GABA(A) receptor activation triggers a Cl- conductance increase and a K+ channel blockade in cerebellar granule cells
| dc.contributor.author | Labrakakis, C. | en |
| dc.contributor.author | Muller, T. | en |
| dc.contributor.author | Schmidt, K. | en |
| dc.contributor.author | Kettenmann, H. | en |
| dc.date.accessioned | 2015-11-24T16:31:47Z | |
| dc.date.available | 2015-11-24T16:31:47Z | |
| dc.identifier.issn | 0306-4522 | - |
| dc.identifier.uri | https://olympias.lib.uoi.gr/jspui/handle/123456789/7481 | |
| dc.rights | Default Licence | - |
| dc.subject | Animals | en |
| dc.subject | Barium/pharmacology | en |
| dc.subject | Bicuculline/*pharmacology | en |
| dc.subject | Cells, Cultured | en |
| dc.subject | Cerebellum/cytology/drug effects/*physiology | en |
| dc.subject | Chloride Channels/*physiology | en |
| dc.subject | Chlorides/*metabolism | en |
| dc.subject | Membrane Potentials/drug effects | en |
| dc.subject | Mice | en |
| dc.subject | Mice, Inbred Strains | en |
| dc.subject | Muscimol/*pharmac | en |
| dc.title | GABA(A) receptor activation triggers a Cl- conductance increase and a K+ channel blockade in cerebellar granule cells | en |
| heal.abstract | GABA(A) receptor activation in cerebellar granule cells induced a complex physiological response, namely the activation of a Cl- conductance in concert with a blockade of the resting K+ outward conductance (by 71% as compared to controls). Both responses were mediated by the activation of GABA(A) receptors, since they were both mimicked by the GABA(A) receptor agonist muscimol and antagonized by picrotoxin and bicuculline. A substantial decrease of the mean open time of single, outwardly rectifying K+ channels was triggered by GABA as revealed from cell-attached recordings; this finding implies that an intracellular pathway links GABA(A) receptors and K+ channels. Furthermore, this action of GABA is mediated through the cytoplasm, as experiments with the cell-attached patch-clamp technique show. GABA induced a prominent membrane depolarization ranging from 10 to 25 mV as revealed by current-clamp recordings of gramicidin (or nystatin) permeabilized patches, thus selecting conditions not to perturb the physiological Cl- gradient across the cell. Our findings imply that the GABA-activated Cl- current depolarized the membrane as described for immature neurons. The blockade of the resting K+ channel conductance acts in concert and both mechanisms lead to this substantial depolarizing event. | en |
| heal.access | campus | - |
| heal.fullTextAvailability | TRUE | - |
| heal.identifier.secondary | http://www.ncbi.nlm.nih.gov/pubmed/9178874 | - |
| heal.identifier.secondary | http://ac.els-cdn.com/S0306452296006446/1-s2.0-S0306452296006446-main.pdf?_tid=2944657a-c388-11e2-8c15-00000aab0f26&acdnat=1369300215_e5b84bc74faaa5e6d6f4b296ec32507e | - |
| heal.journalName | Neuroscience | en |
| heal.journalType | peer reviewed | - |
| heal.language | en | - |
| heal.publicationDate | 1997 | - |
| heal.recordProvider | Πανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών και Τεχνολογιών. Τμήμα Βιολογικών Εφαρμογών και Τεχνολογιών | el |
| heal.type | journalArticle | - |
| heal.type.el | Άρθρο Περιοδικού | el |
| heal.type.en | Journal article | en |
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