Office: 317-274-0547
Fax: 317-278-2040
Email: zxu@anatomy.iupui.edu
My research interest is in the area of anatomical
and neurophysiological changes in the CNS after transient cerebral ischemia.
Cerebrovascular disease (stroke) is the third leading cause of death in
the United States. The long term goal of this laboratory is to reveal
the mechanism of neuronal damage following transient cerebral ischemia
and provide basis for developing potential pharmacological protection.
Pyramidal neurons in CA1 zone of hippocampus
and medium spiny neurons in neostriatum are highly vulnerable to transient
ischemia. It has been postulated that excitotoxic effect of excessive
glutamate release during ischemia triggers the process of neuronal degeneration.
The current project of this laboratory is to study the neurophysiological
changes of hippocampal and neostriatal neurons in rats after transient
forebrain ischemia using contemporary electrophysiological techniques in
vivo and in vitro. By comparing the spontaneous neuronal activity,
evoked synaptic potentials, membrane properties of these neurons before
and after ischemia, the experiments will determine: 1) whether neurophysiological
activity of ischemic vulnerable neurons is increased following ischemia
and if so whether this increase is due to a) enhanced synaptic transmission
or b) increased excitability of these neurons; and 2) whether such neurophysiological
changes differ between the ischemia-sensitive and the ischemia-resistant
neurons, thereby contributing to selective neuronal injury after ischemia.
The dopamine effect on postischemic neuronal injury in neostriatum will
also be studied. The result of this study will improve understanding
of the mechanisms of brain damage upon resuscitation following cardiac
arrest.
PUBLICATIONS:
1. Ren, Yubo, Li Xiaoda and Xu, Z. C. (1997) Asymmetrical protection of neostriatal neurons from transient forebrain ischemia by unilateral dopamine depletion. Exp. Neurol. 146:250-257.
2. Gao, T. M., Pulsinelli, W. A. and Xu, Z. C. (1998) Prolonged potentiation and depression of synaptic transmission in CA1 pyramidal neurons induced by lethal ischemia in vivo. Neuroscience 87:371-383.
3. Howard, E. M. Gao, T. M., Pulsinelli, W. A. and Xu, Z. C. (1998) Electrophysiological changes of CA3 neurons and dentate granule cells following transient forebrain ischemia Brain Res. 798:109-118.