Using the blind patch-clamp technique with the whole-cell mode, we have studied the modulation of pre-synaptic receptor on postsynaptic g-aminobutyric acid (GABA) receptor measuring miniature inhibitory postsy-naptic ...Using the blind patch-clamp technique with the whole-cell mode, we have studied the modulation of pre-synaptic receptor on postsynaptic g-aminobutyric acid (GABA) receptor measuring miniature inhibitory postsy-naptic 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 enhance-ment of mIPSCs frequency induced by nAChR agonists was calcium-dependent. However, the choline, a product of hy-drolyzed acetylcholine, could not increase the frequency of mIPSCs. DH-b-E, a competitive antagonist of nAChR, blocked the increase of mIPSCs frequency induced by car-bachol. Mecamyllamine, an a3b4 subtype of nAChR antago-nist, also blocked the carbachol-induced enhancement of mIPSCs. On the other hand, MLA, a7 subtype of nAChR antagonist, had no effect on it. Thus, it seems that nAChR could presynaptically modulate the mIPSCs and a3b4 sub-type of nAChR might be involved. But a7 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.展开更多
基金the Na-tional Natural Science Foundation of China (Grant No.39670774)
文摘Using the blind patch-clamp technique with the whole-cell mode, we have studied the modulation of pre-synaptic receptor on postsynaptic g-aminobutyric acid (GABA) receptor measuring miniature inhibitory postsy-naptic 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 enhance-ment of mIPSCs frequency induced by nAChR agonists was calcium-dependent. However, the choline, a product of hy-drolyzed acetylcholine, could not increase the frequency of mIPSCs. DH-b-E, a competitive antagonist of nAChR, blocked the increase of mIPSCs frequency induced by car-bachol. Mecamyllamine, an a3b4 subtype of nAChR antago-nist, also blocked the carbachol-induced enhancement of mIPSCs. On the other hand, MLA, a7 subtype of nAChR antagonist, had no effect on it. Thus, it seems that nAChR could presynaptically modulate the mIPSCs and a3b4 sub-type of nAChR might be involved. But a7 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.
