Volume 28 Issue 5
Sep.  2007
Turn off MathJax
Article Contents

LI Hong-bin, HAN Hui-li, MA Wen-pei, DONG Zhi-fang, XU Lin. Enhancement of GABAA Receptor-Mediated Inhibitory Postsynaptic Currents Induced by “Partial Oxygen-Glucose Deprivation”. Zoological Research, 2007, 28(5): 491-496.
Citation: LI Hong-bin, HAN Hui-li, MA Wen-pei, DONG Zhi-fang, XU Lin. Enhancement of GABAA Receptor-Mediated Inhibitory Postsynaptic Currents Induced by “Partial Oxygen-Glucose Deprivation”. Zoological Research, 2007, 28(5): 491-496.

Enhancement of GABAA Receptor-Mediated Inhibitory Postsynaptic Currents Induced by “Partial Oxygen-Glucose Deprivation”

Funds:   
More Information
  • Corresponding author: XU Lin
  • Received Date: 2007-04-03
  • Rev Recd Date: 1900-01-01
  • Publish Date: 2007-10-22
  • Abstract: Oxygen/glucose deprivation (OGD) has been widely used as an in vitro model of focal ischemia, where the blood flow is severely reduced and neurons rapidly die. However, adjacent to the focal region is ‘penumbra’, where residual blood flow remains oxygen and glucose supplies are at low levels. To model this pathological genesis, we developed a partial OGD (pOGD) protocol in a rat brain slice. This model met two requirements: oxygen was partially deprived and glucose was reduced in the perfusion buffer. Therefore we investigated the effect of pOGD on gama-aminobutyric acid (GABAA) receptor-mediated inhibitory postsynaptic currents (IPSCs) in CA1 neurons of a hippocampal slice through whole-cell patch-clamp technique. We found that the amplitude and decay time of IPSCs were increased immediately during pOGD treatment. And the enhancement of IPSCs amplitude resulted from an increase of the synaptic conductance without a significant change in the reversal potential of chloride. These results suggested that the nervous system could increase inhibitory neurotransmission to offset excitation by homeostasis mechanisms during the partial oxygen and glucose attack.
  • 加载中
  • 加载中
通讯作者: 陈斌, bchen63@163.com
  • 1. 

    沈阳化工大学材料科学与工程学院 沈阳 110142

  1. 本站搜索
  2. 百度学术搜索
  3. 万方数据库搜索
  4. CNKI搜索

Article Metrics

Article views(1868) PDF downloads(1923) Cited by()

Related
Proportional views

Enhancement of GABAA Receptor-Mediated Inhibitory Postsynaptic Currents Induced by “Partial Oxygen-Glucose Deprivation”

Funds:   
    Corresponding author: XU Lin

Abstract: Abstract: Oxygen/glucose deprivation (OGD) has been widely used as an in vitro model of focal ischemia, where the blood flow is severely reduced and neurons rapidly die. However, adjacent to the focal region is ‘penumbra’, where residual blood flow remains oxygen and glucose supplies are at low levels. To model this pathological genesis, we developed a partial OGD (pOGD) protocol in a rat brain slice. This model met two requirements: oxygen was partially deprived and glucose was reduced in the perfusion buffer. Therefore we investigated the effect of pOGD on gama-aminobutyric acid (GABAA) receptor-mediated inhibitory postsynaptic currents (IPSCs) in CA1 neurons of a hippocampal slice through whole-cell patch-clamp technique. We found that the amplitude and decay time of IPSCs were increased immediately during pOGD treatment. And the enhancement of IPSCs amplitude resulted from an increase of the synaptic conductance without a significant change in the reversal potential of chloride. These results suggested that the nervous system could increase inhibitory neurotransmission to offset excitation by homeostasis mechanisms during the partial oxygen and glucose attack.

LI Hong-bin, HAN Hui-li, MA Wen-pei, DONG Zhi-fang, XU Lin. Enhancement of GABAA Receptor-Mediated Inhibitory Postsynaptic Currents Induced by “Partial Oxygen-Glucose Deprivation”. Zoological Research, 2007, 28(5): 491-496.
Citation: LI Hong-bin, HAN Hui-li, MA Wen-pei, DONG Zhi-fang, XU Lin. Enhancement of GABAA Receptor-Mediated Inhibitory Postsynaptic Currents Induced by “Partial Oxygen-Glucose Deprivation”. Zoological Research, 2007, 28(5): 491-496.

Catalog

    /

    DownLoad:  Full-Size Img  PowerPoint
    Return
    Return