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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00004118naa a2200733 4500
001oai:gup.ub.gu.se/75505
003SwePub
008240528s2003 | |||||||||||000 ||eng|
024a https://gup.ub.gu.se/publication/755052 URI
024a https://doi.org/10.1002/jnr.106942 DOI
040 a (SwePub)gu
041 a eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
100a Ericson, Mia,d 1970u Gothenburg University,Göteborgs universitet,Institutionen för klinisk neurovetenskap, Sektionen för psykiatri,Institute of Clinical Neurosciences, Section of Psychiatry4 aut0 (Swepub:gu)xerimi
2451 0a Brain-derived neurotrophic factor mitigates chronic ethanol-induced attenuation of gamma-aminobutyric acid responses in cultured cerebellar granule cells.
264 c 2003-08-14
264 1b Wiley,c 2003
520 a This study examined the effect of chronic exposure to ethanol and brain-derived neurotrophic factor (BDNF) on the responsiveness of cerebellar granule cells to gamma-aminobutyric acid (GABA). Cerebellar granule cell cultures were chronically exposed to ethanol (100 mM), BDNF (20 ng/ml), or the combination of ethanol and BDNF. Whole-cell current responses of granule cells to exogenously applied GABA were monitored following at least 5 days of chronic exposure. In the ethanol-treated cultures, granule cell responsiveness to GABA was attenuated. Concomitant exposure of cultures to ethanol and BDNF mitigated the ethanol-induced attenuation of GABA response, although BDNF, by itself, did not affect responsiveness to GABA. BDNF increased the expression of the GABA(A) receptor alpha6 subunit, whereas ethanol had no effect, in chronically treated granule cell cultures. In addition, concomitant treatment with BDNF and ethanol did not increase the expression of the GABA(A) receptor alpha6 subunit, so the subunit expression alone could not account for the mitigating effect of BDNF. We propose that different mechanisms regulating responsiveness to GABA underlie the effects induced by ethanol and BDNF, with the former influencing the expression of functional GABA(A) receptors and the latter involving the activation of the TrkB receptor and its downstream signaling pathways.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Hälsovetenskapx Beroendelära0 (SwePub)303092 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Health Sciencesx Substance Abuse0 (SwePub)303092 hsv//eng
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Fysiologi0 (SwePub)301062 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Physiology0 (SwePub)301062 hsv//eng
653 a Alcohol-Induced Disorders
653 a Nervous System
653 a physiopathology
653 a Animals
653 a Brain-Derived Neurotrophic Factor
653 a metabolism
653 a Cells
653 a Cultured
653 a Central Nervous System Depressants
653 a pharmacology
653 a Cerebellum
653 a physiology
653 a Ethanol
653 a pharmacology
653 a Immunohistochemistry
653 a Mice
653 a Neurons
653 a drug effects
653 a metabolism
653 a Patch-Clamp Techniques
653 a Protein Subunits
653 a drug effects
653 a metabolism
653 a Receptor
653 a trkB
653 a metabolism
653 a Receptors
653 a GABA-A
653 a drug effects
653 a metabolism
653 a gamma-Aminobutyric Acid
653 a drug effects
653 a metabolism
700a Haythornthwaite, Alison R4 aut
700a Yeh, Pamela W L4 aut
700a Yeh, Hermes H4 aut
710a Göteborgs universitetb Institutionen för klinisk neurovetenskap, Sektionen för psykiatri4 org
773t Journal of neuroscience researchd : Wileyg 73:5, s. 722-30q 73:5<722-30x 0360-4012x 1097-4547
8564 8u https://gup.ub.gu.se/publication/75505
8564 8u https://doi.org/10.1002/jnr.10694

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Yeh, Pamela W L
Yeh, Hermes H
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