Edwards Michelle D, Platt Bettina
Department of Biomedical Sciences, Institute of Medical Sciences, University of Aberdeen, Foresterhill, UK.
Exp Brain Res. 2003 Apr;149(3):331-9. doi: 10.1007/s00221-002-1368-2. Epub 2003 Jan 31.
Superficial superior colliculus (SSC) neurones were voltage-clamped and the current-voltage relationship of synaptically evoked currents analyzed in vitro. A strong interplay between excitatory postsynaptic currents (EPSCs) and inhibitory postsynaptic currents (IPSCs) was identified. Glutamate receptor antagonists not only fully blocked EPSCs but IPSCs were also frequently reduced by the specific d,l,-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor antagonist (by 66.9%), indicative of glutamate-driven inhibitory projections. The GABA(A )receptor antagonist bicuculline enhanced EPSCs and either abolished or reduced (by 79.3%) IPSCs. The GABA(C) receptor antagonist 1,2,5,6-tetrahydro-(pyridin-4-yl)methylphosphinic acid decreased IPSCs in 80% of cells tested (by 24.1%), but had no effect on EPSCs. Varying the recording conditions influenced postsynaptic currents. At a holding potential of -60 mV, IPSCs were generally produced with intracellular chloride concentrations of both 5 and 10 mM (total n=24/30). However, with perforated-patch recordings using gramicidin, IPSCs were less frequently encountered (n=5/21), suggesting a higher intracellular chloride concentration in a large proportion of SSC neurones. Further assessment of experimental conditions revealed that two frequently used sodium channel blockers, QX-314 (bromide salt, intracellular) or tetrodotoxin (extracellular), shifted the IPSC reversal potential towards more positive values. Hence, IPSCs were not encountered at -60 mV in their presence. The level of stimulation intensity (minimal or maximal) did not influence IPSC production in these conditions. Thus, the current study describes the pharmacological properties of PSCs in the SSC and highlights the impact of experimental conditions on synaptic transmission, which requires consideration for past and present data reported in this preparation.
在体外对浅层上丘（SSC）神经元进行电压钳制，并分析突触诱发电流的电流-电压关系。研究发现兴奋性突触后电流（EPSC）和抑制性突触后电流（IPSC）之间存在强烈的相互作用。谷氨酸受体拮抗剂不仅能完全阻断EPSC，而且特异性的d，l-α-氨基-3-羟基-5-甲基-4-异恶唑丙酸受体拮抗剂还经常使IPSC减少（减少66.9%），这表明存在谷氨酸驱动的抑制性投射。GABA(A)受体拮抗剂荷包牡丹碱增强了EPSC，并消除或减少了（减少79.3%）IPSC。GABA(C)受体拮抗剂1,2,5,6-四氢-（吡啶-4-基）甲基次膦酸在80%的受试细胞中使IPSC减少（减少24.1%），但对EPSC没有影响。改变记录条件会影响突触后电流。在-60 mV的钳制电位下，细胞内氯化物浓度为5 mM和10 mM时通常都会产生IPSC（总共n = 2４/30）。然而，使用短杆菌肽进行穿孔膜片钳记录时，较少观察到IPSC（n = 5/21），这表明大部分SSC神经元的细胞内氯化物浓度较高。对实验条件的进一步评估表明，两种常用的钠通道阻滞剂，QX-314（溴盐，细胞内）或河豚毒素（细胞外），会使IPSC反转电位向更正的值偏移。因此，在它们存在的情况下，在-60 mV时未观察到IPSC。在这些条件下，刺激强度水平（最小或最大）不影响IPSC的产生。因此，本研究描述了SSC中PSC的药理学特性，并强调了实验条件对突触传递的影响，这对于该制剂过去和现在报道的数据都需要加以考虑。
