Neither forced running nor forced swimming affect acute pyridostigmine toxicity or brain-regional cholinesterase inhibition in rats

Tian, Hailin; Song, Xun; Bressler, Joseph; Pruett, Steve; Pope, Carey

doi:10.1016/s0300-483x(02)00089-6

Cited by 22 publications

(5 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Overall, our studies demonstrated results similar to Grauer et al (2000), Hancock et al (2003), Song et al (2002), and Tian et al (2002), who reported no effects of stress on AChE activity, as opposed to the studies of Beck et al (2003), Friedman et al (1996), and Sunanda, Rao, and Raju (2000), who did. In our studies, restraint, swim, and restraint with swim stress were not sufficient to inhibit AChE in blood or AChE, carboxylesterase, and ChAT in the hippocampus, nor did they further enhance the AChE inhibition caused by chlorpyrifos.…”

Section: Discussionsupporting

confidence: 73%

“…Some studies with carbamate cholinesterase inhibitors have suggested enhanced AChE inhibition and modulation of genes regulating acetylcholine availability following only 4 min of swim or 1 h of restraint (Beck et al 2003;Friedman et al 1996;Kaufer et al 1998). Other studies did not see changes in AChE inhibition following 10 to 90 minutes of stress (Grauer et al 2000;Song et al 2002;Tian et al 2002). Our results demonstrated that repeated restraint, swim, or restraint with occasional swim did not affect activities of blood AChE, or activities of AChE, carboxylesterase, and ChAT in the hippocampus.…”

Section: Indices Of Effects Of Repeated Stress and Chlorpyrifos On Thcontrasting

confidence: 42%

See 1 more Smart Citation

Examination of Concurrent Exposure to Repeated Stress and Chlorpyrifos on Cholinergic, Glutamatergic, and Monoamine Neurotransmitter Systems in Rat Forebrain Regions

et al. 2006

View full text Add to dashboard Cite

Repeated stress has been reported to cause reversible impairment in the central nervous system (CNS). It was proposed that alterations in glutamatergic, cholinergic, and monoamine neurotransmitter systems after exposure to stress are initial CNS events contributing to this impairment and that exacerbation could occur with concurrent exposure to cholinesterase inhibitors. Effects of concurrent exposure to repeated stress and chlorpyrifos on activities of acetylcholinesterase (AChE), carboxylesterase, and choline acetyltransferase (ChAT); concentrations of excitatory amino acids, monoamines, and their metabolites; and maximum binding densities (B(max)) and equilibrium dissociation rate constants (K(d)) of glutamatergic N-methyl-d-aspartate (NMDA) and total muscarinic cholinergic receptors were studied in the blood, hippocampus, cerebral cortex, or hypothalamus of adult Long-Evans rats. Stress treatments extended over 28 days included (1) control rats handled 5 days/week; (2) rats restrained 1 h/day for 5 days/week; (3) rats swum 30 min for 1 day/week; or (4) rats restrained 4 days/week and swum for 1 day/week. On day 24, each stress treatment group was randomly divided and injected either with corn oil or chlorpyrifos, 160 mg/kg subcutaneously (sc) (60% of the maximum tolerated dose), 4 h after restraint. Blood and brain tisssues were collected on day 28. Rats restrained and swum had a statistical trend toward increasing concentrations of glutamate in the hippocampus when compared to rats only swum (p = .064). Chlorpyrifos administration decreased restraint-induced elevated aspartate in the hippocampus, and decreased B(max) of total muscarinic receptors in the cerebral cortex. In addition, chlorpyrifos decreased B(max) and K(d) of total muscarinic receptors in the cerebral cortex of swum rats. Results demonstrated that chlorpyrifos inhibited AChE activity in blood, cerebral cortex, and hippocampus, but stress did not affect AChE activity. Carboxylesterase activity was inhibited by chlorpyrifos and by repeated restraint with swim. Swim stress decreased concentrations of norepinephrine in the hippocampus and hypothalamus, and increased concentrations of dopamine and its metabolite, DOPAC, in the hypothalamus. Both stress and chlorpyrifos altered serotonin concentrations, and the interactions of repeated stress and chlorpyrifos on serotonin approached significance in the hippocampus (p = .06) and hypothalamus (p = .08). Therefore, stress models were demonstrated to alter glutamatergic and monoamine responses, whereas chlorpyrifos alone had effects on cholinergic and monoamine systems in the rat CNS. However, the interactions between stress and chlorpyrifos significant at p < 0.05 were restricted to attenuation of elevated aspartate in the hippocampus of restrained with swim rats and decreased K(d) of acetylcholine receptors in the cerebral cortex of swum rats and restrained rats.

show abstract

Section: Discussionsupporting

confidence: 73%

Section: Indices Of Effects Of Repeated Stress and Chlorpyrifos On Thcontrasting

confidence: 42%

Examination of Concurrent Exposure to Repeated Stress and Chlorpyrifos on Cholinergic, Glutamatergic, and Monoamine Neurotransmitter Systems in Rat Forebrain Regions

et al. 2006

View full text Add to dashboard Cite

show abstract

“…FT-200, Taimeng Instruments, Inc., Chengdu, China) by a grid at the back of the treadmill lane delivering a mild electrical shock (1 mA). Crh +/+ and Crh −/− mice were subjected to running stress in accordance with a modified procedure [32]. Briefly, after 1 day of adaptation to the laboratory environment, the mice were divided into two groups respectively: (1) controls (Con), mice acclimatized to treadmill exercise but not run on the experiment day, and (2) stress group (St), mice were acclimatized to treadmill exercise and run on the experiment day.…”

Section: Model Preparationmentioning

confidence: 99%

Glucocorticoid guides mobilization of bone marrow stem/progenitor cells via FPR and CXCR4 coupling

Gao

Yang

et al. 2021

Stem Cell Res Ther

View full text Add to dashboard Cite

Background Our previous studies have proved the efficient exogenous repairing responses via bone marrow stem and progenitor cells (BMSPCs). However, the trafficking of endogenous bone marrow stem and progenitor cells to and from the bone marrow (BM) is a highly regulated process that remains to be elucidated. We aimed to study the relative importance of the hypothalamic-pituitary-adrenal (HPA) axis in the glucocorticoid-induced BMSPC mobilization. Methods The circulating mesenchymal stem cells (MSCs) and endothelial progenitor cells (EPCs) were examined in Crh (+/+, −/−) mice after running stress or glucocorticoid mini-infusion. The MSCs and EPCs were investigated ex vivo after treatment with glucocorticoid and glucocorticoid receptor (GR) antagonist, RU486. The expression of chemotaxis receptors, N-formyl peptide receptor (FPR), and Cys-X-Cys receptor 4 (CXCR4) of MSCs and EPCs as well as their colocalization were investigated after treatment with glucocorticoid, glucocorticoid receptor (GR) antagonist (RU486), and FPR antagonist (Cyclosporin H). Results Forced running stress increased circulating MSCs and EPCs in mice, which was blunted when Crh was knocked out, and positively related to the levels of serum glucocorticoid. Prolonged glucocorticoid mini-infusion imitated the stress-induced increase in circulating MSCs and EPCs in Crh+/+ mice and rescued the impaired mobilization in circulating MSCs and EPCs in Crh−/− mice. Meanwhile, glucocorticoid promoted the chemotaxis of MSCs and EPCs ex vivo via GR, inhibited by RU486 (10 μM). Concurrently, glucocorticoid increased the expression of FPR of MSCs and EPCs, but inhibited their expression of CXCR4, followed by their changing colocalization in the cytoplasm. The GC-induced colocalization of FPR and CXCR4 was blunted by Cyclosporin H (1 μM). Conclusion Glucocorticoid-induced CXCR4-FPR responsiveness selectively guides the mobilization of BMSPCs, which is essential to functional tissue repair. Graphical abstract Schematic view of the role of glucocorticoid on the mobilization of bone marrow-derived stem/progenitor cells subsets in the present study. The HPA axis activation promotes the release of glucocorticoid, which regulates the directional migration of MSCs and EPCs mainly via GR. The possible mechanisms refer to the signal coupling of FPR and CXCR4. Their two-sided changes regulated by glucocorticoid are involved in the egress of MSCs and EPCs from BM, which is helpful for wound healing. MSCs, mesenchymal stem cells; EPCs, endothelial progenitor cells.

show abstract

“…While very few studies have looked directly at neuroinflammation as a result of PB exposure, those that have investigated this directly, found very minimal proinflammatory effects of the drug with an inclination towards anti-inflammatory outcomes ( Locker et al, 2017 ; Hernandez et al, 2019 ). Moreover, while it has been suggested that stress may increase the permeability of the BBB allowing for PB to gain access to the brain ( Friedman et al, 1996 ; Hanin, 1996 ; Shen, 1998 ; Shaikh et al, 2003 ), several studies investigating the possibility that wartime stress affected the brain accessibility of PB have found that multiple stressor methods do not increase BBB permeability, affect PB’s reduction of brain ChE activity, nor elicit the elaboration of inflammatory markers in the brain or blood in animal models of GWI ( Sinton et al, 2000 ; Song et al, 2002 ; Tian et al, 2002 ; Amourette et al, 2009 ; Locker et al, 2017 ; Macht et al, 2018 ). These results suggest that the relationship between PB exposure and GWI that has been supported by epidemiological studies is not straightforward but does not seem to support a role for PB alone in the neuroimmune dysfunction hypothesis.…”

Section: Introductionmentioning

confidence: 99%

Acetylcholinesterase inhibitor exposures as an initiating factor in the development of Gulf War Illness, a chronic neuroimmune disorder in deployed veterans

et al. 2020

View full text Add to dashboard Cite

Gulf War Illness (GWI) is a chronic multi-symptom disorder, characterized by symptoms such as fatigue, pain, cognitive and memory impairment, respiratory, skin and gastrointestinal problems, that is experienced by approximately one-third of 1991 Gulf War veterans. Over the nearly three decades since the end of the war, investigators have worked to elucidate the initiating factors and underlying causes of GWI. A significant portion of this research has indicated a strong correlation between GWI and exposure to a number of different acetycholinesterase inhibitors (AChEIs) in theater, such as sarin and cyclosarin nerve agents, chlorpyrifos and dichlorvos pesticides, and the anti-nerve agent prophylactic pyridostigmine bromide. Through studying these exposures and their relationship to the symptoms presented by ill veterans, it has become increasingly apparent that GWI is the likely result of an underlying neuroimmune disorder. While evidence indicates that AChEIs are a key exposure in the development of GWI, particularly organophosphate AChEIs, the mechanism(s) by which these chemicals instigate illness appears to be related to “off-target”, non-cholinergic effects. In this review, we will discuss the role of AChEI exposure in the development and persistence of GWI; in particular, how these chemicals, combined with other exposures, have led to a chronic neuroimmune disorder. This article is part of the special issue entitled ‘Acetylcholinesterase Inhibitors: From Bench to Bedside to Battlefield’.

show abstract

Neither forced running nor forced swimming affect acute pyridostigmine toxicity or brain-regional cholinesterase inhibition in rats

Cited by 22 publications

References 26 publications

Examination of Concurrent Exposure to Repeated Stress and Chlorpyrifos on Cholinergic, Glutamatergic, and Monoamine Neurotransmitter Systems in Rat Forebrain Regions

Examination of Concurrent Exposure to Repeated Stress and Chlorpyrifos on Cholinergic, Glutamatergic, and Monoamine Neurotransmitter Systems in Rat Forebrain Regions

Glucocorticoid guides mobilization of bone marrow stem/progenitor cells via FPR and CXCR4 coupling

Acetylcholinesterase inhibitor exposures as an initiating factor in the development of Gulf War Illness, a chronic neuroimmune disorder in deployed veterans

Contact Info

Product

Resources

About