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NMDA 受体、SK 通道和电压门控 Ca2+通道之间的功能相互作用调节前额叶皮质中的突触兴奋性。

Functional interplay between NMDA receptors, SK channels and voltage-gated Ca2+ channels regulates synaptic excitability in the medial prefrontal cortex.

机构信息

Queensland Brain Institute, The University of Queensland, Brisbane, QLD 4072, Australia.

出版信息

J Physiol. 2010 Apr 15;588(Pt 8):1281-92. doi: 10.1113/jphysiol.2009.185645. Epub 2010 Mar 1.

DOI:10.1113/jphysiol.2009.185645
PMID:20194128
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2872733/
Abstract

Synaptic activity in the medial prefrontal cortex (mPFC) is fundamental for higher cognitive functions such as working memory. The present study shows that small conductance (SK) calcium-activated potassium channels attenuate excitatory synaptic transmission at layer 2/3 and layer 5 inputs to layer 5 pyramidal neurons in the mPFC. SK channels are located postsynaptically at synapses where they are activated during synaptic transmission by calcium influx through NMDA receptors, L-type calcium channels, R-type calcium channels and by calcium release from IP(3)-sensitive stores. Removal of the SK channel-mediated shunt of synaptic transmission reveals significant NMDA receptor-mediated activation during basal synaptic transmission, which is greater at layer 5 inputs (approximately 30%) than at layer 2/3 inputs (approximately 20%). These findings show that interactions between NMDA receptors, SK channels and voltage-gated calcium channels play a critical role in regulating excitatory synaptic transmission in layer 5 pyramidal neurons in the mPFC.

摘要

前额叶皮质（mPFC）中的突触活动对于工作记忆等高级认知功能至关重要。本研究表明，小电导（SK）钙激活钾通道可减弱 mPFC 中第 2/3 层和第 5 层输入到第 5 层锥体神经元的兴奋性突触传递。SK 通道位于突触后，在突触处，它们通过 NMDA 受体、L 型钙通道、R 型钙通道内流的钙以及 IP3 敏感储存器内的钙释放而在突触传递过程中被激活。去除 SK 通道介导的突触传递分流会揭示基础突触传递过程中 NMDA 受体介导的显著激活，而在第 5 层输入（约 30%）中比在第 2/3 层输入（约 20%）中更为明显。这些发现表明，NMDA 受体、SK 通道和电压门控钙通道之间的相互作用在调节 mPFC 中第 5 层锥体神经元的兴奋性突触传递中起着关键作用。

相似文献

[1]
Functional interplay between NMDA receptors, SK channels and voltage-gated Ca2+ channels regulates synaptic excitability in the medial prefrontal cortex.

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[3]
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[6]
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[7]
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[8]
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[9]
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[10]
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本文引用的文献

[1]
Reporting ethical matters in the Journal of Physiology: standards and advice.

J Physiol. 2009-2-15

[2]
Modulation of SK channel trafficking by beta adrenoceptors enhances excitatory synaptic transmission and plasticity in the amygdala.

J Neurosci. 2008-10-22

[3]
A specialized NMDA receptor function in layer 5 recurrent microcircuitry of the adult rat prefrontal cortex.

Proc Natl Acad Sci U S A. 2008-10-28

[4]
Blockade of IP3-mediated SK channel signaling in the rat medial prefrontal cortex improves spatial working memory.

Learn Mem. 2008-2-19

[5]
SK2 channel plasticity contributes to LTP at Schaffer collateral-CA1 synapses.

Nat Neurosci. 2008-2

[6]
Functions of SK channels in central neurons.

Clin Exp Pharmacol Physiol. 2007-10

[7]
MGluR-mediated calcium waves that invade the soma regulate firing in layer V medial prefrontal cortical pyramidal neurons.

Cereb Cortex. 2008-2

[8]
Increased threshold for spike-timing-dependent plasticity is caused by unreliable calcium signaling in mice lacking fragile X gene FMR1.

Neuron. 2007-5-24

[9]
Catecholamine and second messenger influences on prefrontal cortical networks of "representational knowledge": a rational bridge between genetics and the symptoms of mental illness.

Cereb Cortex. 2007-9

[10]
Nonlinear regulation of unitary synaptic signals by CaV(2.3) voltage-sensitive calcium channels located in dendritic spines.

Neuron. 2007-1-18

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