5 results on '"Pomierny B"'
Search Results
2. Extinction training following cocaine or MDMA self-administration produces discrete changes in D 2 -like and mGlu 5 receptor density in the rat brain.
- Author
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Frankowska M, Miszkiel J, Pomierny-Chamioło L, Pomierny B, Borelli AC, Suder A, and Filip M
- Subjects
- Animals, Behavior, Animal drug effects, Brain metabolism, Cocaine administration & dosage, Male, N-Methyl-3,4-methylenedioxyamphetamine administration & dosage, Rats, Wistar, Reinforcement Schedule, Self Administration, Brain drug effects, Cocaine pharmacology, Drug-Seeking Behavior drug effects, Extinction, Psychological, N-Methyl-3,4-methylenedioxyamphetamine pharmacology, Receptor, Metabotropic Glutamate 5 metabolism, Receptors, Dopamine D2 metabolism
- Abstract
Background: Several studies strongly support the role of the dopamine D
2 -like and glutamate mGlu5 receptors in psychostimulant reward and relapse., Methods: The present study employed cocaine or MDMA self-administration with yoked-triad procedure in rats to explore whether extinction training affects the drug-seeking behavior and the D2 -like and mGlu5 receptor Bmax and Kd values in several regions of the animal brain., Results: Both cocaine and MDMA rats developed maintenance of self-administration, but MDMA evoked lower response rates and speed of self-administration acquisition. During reinstatement tests, cocaine or MDMA seeking behavior was produced by either exposure to the drug-associated cues or drug-priming injections. The extinction training after cocaine self-administration did not alter significantly D2 -like receptor expression the in the limbic and subcortical brain areas, while MDMA yoked rats showed a decrease of the D2- like binding density in the nucleus accumbens and increase in the hippocampus and a rise of affinity in the striatum and hippocampus. Interestingly, in the prefrontal cortex a reduction in the mGlu5 receptor density in cocaine- or MDMA-abstinent rats was demonstrated, with significant effects being observed after previous MDMA exposure. Moreover, rats self-administered cocaine showed a rise in the density of mGlu5 receptor for the nucleus accumbens., Conclusion: This study first time shows that abstinence followed extinction training after cocaine or MDMA self- or passive-injections changes the D2 -like and mGlu5 density and affinity. The observed changes in the expression of both receptors are brain-region specific and related to either pharmacological and/or motivational features of cocaine or MDMA., (Copyright © 2019 Institute of Pharmacology, Polish Academy of Sciences. Published by Elsevier B.V. All rights reserved.)- Published
- 2019
- Full Text
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3. Ethylene glycol ethers induce apoptosis and disturb glucose metabolism in the rat brain.
- Author
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Pomierny B, Krzyżanowska W, Niedzielska E, Broniowska Ż, and Budziszewska B
- Subjects
- Animals, Apoptosis physiology, Ethers toxicity, Male, Rats, Rats, Wistar, Apoptosis drug effects, Brain drug effects, Brain metabolism, Ethylene Glycols toxicity, Glucose metabolism
- Abstract
Background: Ethylene glycol ethers (EGEs) are compounds widely used in industry and household products, but their potential, adverse effect on brain is poorly understood, so far. The aim of the present study was to determine whether 4-week administration of 2-buthoxyethanol (BE), 2-phenoxyethanol (PHE), and 2-ethoxyethanol (EE) induces apoptotic process in the rat hippocampus and frontal cortex, and whether their adverse effect on the brain cells can result from disturbances in the glucose metabolism., Methods: Experiments were conducted on 40 rats, exposed to BE, PHE, EE, saline or sunflower oil for 4 weeks. Markers of apoptosis and glucose metabolism were determined in frontal cortex and hippocampus by western blot, ELISA, and fluorescent-based assays., Results: BE and PHE, but not EE, increased expression of the active form of caspase-3 in the examined brain regions. BE and PHE increased caspase-9 level in the cortex and PHE also in the hippocampus. BE and PHE increased the level of pro-apoptotic proteins (Bax, Bak) and/or reduced the concentration of anti-apoptotic proteins (Bcl-2, Bcl-xL); whereas, the effect of BE was observed mainly in the cortex and that of PHE in the hippocampus. It has also been found that PHE increased brain glucose level, and both BE and PHE elevated pyruvate and lactate concentration., Conclusions: It can be concluded that chronic treatment with BE and PHE induced mitochondrial pathway of apoptosis, and disturbed glucose metabolism in the rat brain., (Copyright © 2015 Institute of Pharmacology, Polish Academy of Sciences. Published by Elsevier Urban & Partner Sp. z o.o. All rights reserved.)
- Published
- 2016
- Full Text
- View/download PDF
4. Potential neurotoxic effect of ethylene glycol ethers mixtures.
- Author
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Pomierny B, Starek A, Krzyżanowska W, Starek-Swiechowicz B, Smaga I, Pomierny-Chamioło L, Regulska M, and Budziszewska B
- Subjects
- Animals, Apoptosis drug effects, Caspase 3 metabolism, Cerebral Cortex metabolism, Frontal Lobe metabolism, Frontal Lobe pathology, Hippocampus metabolism, Lipid Peroxidation drug effects, Nerve Degeneration, Neurotoxicity Syndromes metabolism, Neurotoxicity Syndromes pathology, Oxidative Stress drug effects, Rats, Rats, Wistar, Cerebral Cortex drug effects, Ethers toxicity, Ethylene Glycols toxicity, Frontal Lobe drug effects, Hippocampus drug effects, Neurotoxicity Syndromes etiology
- Abstract
Background: Ethylene glycol ethers (EGEs) are widely used as mixtures in various industrial processes and in many household products. 2-Methoxyethanol and 2-ethoxyethanol primarily exert gonadotoxic effect, while 2-butoxyethanol and 2-isopropoxyethanol have potent hemolytic activity. EGEs can cross the blood-brain barrier, but their potential neurodegenerative action in vivo has not been investigated, yet. In the present work, we examined potential adverse effects of EGEs on some selected brain structures., Methods: A mixture of two compounds: one with stronger hydrophilic properties (2-methoxyethanol or 2-ethoxyethanol) and the second more lipophilic (2-butoxyethanol or 2-isopropoxyethanol) were administered sc for 4 weeks. Total antioxidant capacity, lipid peroxidation and caspase-3 activity were determined in the frontal cortex and hippocampus., Results: It has been found that 4-week administration of a mixture of two EGEs, with various intensity, decreased total antioxidant capacity, enhanced lipid peroxidation and increased caspase-3 activity in the frontal cortex and hippocampus of Wistar rat., Conclusion: The obtained results suggested that EGEs exerted adverse effects on the CNS cells and may contribute in pathogenesis of neurodegenerative disorders.
- Published
- 2013
- Full Text
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5. Effects of ethylene glycol ethers on cell viability in the human neuroblastoma SH-SY5Y cell line.
- Author
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Regulska M, Pomierny B, Basta-Kaim A, Starek A, Filip M, Lasoń W, and Budziszewska B
- Subjects
- Cell Line, Tumor, Humans, Hydrogen Peroxide pharmacology, Hydrogen Peroxide toxicity, Neuroblastoma, Neurons physiology, Cell Survival drug effects, Ethylene Glycols pharmacology, Neurons drug effects
- Abstract
Ethylene glycol ethers (EGEs) are a class of chemicals used extensively in the manufacture of a wide range of domestic and industrial products, which may result in human exposure and toxicity. Hematologic and reproductive toxicity of EGEs are well known whereas their action on neuronal cell viability has not been studied so far. In the present study, we investigated the effects of some EGEs on cell viability and on the hydrogen peroxide-induced damage in the human neuroblastoma (SH-SY5Y) cells. It has been found that 2-phenoxyethanol in a concentration-dependent manner (5-25 mM, 24 h) increased the basal and H(2)O(2)-induced lactate dehydrogenase (LDH) release and 3-[4,5-dimethylthiazol-2-yl]2,5-diphenyl tetrazolium bromide (MTT) reduction. 2-Butoxyethanol given alone did not affect LDH release and MTT reduction but concentration-dependently enhanced the cytotoxic effect of H(2)O(2). 2-Isopropoxyethanol significantly and concentration-dependently (1-25 mM) increased the basal LDH release and attenuated MTT reduction, but did not potentiate the cytotoxic effect of H(2)O(2). Contrary to this, 2-methoxyethanol did not show a cytotoxic effect while 2-ethoxyethanol at high concentrations intensified the hydrogen peroxide action. This study demonstrated that among the EGEs studied, 2-phenoxyethanol showed the most consistent cytotoxic effect on neurons in in vitro conditions and enhanced the hydrogen peroxide action. 2-Isopropoxyethanol had also a potent cytotoxic effect, but it did not enhance the hydrogen peroxide action, whereas 2-butoxyethanol only potentiated cytotoxic effect of H(2)O(2). It is concluded that the results of the present study should be confirmed in in vivo conditions and that some EGEs, especially 2-phenoxyethanol, 2-butoxyethanol and 2-isopropoxyethanol, may be responsible for initiation or exacerbation of neuronal cell damage.
- Published
- 2010
- Full Text
- View/download PDF
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