Gerasimov V D, Artemenko D P
Neirofiziologiia. 1990;22(5):627-33.
The action of various gamma-aminobutyric (GABA) concentrations on the amplitude of population EPSPs (PEPSPs) recorded from dendrites was examined in hippocampal slices. GABA produced reversible dose-dependent diminishing of the amplitude of PEPSPs without features of desensitization. CA1 hippocampal PEPSPs were much more sensitive to GABA (threshold concentrations--3.10(-5)-2.10(-4)mol/l; IC50--5.10(-4)-1.10(-3) mol/l) the action of GABA on PEPSPs was not depressed by bicuculline, picrotoxin or penicillin. The inhibitory action of GABA on dendritic antidromic population spike (DAPS) (post-synaptic inhibitory effect) was greatly reduced by these drugs. Baclofen was more potent inhibitor of CA1 PEPSPs than GABA (threshold concentration--1.10(-6)mol/l; IC50--3.10(-6)mol/l), but even in high concentration it induced only slight reduction of DAPS amplitude. It is concluded that GABA inhibitory effects on CA1 hippocampal PEPSPs are caused in the main by its presynaptic action mediated by GABA(B)-receptors located probably on axon terminals of the Schaffer collaterals.
在海马切片中研究了不同浓度的γ-氨基丁酸(GABA)对从树突记录的群体兴奋性突触后电位(pEPSP)幅度的作用。GABA使pEPSP幅度出现可逆的剂量依赖性降低,且无脱敏特征。海马CA1区的pEPSP对GABA更为敏感(阈值浓度为3×10⁻⁵ - 2×10⁻⁴mol/L;半数抑制浓度为5×10⁻⁴ - 1×10⁻³mol/L),GABA对pEPSP的作用不受荷包牡丹碱、印防己毒素或青霉素的抑制。这些药物可大大降低GABA对树突逆向群体峰电位(DAPS)的抑制作用(突触后抑制效应)。巴氯芬对海马CA1区pEPSP的抑制作用比GABA更强(阈值浓度为1×10⁻⁶mol/L;半数抑制浓度为3×10⁻⁶mol/L),但即使在高浓度时,它也仅使DAPS幅度略有降低。得出的结论是,GABA对海马CA1区pEPSP的抑制作用主要由其通过可能位于谢弗侧支轴突终末上的GABA(B)受体介导的突触前作用引起。