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Tytuł pozycji:

Inhibition of constitutive inward rectifier currents in cerebellar granule cells by pharmacological and synaptic activation of GABA receptors.

Tytuł :
Inhibition of constitutive inward rectifier currents in cerebellar granule cells by pharmacological and synaptic activation of GABA receptors.
Index Terms :
Sciences bio-médicales et agricoles
Animals
Cerebellar Cortex -- drug effects
Cerebellar Cortex -- metabolism
GABA Agonists -- pharmacology
GABA Antagonists -- pharmacology
Membrane Potentials -- drug effects
Membrane Potentials -- physiology
Mice
Neural Inhibition -- drug effects
Neural Inhibition -- physiology
Neurons -- drug effects
Neurons -- metabolism
Organ Culture Techniques
Patch-Clamp Techniques
Phosphoprotein Phosphatases -- antagonists & inhibitors
Phosphoprotein Phosphatases -- metabolism
Potassium Channels, Inwardly Rectifying -- drug effects
Potassium Channels, Inwardly Rectifying -- metabolism
Receptors, G-Protein-Coupled -- drug effects
Receptors, G-Protein-Coupled -- metabolism
Receptors, GABA-B -- drug effects
Receptors, GABA-B -- metabolism
Synaptic Transmission -- drug effects
Synaptic Transmission -- physiology
Cerebellum
GABAB receptors
Granule cells
Inward rectifier
Non-synaptic plasticity
info:eu-repo/semantics/article
info:ulb-repo/semantics/articlePeerReview
info:ulb-repo/semantics/openurl/article
Wydawca :
2006-07
Dodane szczegóły :
Rossi, Pier Luca
Roggeri, L.
Gall, David
de Kerchove d'Exaerde, Alban
Schiffmann, Serge N.
D'Angelo, E.
Typ dokumentu :
Zasób elektroniczny
URL :
http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/50718">http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/50718
http://worldcat.org/search?q=on:EQY+http://difusion-oai.ulb.ac.be/oai/request+DCG_ENTIRE_REPOSITORY+CNTCOLL">http://worldcat.org/search?q=on:EQY+http://difusion-oai.ulb.ac.be/oai/request+DCG_ENTIRE_REPOSITORY+CNTCOLL
Dostępność :
Open access content. Open access content
2 full-text file(s): info:eu-repo/semantics/restrictedAccess | info:eu-repo/semantics/openAccess
Pozostałe numery :
EQY oai:dipot.ulb.ac.be:2013/50718
uri/info:doi/10.1111/j.1460-9568.2006.04914.x
uri/info:pii/EJN4914
uri/info:pmid/16903850
uri/info:scp/33746210832
https://dipot.ulb.ac.be/dspace/bitstream/2013/50718/4/50718.pdf
https://dipot.ulb.ac.be/dspace/bitstream/2013/50718/1/EJNKir2006.pdf
803419669
Źródło wspomagające :
UNIV LIBR DE BRUXELLES
From OAIster®, provided by the OCLC Cooperative.
Numer akcesji :
edsoai.ocn803419669
Zasób elektroniczny
gamma-Aminobutyric acid (GABA)(B) receptors are known to enhance activation of Kir3 channels generating G-protein-dependent inward rectifier K(+)-currents (GIRK). In some neurons, GABA(B) receptors either cause a tonic GIRK activation or generate a late K(+)-dependent inhibitory postsynaptic current component. However, other neurons express Kir2 channels, which generate a constitutive inward rectifier K(+)-current (CIRK) without requiring G-protein activation. The functional coupling of CIRK with GABA(B) receptors remained unexplored so far. About 50% of rat cerebellar granule cells in the internal granular layer of P19-26 rats showed a sizeable CIRK current. Here, we have investigated CIRK current regulation by GABA(B) receptors in cerebellar granule cells, which undergo GABAergic inhibition through Golgi cells. By using patch-clamp recording techniques and single-cell reverse transcriptase-polymerase chain reaction in acute cerebellar slices, we show that granule cells co-express Kir2 channels and GABA(B) receptors. CIRK current biophysical properties were compatible with Kir2 but not Kir3 channels, and could be inhibited by the GABA(B) receptor agonist baclofen. The action of baclofen was prevented by the GABA(B) receptor blocker CGP35348, involved a pertussis toxin-insensitive G-protein-mediated pathway, and required protein phosphatases inhibited by okadaic acid. GABA(B) receptor-dependent CIRK current inhibition could also be induced by repetitive GABAergic transmission at frequencies higher than the basal autorhythmic discharge of Golgi cells. These results suggest therefore that GABA(B) receptors can exert an inhibitory control over CIRK currents mediated by Kir2 channels. CIRK inhibition was associated with an increased input resistance around rest and caused a approximately 5 mV membrane depolarization. The pro-excitatory action of these effects at an inhibitory synapse may have an homeostatic role re-establishing granule cell readiness under conditions of
Journal Article
Research Support, Non-U.S. Gov't
FLWIN
info:eu-repo/semantics/published

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