Unbound MEDLINE

Activity-mediated plasticity of GABA equilibrium potential in rat hippocampal CA1 neurons. Experimental neurology [Exp Neurol] Journal article

 
TitleActivity-mediated plasticity of GABA equilibrium potential in rat hippocampal CA1 neurons.
Author(s)Yang B, Tadavarty R, Xu JY, Sastry BR 
InstitutionNeuroscience Research Laboratory, Department of Anesthesiology, Pharmacology and Therapeutics, Faculty of Medicine, The University of British Columbia, Vancouver V6T 1Z3, Canada.
SourceExp Neurol 2009 Oct 28.
AbstractThe equilibrium potential (E(GABA-PSC)) for gamma-aminobutyric acid (GABA) A receptor mediated inhibitory postsynaptic currents (PSCs) in hippocampal CA1 pyramidal neurons shifts when theta-burst stimulation (4 pulses at 100 Hz in each burst in a train consisting of 5 bursts with an inter-burst interval of 200 ms, the train repeated thrice at 30 s intervals) is applied to the input. E(GABA-PSC) is regulated by K(+)/Cl(-)co-transporter (KCC2). GABA(B) receptors are implicated in modulating KCC2 levels. In the current study, the involvement of KCC2 as well as GABA(B) receptors in theta-burst-mediated shifts in E(GABA-PSC,) were examined. Whole-cell patch recordings were made from hippocampal CA1 pyramidal neurons (from 9-12 day old rats), in a slice preparation. Glutamatergic excitatory postsynaptic currents were blocked with dl-2-Amino-5-phosphonovaleric acid (50 microM) and 6,7-dinitroquinoxaline-2,3-dione (20 microM). The PSC as well as the E(GABA-PSC) were stable when stimulated at 0.05 Hz. However, both changed following a 30 min stimulation at 0.5 or 1 Hz. Furosemide (500 microM) and KCC2 anti-sense in the recording pipette but not bumetanide (20 or 100 microM) or KCC2 sense, blocked the changes, suggesting KCC2 involvement. Theta-burst stimulation induced a negative shift in E(GABA-PSC,) which was prevented by KCC2 anti-sense; however, KCC2 sense had no effect. CGP55845 (2 microM), a GABA(B) antagonist, applied in the superfusing medium, or GDP-beta-S in the recording pipette, blocked the shift in E(GABA-PSC.) These results indicate that activity-mediated plasticity in E(GABA-PSC) occurs in hippocampal CA1 pyramidal neurons and theta-burst-induced negative shift in E(GABA-PSC) requires KCC2, GABA(B) receptors and G-protein activation.
LanguageENG
Pub Type(s)JOURNAL ARTICLE
PubMed ID19879261
  
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