Wyniki wyszukiwania

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The role of GABAA and GABAB receptors in the control of GnRH release in anestrous ewes

100%

Tomaszewska-Zaremba D., Przekop F.

Reproductive Biology

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2006

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tom 06

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nr Suppl.2

2

Electrophysiological study of the mechanism of modulation of gabaergic synaptic currents by hydrogen ions

100%

Mandat M., Zarnowska E. D., Mercik K., Mozrzymas J. W.

Cellular and Molecular Biology Letters

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2002

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tom 07

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nr 3

3

Zolpidem withdrawal induced uncoupling of GABAA receptors in vitro associated with altered GABAA receptor subunit mRNA expression

84%

Jazvinscak Jembrek M., Vlainic J., Suran J.

Acta Neurobiologiae Experimentalis

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2015

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tom 75

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nr 2

Hypnotic Zolpidem produces its effects via the benzodiazepine binding site in a1-containing GABAA receptors. The aim of the study was to assess the influence of duration of Zolpidem treatment and its withdrawal, as well as the role of a1-containing GABAA receptors in the development of physical dependence and tolerance. Namely, recombinant receptors can be used to characterize mechanisms involved in different processes in the brain and to delineate the contribution of specific receptor subtypes. To address the influence of chronic Zolpidem treatment we exposed HEK293 cells stably expressing a102y2S recombinant GABAA receptors for seven consecutive days, while withdrawal periods lasted for 24, 48, 72 and 96 hours. Using radioligand binding studies we determined that chronic Zolpidem treatment did not induce changes in either GABAA receptor number or in the expression of subunit mRNAs. We observed the enhancement of binding sites and upregulated expression of subunit mRNAs only following 96-hour withdrawal. Moreover, Zolpidem treatment and its withdrawal (all time points) induced functional uncoupling between GABA and benzodiazepine binding sites in the GABAA receptor complex. Accordingly, it might be assumed that Zolpidem withdrawal-induced uncoupling of GABAA receptors is associated with altered GABAA receptor subunit mRNA expression. The results presented here provide an insight into molecular and cellular mechanisms probably underlying adaptive changes of GABAA receptor function in response to chronic usage and withdrawal of zolpidem and perhaps the observed molecular changes could be linked to the tolerance and dependence produced upon prolonged treatment with other GABAergic drugs.

4

Intermingled modulatory and neurotoxic effects of thimerosal and mercuric ions on electrophysiological responses to GABA and NMDA in hippocampal neurons

84%

Wyrembek P., Szczuraszek K., Majewska M. D., Mozrzymas J. W.

Journal of Physiology and Pharmacology

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2010

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tom 61

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nr 6

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Propofol alters vesicular transport in rat cortical neuronal cultures

67%

Turina D., Bjornstrom K., Sundovist T., Eintrei C.

Journal of Physiology and Pharmacology

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2011

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tom 62

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nr 1

Neuronal intracellular transport is performed by motor proteins, which deliver vesicles, organelles and proteins along cytoskeletal tracks inside the neuron. We have previously shown that the anesthetic propofol causes dose- and time-dependent, reversible retraction of neuronal neurites. We hypothesize that propofol alters the vesicular transport of cortical neurons due to this neurite retraction. Primary cultures of co-cultivated rat cortical neurons and glial cells were exposed to either 2 µM propofol, control medium or the lipid vehicle, in time-response experiments. Reversibility was tested by washing propofol off the cells. The role of the GABAA receptor (GABAAR) was assessed with the GABAAR antagonist gabazine. Vesicles were tracked using differential interference contrast video microscopy. Propofol caused a retrograde movement in 83.4±5.2% (mean±S.E.M.) of vesicles, which accelerated over the observed time course (0.025±0.012 µm·s-1). In control medium, vesicles moved predominantly anterograde (84.6±11.1%) with lower velocity (0.011±0.004 µm·s-1). Cells exposed to the lipid vehicle showed the same dynamic characteristics as cells in control medium. The propofol-induced effect on vesicle transport was reversible and blocked by the GABAAR antagonist gabazine in low concentration. Our results show that propofol causes a reversible, accelerating vesicle movement toward the neuronal cell body that is mediated via synaptic GABAAR. We have previously reported that propofol initiates neurite retraction, and we propose that propofol causes vesicle movement by retrograde flow of cytoplasm from the narrowed neurite.

6

Exogenous melatonin abolishes mechanical allodynia but not thermal hyperalgesia in neuropathic pain. The role of the opioid system and benzodiazepine-GABAergic mechanism

67%

Zurowski D., Nowak L., Machowska A., Wordliczek J., Thor P. J.

Journal of Physiology and Pharmacology

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2012

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tom 63

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nr 6

7

Ischemia-related alteration of GABA A-operated chloride channel properties in gerbil hippocampus and cerebral cortex

67%

Strosznajder J., Koladkiewicz I., Chalimoniuk M., Samochocki M.

Acta Neurobiologiae Experimentalis

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1998

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tom 58

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nr 2

Ograniczanie wyników

The role of GABAA and GABAB receptors in the control of GnRH release in anestrous ewes

Electrophysiological study of the mechanism of modulation of gabaergic synaptic currents by hydrogen ions

Zolpidem withdrawal induced uncoupling of GABAA receptors in vitro associated with altered GABAA receptor subunit mRNA expression

Intermingled modulatory and neurotoxic effects of thimerosal and mercuric ions on electrophysiological responses to GABA and NMDA in hippocampal neurons

Propofol alters vesicular transport in rat cortical neuronal cultures

Exogenous melatonin abolishes mechanical allodynia but not thermal hyperalgesia in neuropathic pain. The role of the opioid system and benzodiazepine-GABAergic mechanism

Ischemia-related alteration of GABA A-operated chloride channel properties in gerbil hippocampus and cerebral cortex