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2
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本文引用的文献

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Functional respiratory rhythm generating networks in neonatal mice lacking NMDAR1 gene.缺乏NMDAR1基因的新生小鼠的功能性呼吸节律产生网络。
J Neurophysiol. 1997 Sep;78(3):1414-20. doi: 10.1152/jn.1997.78.3.1414.
2
Regulatory phosphorylation of AMPA-type glutamate receptors by CaM-KII during long-term potentiation.在长时程增强过程中,CaM-KII对AMPA型谷氨酸受体的调节性磷酸化作用。
Science. 1997 Jun 27;276(5321):2042-5. doi: 10.1126/science.276.5321.2042.
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Characterization of multiple phosphorylation sites on the AMPA receptor GluR1 subunit.AMPA受体GluR1亚基上多个磷酸化位点的表征
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Phosphorylation and regulation of glutamate receptors by calcium/calmodulin-dependent protein kinase II.钙/钙调蛋白依赖性蛋白激酶II对谷氨酸受体的磷酸化作用及调控
Nature. 1993 Apr 15;362(6421):640-2. doi: 10.1038/362640a0.
7
Generation and transmission of respiratory oscillations in medullary slices: role of excitatory amino acids.延髓切片中呼吸振荡的产生与传导:兴奋性氨基酸的作用
J Neurophysiol. 1993 Oct;70(4):1497-515. doi: 10.1152/jn.1993.70.4.1497.
8
Regulation of NMDA receptors in cultured hippocampal neurons by protein phosphatases 1 and 2A.蛋白磷酸酶1和2A对培养海马神经元中NMDA受体的调节作用
Nature. 1994 May 19;369(6477):230-2. doi: 10.1038/369230a0.
9
NMDA and non-NMDA receptors may play distinct roles in timing mechanisms and transmission in the feline respiratory network.N-甲基-D-天冬氨酸(NMDA)受体和非NMDA受体可能在猫呼吸网络的计时机制和信号传递中发挥不同作用。
J Physiol. 1994 Feb 1;474(3):509-23. doi: 10.1113/jphysiol.1994.sp020041.
10
Modulation of AMPA/kainate receptors in cultured murine hippocampal neurones by protein kinase C.蛋白激酶C对培养的小鼠海马神经元中AMPA/海人藻酸受体的调节作用
J Physiol. 1994 Mar 15;475(3):431-7. doi: 10.1113/jphysiol.1994.sp020083.

α-氨基-3-羟基-5-甲基-4-异恶唑丙酸(AMPA)受体激活和磷酸酶抑制影响新生大鼠呼吸节律的产生。

AMPA receptor activation and phosphatase inhibition affect neonatal rat respiratory rhythm generation.

作者信息

Ge Q, Feldman J L

机构信息

Department of Physiological Science, University of California, Los Angeles, CA 90095-1763, USA.

出版信息

J Physiol. 1998 May 15;509 ( Pt 1)(Pt 1):255-66. doi: 10.1111/j.1469-7793.1998.255bo.x.

DOI:10.1111/j.1469-7793.1998.255bo.x
PMID:9547398
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2230945/
Abstract
  1. We investigated the role of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptors and their regulation in affecting respiratory-related neurones in a neonatal rat medullary slice that spontaneously generates respiratory-related rhythm and motor output in the hypoglossal (XII) nerve. 2. Bath application of the AMPA receptor antagonist 1-(4-aminophenyl)-4-methyl-7,8-methylenedioxy-5H-2, 3-benzodiazepine (GYKI) completely blocked XII nerve activity, as well as respiratory-related synaptic drives in neurones within the preBötzinger Complex (preBotC), site of rhythm generation in the slice. 3. Local application of GYKI to the preBötC blocked respiratory rhythm. Local application of AMPA to the preBötC increased rhythm frequency and depolarized respiratory-related neurones. 4. In the presence of tetrodotoxin (TTX), GYKI completely blocked the inward current induced by local application of AMPA, but not that induced by kainate. 5. Local application of okadaic acid, a membrane-permeable inhibitor of phosphatase 1 and 2A, to the preBotC increased the frequency of respiratory motor discharge. 6. Intracellular application of microcystin, a membrane-impermeable inhibitor of phosphatase 1 and 2A, enhanced endogenous inspiratory drive and exogenous AMPA-induced current (in the presence of TTX) in preBotC inspiratory neurones. Both the enhanced inspiratory drive and the increased AMPA-induced current were completely blocked by GYKI. 7. We suggest that AMPA receptor activation and AMPA receptor modulation by phosphorylation are crucial for the rhythm generation within the preBötC.
摘要
  1. 我们研究了α-氨基-3-羟基-5-甲基异恶唑-4-丙酸(AMPA)受体的作用及其调节,其对新生大鼠延髓切片中与呼吸相关的神经元产生影响,该切片能自发产生呼吸相关节律和舌下神经(XII)的运动输出。2. 浴用AMPA受体拮抗剂1-(4-氨基苯基)-4-甲基-7,8-亚甲基二氧基-5H-2,3-苯并二氮杂卓(GYKI)完全阻断了XII神经活动以及前包钦格复合体(preBotC,切片中的节律产生部位)内神经元的呼吸相关突触驱动。3. 向preBotC局部应用GYKI可阻断呼吸节律。向preBotC局部应用AMPA可增加节律频率并使与呼吸相关的神经元去极化。4. 在存在河豚毒素(TTX)的情况下,GYKI完全阻断了局部应用AMPA诱导的内向电流,但未阻断由海人酸诱导的内向电流。5. 向preBotC局部应用冈田酸(一种可透过膜的蛋白磷酸酶1和2A抑制剂)可增加呼吸运动放电频率。6. 向preBotC吸气神经元细胞内应用微囊藻毒素(一种不能透过膜的蛋白磷酸酶1和2A抑制剂)可增强内源性吸气驱动和外源性AMPA诱导电流(在存在TTX的情况下)。增强的吸气驱动和增加的AMPA诱导电流均被GYKI完全阻断。7. 我们认为,AMPA受体激活以及通过磷酸化对AMPA受体的调节对于preBotC内的节律产生至关重要。