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Neuroscience. 1995 Aug;67(4):823-36.

Neurophysiological changes of spiny neurons in rat neostriatum after transient forebrain ischemia: an in vivo intracellular recording and staining study.

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Department of Neurology, College of Medicine, University of Tennessee, Memphis 38163, USA.


The spontaneous activities, evoked postsynaptic potentials and membrane properties of spiny neurons in rat neostriatum were compared before, during and after 5-8 min ischemia using intracellular recording and staining techniques in vivo. Severe forebrain ischemia was induced with the four-vessel occlusion method. Approximately 2.5 min after the onset of ischemia the baseline membrane potential quickly depolarized to -20 mV and remained at this level during ischemia. Repolarization began within 2 min after recirculation. The onset of ischemic depolarization was directly related to the severity of ischemia and its latency was inversely related to brain temperature. Spontaneous firing and membrane potential fluctuation of spiny neurons ceased immediately after ischemia and slowly recovered several hours after recirculation. No neuronal hyperactivity was observed up to 7 h after recirculation. Cortically evoked inhibitory postsynaptic potentials and late depolarizations disappeared earlier after ischemia and recovered later following recirculation than the initial excitatory postsynaptic potentials. Membrane input resistance of spiny neurons was significantly increased but the time constant remained the same following recirculation. The rheobase and spike threshold of spiny neurons were significantly increased and the repetitive firing evoked by depolarizing current pulse was suppressed shortly after recirculation. The results of the present study indicated that the spontaneous activity and evoked postsynaptic responses of spiny neurons are suppressed and the excitability of spiny neurons is decreased after transient ischemia. The polysynaptic responses are more sensitive to ischemia than the monosynaptic ones.

[Indexed for MEDLINE]

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