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Sometimes you see them, sometimes you don't: IPSCs in the rat superficial superior colliculus

机译:有时您看到它们,有时却看不到:大鼠浅表上丘中的IPSC

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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,-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor antagonist (by 66.9%), indicative of glutamate-driven inhibitory projections. The GABAA receptor antagonist bicuculline enhanced EPSCs and either abolished or reduced (by 79.3%) IPSCs. The GABAC 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.
机译:浅表上丘(SSC)神经元被电压钳,并在体外分析突触诱发电流的电流-电压关系。兴奋性突触后电流(EPSCs)和抑制性突触后电流(IPSCs)之间强烈相互作用。谷氨酸受体拮抗剂不仅可以完全阻断EPSC,而且特定的d,l,-α-氨基-3-羟基-5-甲基-5-甲基-4-异恶唑丙酸受体拮抗剂(66.9%)还经常降低IPSC,表明谷氨酸驱动的抑制性预测。 GABAA 受体拮抗剂bicuculline增强了EPSC,并且废除了或减少了IPSC(降低了79.3%)。 GABAC受体拮抗剂1,2,5,6-四氢-(吡啶-4-基)甲基次膦酸可降低80%受测细胞的IPSC(24.1%),但对EPSC无影响。记录条件的变化会影响突触后电流。在保持电位为–60 mV的情况下,通常产生的IPSC的细胞内氯浓度为5和10 mM(总n = 24/30)。然而,在使用短杆菌肽的穿孔补丁记录中,IPSC的出现频率较低(n = 5/21),这表明在很大比例的SSC神经元中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(溴化物盐,在细胞内)或河豚毒素(在细胞外)使IPSC逆转潜力向更正值转移。因此,在存在时,在-60 mV时未遇到IPSC。在这些条件下,刺激强度(最小或最大)水平不会影响IPSC的产生。因此,本研究描述了SSC中PSC的药理特性,并强调了实验条件对突触传递的影响,这需要考虑该制剂中报道的过去和现在的数据。

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