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2 results on '"Cultured cerebellar granule cells"'

1. The effect of modulation of Na+/К+-АТPase activity on viability of cerebellar granule cells exposed to oxidative stress in vitro

Author

Elena V. Stelmashook, Nikolay K. Isaev, Elizaveta E. Genrikhs, and Leonid G. Khaspekov

Subjects
cultured cerebellar granule cells, na+/к+-атpase, ouabain, oxidative stress, Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571
Abstract

Introduction. Oxidative stress is an important pathogenic factor in cerebral ischemia, which occupies one of the leading places among various forms of cerebral pathology in mortality and disability of the working-age population and is recognized as an actual problem of experimental and clinical neurology. Naturally, modeling of neurodestructive processes and their correction under the action of oxidative stress in vitro contributes to the study of protective mechanisms that counteract ischemic damage of neurons. Objective. To reveal the influence of chemical preconditioning induced by transient inhibition of Na+/K+-ATPase activity on tolerance of cultured cerebellar granule neurons to oxidative stress at different stages of their differentiation in vitro. Materials and methods. The activity of Na+/K+-ATPase was inhibited with ouabain, which was added at 34 and 78 days in vitro to cerebellar cell cultures of 7-day rats at a concentration of 0.1 mM for 24 hours before induction of oxidative stress by hydrogen peroxide (0.05 and 0.075 mM, 4 hours) or paraquat (0.15 and 0.2 mM, 24 hours). Results. Oxidative stress induced by paraquat causes the most pronounced death of cultured granular neurons in immature (34 days) cultures, in which survival was 442,5% of neurons, compared to mature (78 days) cultures, in which survival was 615,4%. Pretreatment of cultures with ouabain has a protective effect, the most significant in mature cultures. The exposure of mature cultures with hydrogen peroxide kills more than 90% of neurons, whereas pretreatment with ouabain increases the survival rate by 44%. At the same time in the immature cultures the damaging effects of H2O2 and the protective effect of ouabain is less pronounced. Conclusion. The increased tolerance of cultured cerebellar granule cells to oxidative stress after transient inhibition of Na+/K+-ATPase activity by ouabain is shown. The direct dependence of the efficiency of the ouabain protection on the degree of neuronal morphochemical differentiation in vitro is revealed.

Published
2018
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2. Mercury interaction with the GABA(A) receptor modulates the benzodiazepine binding site in primary cultures of mouse cerebellar granule cells

Author

Elena Fonfría, E Rodríguez-Farré, Cristina Suñol, Ministerio de Sanidad y Seguridad Social (España), Generalitat de Catalunya, and Institut d'Investigacions Biomèdiques August Pi i Sunyer

Subjects
Cerebellum, Alkylation, Benzodiazepine binding, Flunitrazepam, Pharmacology, Antioxidants, Ion Channels, GABAA-rho receptor, Cellular and Molecular Neuroscience, chemistry.chemical_compound, Mice, Neurotoxicity, medicine, Animals, GABA-A Receptor Antagonists, Sulfhydryl Compounds, Enzyme Inhibitors, Receptor, Cells, Cultured, Protein Kinase C, gamma-Aminobutyric Acid, Binding Sites, Dose-Response Relationship, Drug, GABAA receptor, Mercury Compounds, musculoskeletal, neural, and ocular physiology, Methylmercury, Bicuculline, Methylmercury Compounds, Receptors, GABA-A, Cyclic AMP-Dependent Protein Kinases, Enzyme Activation, Mercuric chloride, medicine.anatomical_structure, chemistry, Mechanism of action, Biochemistry, Anti-Anxiety Agents, DIDS, Mercuric Chloride, medicine.symptom, Cultured cerebellar granule cells, medicine.drug
Abstract

Mercury compounds are neurotoxic compounds with a great specificity for cerebellar granule cells. The interaction of mercury compounds with proteins in the central nervous system may underlie some of their effects on neurotransmission. In this work we study the interaction of mercuric chloride (HgCl2) and methylmercury (MeHg) with the GABAA receptor in primary cultures of cerebellar granule cells. Both compounds increased, dose dependently, the binding of flunitrazepam to the benzodiazepine recognition site. EC50 values for this effect were 3.56 and 15.24 μM for HgCl2 and MeHg, respectively, after 30 min exposure of intact cultured cerebellar granule cells. The increase of flunitrazepam binding by mercury compounds was completely inhibited by the GABAA receptor antagonists bicuculline and picrotoxinin, and by the organochlorine pesticide α-endosulfan. It was also partially inhibited by the anion transporter blocker DIDS, however this effect could be due to a possible chelation of mercury by DIDS. Intracellular events, like intracellular calcium, kinase activation/inactivation or antioxidant conditions did not affect flunitrazepam binding or its increase induced by mercury compounds. The sulfhydryl alkylating agent N-ethylmaleimide mimicked the effect of mercury compounds on flunitrazepam binding suggesting a common mechanism. We conclude that mercury compounds interact with the GABAA receptor by the way of alkylation of SH groups of cysteinyl residues found in GABAA receptor subunit sequences., This research was supported by Grant number 00/1094 and 01/1318 from FIS (Spanish Fondo de Investigaciones Sanitarias de la Seguridad Social) and Grant numbers 1999SGR00210 and 1999SGR00212 from CIRIT (Generalitat de Catalunya, Spain). E. Fonfrı́a is recipient of a fellowship from the Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS).

Published
2001

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