Using the blind patch-clamp technique with the whole-cell mode, we have studied the modulation of presynaptic receptor on postsynaptic γ-aminobutyric acid (GABA) receptor measuring miniature inhibitory postsynaptic currents (mIPSCs) in optic tectum of Xenopus during critical peroid. It was demonstrated that compared with mature neurons, mIPSCs recorded from immature neurons had smaller amplitude and longer decay time. mIPSCs are mediated by GABAa receptor. The nicotinic acetylcholine receptor agonists (carbachol, cytisine, nicotine, DMPP and so on) could increase the frequency of mIPSCs. The enhancement of mIPSCs frequency induced by nAChR agonists was calcium-dependent. However, the choline, a product of hydrolyzed acetylcholine, could not increase the frequency of mIPSCs. DH-β-E, a competitive antagonist of nAChR, blocked the increase of mIPSCs frequency induced by carbachol. Mecamyllamine, an α3β4 subtype of nAChR antagonist, also blocked the carbachol-induced enhancement of mIPSCs. On the other hand, MLA, α7 subtype of nAChR antagonist, had no effect on it. Thus, it seems that nAChR could presynaptically modulate the mIPSCs and α3β4 subtype of nAChR might be involved. But α7 nAChR subtype of nAChR would not be involved. The modulation is calcium- dependent. Meanwhile, we found that Ca2+-free solution could elicit giant PSCs. The frequency of mIPSCs also is related with the level of HP.