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AMPA受体参与大鼠体内展神经运动神经元记录的三叉神经突触后电位。

Involvement of AMPA receptors in trigeminal post-synaptic potentials recorded in rat abducens motoneurons in vivo.

作者信息

Ouardouz M, Durand J

机构信息

Unité de Neurocybernétique Cellulaire, CNRS UPR 418, Marseille, France.

出版信息

Eur J Neurosci. 1994 Nov 1;6(11):1662-8. doi: 10.1111/j.1460-9568.1994.tb00558.x.

Abstract

The pharmacology of trigeminal excitatory postsynaptic potentials (EPSPs) evoked by electrical stimulation of the vibrissal pad was investigated in vivo in rat abducens motoneurons using intracellular recordings combined with microionophoretic applications of excitatory amino acid agonists [alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA), NMDA, kainate] and a selective non-NMDA receptor antagonist (GYKI-52466). Intravenous applications of GYKI-52466 were also performed during synaptic and amino acid excitations. GYKI-52466, applied intravenously or microionophoretically, reversibly antagonized AMPA-induced depolarizations and trigeminal EPSPs in rat abducens motoneurons without affecting NMDA and kainate responses. The inhibition of AMPA-induced depolarizations was similar following i.v. and ionophoretic applications of GYKI-52466. Intravenous applications of GYKI-52466 (0.3-4 mg/kg) reversibly and dose-dependently reduced trigeminal EPSPs, which could be totally suppressed at the highest doses of GYKI-52466 (2-4 mg/kg). The antagonist effect, which developed very quickly, could last several minutes and recovered gradually. The effect of GYKI-52466 on the EPSPs and AMPA responses were compared in the same motoneurons. The partial inhibition of trigeminal EPSPs during microionophoretic applications of GYKI-52466 was probably due to the distribution of the synapses in the dendritic arborization of abducens motoneurons. Our results show that AMPA receptors are involved in the generation of trigeminal EPSPs in rat abducens motoneurons in vivo.

摘要

采用细胞内记录结合兴奋性氨基酸激动剂(α-氨基-3-羟基-5-甲基-4-异恶唑丙酸(AMPA)、N-甲基-D-天冬氨酸(NMDA)、海人藻酸)和选择性非NMDA受体拮抗剂(GYKI-52466)的微量离子电泳应用,在大鼠展神经运动神经元体内研究了电刺激触须垫诱发的三叉神经兴奋性突触后电位(EPSP)的药理学特性。在突触和氨基酸激发过程中,还进行了GYKI-52466的静脉注射。静脉或微量离子电泳应用GYKI-52466可可逆性拮抗大鼠展神经运动神经元中AMPA诱导的去极化和三叉神经EPSP,而不影响NMDA和海人藻酸反应。静脉注射和离子电泳应用GYKI-52466后,对AMPA诱导的去极化的抑制作用相似。静脉注射GYKI-52466(0.3 - 4 mg/kg)可可逆性且剂量依赖性地降低三叉神经EPSP,在最高剂量的GYKI-52466(2 - 4 mg/kg)时可完全抑制。拮抗剂作用起效非常迅速,可持续数分钟并逐渐恢复。在同一运动神经元中比较了GYKI-52466对EPSP和AMPA反应的影响。在微量离子电泳应用GYKI-52466期间,三叉神经EPSP的部分抑制可能是由于展神经运动神经元树突分支中突触的分布所致。我们的结果表明,AMPA受体参与了大鼠展神经运动神经元体内三叉神经EPSP的产生。

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