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GABAB receptor-mediated inhibition of spontaneous inhibitory synaptic currents in rat midbrain culture.

机译:GABA B受体介导的大鼠中脑培养物中自发抑制突触电流的抑制。

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摘要

1. Tight-seal, whole-cell recording was used to study GABAB receptor-mediated inhibition of spontaneous inhibitory synaptic currents in cultured rat midbrain neurones. 2. Spontaneous miniature inhibitory postsynaptic currents (mIPSCs) were recorded in tetrodotoxin (TTX), Cd2+ and Ba2+. (R)-(-)-baclofen reduced the frequency of mIPSCs through a presynaptic mechanism. The EC50 for this effect was 7 microM. It was antagonized by the GABAB receptor antagonist CGP55845A (0.5 microM). 3. In pertussis toxin (PTX)-treated cultures, some GABAB receptor-mediated reduction of the frequency of mIPSCs persisted. In contrast, PTX treatment totally abolished inhibition of miniature excitatory postsynaptic currents (mEPSCs). 4. In PTX-treated cultures, a saturating concentration of (R)-(-)-baclofen inhibited action potential-generated IPSCs but no EPSCs. 5. PTX treatment abolished the (R)-(-)-baclofen-mediated inhibition of high voltage-activated somatic Ca2+ currents and of spontaneous IPSCs depending on presynaptic Ca2+ entry. 6. We conclude that cellular mechanisms underlying GABAB receptor-mediated inhibition of mIPSCs contribute to auto-inhibition of GABA release.
机译:1.密闭全细胞记录用于研究GABA B受体介导的对大鼠中脑神经元自发抑制突触电流的抑制作用。 2.河豚毒素(TTX),Cd2 +和Ba2 +中记录了自发的微型抑制性突触后电流(mIPSC)。 (R)-(-)-baclofen通过突触前机制降低了mIPSC的频率。该效应的EC50为7 microM。它被GABAB受体拮抗剂CGP55845A(0.5 microM)拮抗。 3.在百日咳毒素(PTX)处理的培养物中,某些GABA B受体介导的mIPSC频率降低持续存在。相反,PTX治疗完全取消了对小型兴奋性突触后突触电流(mEPSC)的抑制。 4.在PTX处理的​​培养物中,饱和浓度的(R)-(-)-巴洛克芬抑制了动作电位产生的IPSC,但没有EPSC。 5. PTX治疗取消了(R)-(-)-baclofen介导的对高电压激活的体细胞Ca2 +电流和自发IPSC的抑制,这取决于突触前的Ca2 +进入。 6.我们得出结论,基于GABAB受体介导的mIPSC抑制的细胞机制有助于GABA释放的自抑制。

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