中文摘要：

目的：研究急性缺氧对非洲电鱼小脑浦肯野细胞（Pc）之间γ-氨基丁酸（GABA）能突触传递的影响。方法：采用配对全细胞膜片钳记录法,记录电鱼小脑Pc-Pc之间的抑制性突触后电流（IPSC）,观察急性缺氧对Pc-Pc IPSC的影响,以及GABAA受体拮抗剂和谷氨酸α-氨基-3-羟基-5-甲基-4-异噁唑丙酸（AMPA）受体拮抗剂对Pc-Pc IPSC缺氧反应的调节作用。结果：短暂缺氧使Pc-Pc IPSC的幅值显著增大,表现为长时程增强（LTP）;GABAA受体拮抗剂荷包牡丹碱逆转了Pc-Pc IPSC的LTP,表现为长时程抑制;AMPA受体拮抗剂6-氰基-7-硝基喹喔啉-2,3-二酮（CNQX）阻断了Pc-Pc IPSC的LTP,表现为短时程增强。结论：急性缺氧引起电鱼小脑Pc之间的GABA能突触活动持续增强,GABAA受体和AMPA受体共同介导这种反应,提示GABA能和谷氨酸能突触活动的平衡可能是电鱼以及其他缺氧耐受动物缺氧保护反应的关键机制。

英文摘要：

AIM： To study the effects of acute hypoxia on GABAergic synaptic transmission between Purkinje cell（ Pc） and Pc of mormyrid cerebellum. METHODS： The technique of dual whole-cell patch clamp was used to record the inhibitory postsynaptic current（ IPSC） between two Pcs. The responses of Pc-Pc IPSC to acute hypoxic episode were observed. The effects of GABAA receptor antagonist and glutamate AMPA receptor antagonist on the hypoxic responses of Pc-Pc IPSC were also investigated. RESULTS： Brief exposure to hypoxia led to long-term potentiation（ LTP） of Pc-Pc IPSC. The GABAA receptor antagonist bicuculline completely abolished this LTP,reversed to long-term depression,whereas an AMPA receptor inhibitor CNQX partially prevented the formation of the LTP induced by hypoxia,only displaying a shortterm potentiation. CONCLUSION： Acute hypoxia induced LTP of Pc-Pc IPSC,which requires the contribution of both GABAAreceptors and AMPA receptors,indicating that a balance between the GABAergic and glutamatergic activities might be critical to the hypoxia-induced protective response in hypoxia-tolerant animals such as mormyrid fish.