs) that are known neuroendocrine disrupting chemicals with adverse neurodevelopmental effects. PBDEs may act as risk factors for autism spectrum disorders (ASD), characterized by abnormal psychosocial functioning, although direct evidence is currently lacking. Using a translational exposure model, we tested the hypothesis that maternal transfer of a commercial mixture of PBDEs, DE-71, produces ASD-relevant behavioral and neurochemical deficits in female offspring. C57Bl6/N mouse dams (F0) were exposed to DE-71 via oral administration of 0 (VEH/CON), 0.1 (L-DE-71) or 0.4 (H-DE-71) mg/kg bw/d from 3 wk prior to gestation through end of lactation. Mass spectrometry analysis indicated in utero and lactational transfer of PBDEs (in ppb) to F1 female offspring brain tissue at postnatal day (PND) 15 which was reduced by PND 110. Neurobehavioral testing of social novelty preference (SNP) and social recognition memory (SRM) revealed that adult L-DE-71 F1 offspring display deficient short- and long-term SRM, in the absence of reduced sociability, and increased repetitive behavior. These effects were concomitant with reduced olfactory discrimination of social odors. Additionally, L-DE-71 exposure also altered short-term novel object recognition memory but not anxiety or depressive-like behavior. Moreover, F1 L-DE-71 displayed downregulated mRNA transcripts for oxytocin (Oxt) in the bed nucleus of the stria terminalis (BNST) and supraoptic nucleus, and vasopressin (Avp) in the BNST and upregulated Avp1ar in BNST, and Oxtr in the paraventricular nucleus. Our work demonstrates that developmental PBDE exposure produces ASD-relevant neurochemical, olfactory processing and behavioral phenotypes that may result from early neurodevelopmental reprogramming within central social and memory networks.

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Permanently compromised NADPH-diaphorase activity within the osmotically activated supraoptic nucleus after in utero but not adult exposure to Aroclor 1254

Cited by 10 publications

References 88 publications

Perinatal exposure to organohalogen pollutants decreases vasopressin content and its mRNA expression in magnocellular neuroendocrine cells activated by osmotic stress in adult rats

Perinatal exposure to organohalogen pollutants decreases vasopressin content and its mRNA expression in magnocellular neuroendocrine cells activated by osmotic stress in adult rats

Dirty Minds: How Endocrine Disrupting Chemicals (EDCs) and Other Pollutants Affect the Neuroendocrinology of Behavior and Emotions

Persistent autism-relevant behavioral phenotype and social neuropeptide alterations in female mice offspring induced by maternal transfer of PBDE congeners in the commercial mixture DE-71

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