Zao C. Xu

Indiana University – Purdue University Indianapolis

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Ping Deng

Qinghai University

Zhigang Lei

Indiana University – Purdue University Indianapolis

Yiwen Ruan

Jinan University

Zhiping P. Pang

Sun Yat-sen University

Charles J. Wilson

The University of Texas at San Antonio

Yuchun Zhang

Shandong University of Technology

Tian-Ming Gao

Southern Medical University

Yuan Fan

Yunnan University of Traditional Chinese Medicine

Min Zhuo

University of Toronto

Bende Zou

University of Oxford

Cooperative Institutions

Indiana University – Purdue University Indianapolis

Indiana University School of Medicine

Guangzhou Medical University

Sun Yat-sen University

University of Toronto

Indiana University

Second Affiliated Hospital of Guangzhou Medical University

Johns Hopkins University

University of California, Irvine

University of Tennessee Health Science Center

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Morphological heterogeneity of CA1 pyramidal neurons in response to ischemia

Journal of Neuroscience Research (2006)

Yiwen Ruan Bende Zou Yuan Fan Yan Li Nan Lin

We have found, based on the electrophysiological properties, two subtypes of CA1 pyramidal neurons in the CA1 region of the normal hippocampus, late postsynaptic potential (L-PSP) neurons and non-L-PSP neurons. In addition, our previous study has shown that the electrophysiological properties of these two subtypes of pyramidal neurons were differentially modified after ischemia. In the present study, we hypothesized that ischemia might also induce different morphological alterations in these two subtypes of neuron. To test the hypothesis, we compared the changes in the dendritic arborization and soma volume of these two subtypes of neurons in rats subjected to transient global ischemia. We found a significant decrease in the basal dendritic length of L-PSP neurons at 12 hr after reperfusion, resulting mainly from a significant decrease in the dendrite terminal length. The apical dendritic length of L-PSP neurons markedly increased at 24 hr after ischemia, resulting mainly from an increase in the number of branching arbors in the middle part of the apical dendritic trees. The soma size of L-PSP neurons was significantly reduced at 12 hr, but they became slightly larger at 24 hr and 48 hr after reperfusion. In contrast to L-PSP neurons, non-L-PSP neurons showed slight modifications in the dendritic arborization but had persistent swelling of their soma after ischemia. These results indicate that pathological changes in these two subtypes of neurons are different after ischemia.

Dendrite (mathematics)

10.1002/jnr.21101

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Citations (9)

Involvement of I(h) in dopamine modulation of tonic firing in striatal cholinergic interneurons

PMC (2007)

Ping Deng Yuchun Zhang Zao C. Xu

Tonic (physiology)

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Citations (3)

Inhibition ofI_hin Striatal Cholinergic Interneurons Early after Transient Forebrain Ischemia

Journal of Cerebral Blood Flow & Metabolism (2007)

Ping Deng Yuchun Zhang Zao C. Xu

Striatal cholinergic interneurons are relatively resistant to ischemic insults. These neurons express hyperpolarization-activated cation current (I(h)) that profoundly regulates neuronal excitability. Changes in neuronal excitability early after ischemia may be crucial for determining neuronal injury. Here we report that I(h) in cholinergic interneurons was decreased 3 h after transient forebrain ischemia, which was accompanied by a negative shift of the voltage dependence of activation. The inhibition of I(h) might be due to the tonic activation of adenosine A1 receptors, as blockade of A1 receptors significantly increased I(h) in postischemic neurons, but had no effect on control neurons. Consistent with the inhibition of I(h), postischemic neurons showed a reduction in both spontaneous firing and hyperpolarization-induced rebound depolarization. These findings indicate that I(h) may play excitatory roles in striatal cholinergic interneurons. Postischemic inhibition of I(h) might be a novel mechanism by which adenosine confers neuronal resistance to cerebral ischemia.

Transient (computer programming)

Forebrain

10.1038/sj.jcbfm.9600583

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Citations (16)

A-type potassium currents and neuroprotection after ischemia

Journal of Cerebral Blood Flow & Metabolism (2005)

Ping Deng Zhiping P. Pang Zhigang Lei Sojin Shikano Qiaoxi Xiong

Brain ischemia

10.1038/sj.jcbfm.9591524.0287

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Citations (0)

Brain Ischemia and Neuronal Excitability

Contemporary clinical neuroscience (2009)

Ping Deng Zao C. Xu

Premovement neuronal activity

10.1007/978-1-60327-579-8_3

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Citations (1)

Transient Neurophysiological Changes in CA3 Neurons and Dentate Granule Cells After Severe Forebrain Ischemia In Vivo

Journal of Neurophysiology (1998)

Tian-Ming Gao Eugene M. Howard Zao C. Xu

Gao, T. M., E. M. Howard, and Z. C. Xu. Transient neurophysiological changes in CA3 neurons and dentate granule cells after severe forebrain ischemia in vivo. J. Neurophysiol. 80: 2860–2869, 1998. The spontaneous activities, evoked synaptic responses, and membrane properties of CA3 pyramidal neurons and dentate granule cells in rat hippocampus were compared before ischemia and ≤7 days after reperfusion with intracellular recording and staining techniques in vivo. A four-vessel occlusion method was used to induce ∼14 min of ischemic depolarization. No significant change in spontaneous firing rate was observed in both cell types after reperfusion. The amplitude and slope of excitatory postsynaptic potentials (EPSPs) in CA3 neurons decreased to 50% of control values during the first 12 h reperfusion and returned to preischemic levels 24 h after reperfusion. The amplitude and slope of EPSPs in granule cells slightly decreased 24–36 h after reperfusion. The amplitude of inhibitory postsynaptic potentials in CA3 neurons transiently increased 24 h after reperfusion, whereas that in granule cells showed a transient decrease 24–36 h after reperfusion. The duration of spike width of CA3 and granule cells became longer than that of control values during the first 12 h reperfusion. The spike threshold of both cell types significantly increased 24–36 h after reperfusion, whereas the frequency of repetitive firing evoked by depolarizing current pulse was decreased during this period. No significant change in rheobase and input resistance was observed in CA3 neurons. A transient increase in rheobase and a transient decrease in input resistance were detected in granule cells 24–36 h after reperfusion. The amplitude of fast afterhyperpolarization in both cell types increased for 2 days after ischemia and returned to normal values 7 days after reperfusion. The results from this study indicate that the neuronal excitability and synaptic transmission in CA3 and granule cells are transiently suppressed after severe forebrain ischemia. The depression of synaptic transmission and neuronal excitability may provide protection for neurons after ischemic insult.

Rheobase

Postsynaptic Current

Granule cell

10.1152/jn.1998.80.6.2860

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Citations (33)

Alterations of Synaptic Transmission Following Transient Cerebral Ischemia

Springer eBooks (2003)

Zao C. Xu

10.1007/978-1-4615-0282-1_5

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Citations (0)

Transient cerebral ischemia increases CA1 pyramidal neuron excitability

Experimental Neurology (2008)

Yuan Fan Ping Deng Yu-Chi Wang Hui‐Chen Lu Zao C. Xu

Transient (computer programming)

Pyramidal tracts

10.1016/j.expneurol.2008.04.032

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Citations (32)

Animal Models of Acute Neurological Injuries II

Springer protocols handbooks/Springer protocols (2012)

Jun Chen Xiao‐Ming Xu Zao C. Xu John H. Zhang

The successful previous volume on this topic provided a detailed benchwork manual for the most commonly used animal models of acute neurological injuries including cerebral ischemia, hemorrhage, vasos

10.1007/978-1-61779-782-8

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Citations (12)

Restoration of the corticostriatal projection in rat neostriatal grafts: electron microscopic analysis

Neuroscience (1989)

Zao C. Xu Charles J. Wilson P.C. Emson

10.1016/0306-4522(89)90129-2

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Citations (92)