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首页> 外文期刊>Journal of Neurophysiology >Abnormal synaptic transmission in the olfactory bulb of Fyn-kinase-deficient mice.
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Abnormal synaptic transmission in the olfactory bulb of Fyn-kinase-deficient mice.

机译：Fyn激酶缺陷小鼠嗅球中的突触传递异常。

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摘要

We studied synaptic transmission in the granule cells in the olfactory bulb of the homozygous Fyn (a nonreceptor type tyrosine kinase)-deficient (fynz/fynz) and heterozygous Fyn-deficient (+/fynz) mice by using slice preparations from the olfactory bulb. Stimulation to the lateral olfactory tract and/or centrifugal fibers to the olfactory bulb evoked field excitatory postsynaptic potentials (fEPSPs) in the granule cells. In +/fynz mice, fEPSPs were augmented by bicuculline, a gamma-aminobutyric acid (GABAA) antagonist and picrotoxin, whereas fEPSPs in fynz/fynz mice were much less sensitive to bicuculline and picrotoxin. Application of D-2-amino-5-phosphonopentanoic acid had no effect but 6-cyano-7-nitroquinoxaline-2,3-dione produced almost complete block of fEPSPs in both +/fynz mice and fynz/fynz mice. (1S,3R)-1-aminocyclo-pentane-1.3-dicarboxylate, an agonist of metabotropic glutamate receptors caused a similar depression of fEPSPs in both +/fynz and fynz/fynz mice. In +/fynz mice tetanic stimulation to the lateral olfactory tract and/or centrifugal fibers induced N-methyl-D-aspartate (NMDA)-dependent long-term potentiation (LTP) of fEPSPs, whereas LTP was impaired in fynz/fynz mice. Our results demonstrate altered functions of GABAA and NMDA receptors in the olfactory system of Fyn-deficient mice.
机译：我们通过使用嗅球的切片制剂研究了纯合Fyn（一种非受体型酪氨酸激酶）缺陷（fynz / fynz）和杂合Fyn缺陷（+ / fynz）小鼠嗅球中颗粒细胞中的突触传递。刺激嗅球外侧和/或离心纤维诱发颗粒细胞中的场兴奋性突触后突触电位（fEPSPs）。在+ / fynz小鼠中，γ-氨基丁酸（GABAA）拮抗剂比库克林和苦瓜毒素增强了fEPSPs，而在fynz / fynz小鼠中的fEPSPs对股瓜碱和苦瓜毒素的敏感性低得多。 D-2-氨基-5-膦基戊酸的应用没有效果，但是6-氰基-7-硝基喹喔啉-2,3-二酮在+ / fynz小鼠和fynz / fynz小鼠中产生了几乎完全的fEPSP阻滞。 （1S，3R）-1-氨基环戊烷-1.3-二羧酸盐是代谢型谷氨酸受体的激动剂，在+ / fynz和fynz / fynz小鼠中均引起fEPSP的类似降低。在+ / fynz小鼠中，强直性刺激外侧嗅道和/或离心纤维诱导了fEPSP的N-甲基-D-天冬氨酸（NMDA）依赖性长期增强（LTP），而在fynz / fynz小鼠中，LTP受损。我们的研究结果表明，Fyn缺陷小鼠的嗅觉系统中GABAA和NMDA受体的功能发生了改变。

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