Z C Xu

Publications (42)121.7 Total impact

• Article: Changes in membrane properties of CA1 pyramidal neurons after transient forebrain ischemia in vivo

  T.M. Gao, W.A. Pulsinelli, Z.C. Xu
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  ABSTRACT: We have previously identified three distinct populations of CA1 pyramidal neurons after reperfusion based on differences in synaptic response, and named these late depolarizing postsynaptic potential neurons (enhanced synaptic transmission), non-late depolarizing postsynaptic potential and small excitatory postsynaptic neurons (depressed synaptic transmission). In the present study, spontaneous activity and membrane properties of CA1 neurons were examined up to 48 h following ∼14 min ischemic depolarization using intracellular recording and staining techniques in vivo. In comparison with preischemic properties, the spontaneous firing rate and the spontaneous synaptic activity of CA1 neurons decreased significantly during reperfusion; spontaneous synaptic activity ceased completely 36–48 h after reperfusion, except for a low level of activity which persisted in non-late depolarizing postsynaptic potential neurons. Neuronal hyperactivity as indicated by increasing firing rate was never observed in the present study. The membrane input resistance and time constant decreased significantly in late depolarizing postsynaptic potential neurons at 24–48 h reperfusion. In contrast, similar changes were not observed in non-late depolarizing postsynaptic potential neurons. The rheobase, spike threshold and spike frequency adaptation in late depolarizing postsynaptic potential neurons increased progressively following reperfusion. Only a transient increase in rheobase and spike threshold was detected in non-late depolarizing postsynaptic potential neurons and spike frequency adaptation remained unchanged in these neurons. The amplitude of fast afterhyperpolarization increased in all neurons after reperfusion, with the smallest increment in non-late depolarizing postsynaptic potential neurons. Small excitatory postsynaptic potential neurons shared similar changes to those of late depolarizing postsynaptic potential neurons.These results suggest that the enhancement and depression of synaptic transmission following ischemia are probably due to changes in synaptic efficacy rather than changes in intrinsic membrane properties. The neurons with enhanced synaptic transmission following ischemia are probably the degenerating neurons, while the neurons with depressed synaptic transmission may survive the ischemic insult.
  Neuroscience.
• Article: Grafted neostriatal neurons express a late-developing transient potassium current

  D.J. Surmeier, Z.C. Xu, C.J. Wilson, A. Stefani, S.T. Kitai
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  ABSTRACT: Previous anatomical and physiological studies of neostriatal grafts have suggested that transplanted neurons do not develop beyond an early postnatal stage. We have tested whether this hypothesis can be generalized by characterizing the developmentally regulated Ca-independent potassium currents in graft neurons. These currents were studied using a combination of the whole-cell voltage-clamp technique with acutely-dissociated neurons and intracellular recording in slices. In all of the graft neurons examined with voltage-clamp techniques (n = 13), evidence was found for a slowly-inactivating potassium current that is seen only beyond the third or fourth postnatal week in normal rats. A current resembling the delayed rectifier was also seen in all sample neurons. The rapidly inactivating A-current which dominates recordings from nearly all immature neurons was seen in only about half (54%, 7/13) of the graft neurons; in a sample of normal adult striatal neurons, the A-current was detected in a similar percentage of neurons (41%, 25/62). Recordings of graft neurons in slices corroborated the voltage-clamp findings in revealing a slowly inactivating outward current that acts in the subthreshold potential range.These findings suggest that graft neurons express the normal complement of depolarization-activated potassium channel proteins seen in adult neurons.
  Neuroscience.