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* To whom correspondence should be addressed. E-mail: zxu{at}anatomy.iupui.edu.
Previous studies have shown that GABA can have a depolarizing and excitatory action through GABAA receptors in mature CNS neurons in vitro. However, it remains unknown whether this occurs under physiological conditions. In the present study, using intracellular recording and staining in vivo technique, we demonstrate a late depolarizing post-synaptic potential (L-PSP) in CA1 pyramidal neurons of adult Wistar rats under halothane anesthesia. This L-PSP was elicited in approximately 70% of the recorded neurons upon stimulation of the Schaffer collaterals or the contralateral commissural path. The size of L-PSP was linearly correlated to the decay time constant but not the rising slope of the initial EPSP. Intravenous administration of the NMDA receptor blocker MK-801 and the GABAA receptor blocker picrotoxin significantly reduced the size of the L-PSP. The spine density and apical dendritic branching length of the neurons that displayed L-PSPs was significantly greater than those that do not. These results indicate that NMDA receptor and GABAA receptor-mediated depolarizing post-synaptic potentials can be revealed in CA1 pyramidal neurons of adult rats in vivo, supporting the physiological relevance of GABAA-mediated depolarization in normal neuronal information processing. The difference in electrophysiological properties and morphological features between neurons that display the L-PSP and the other neurons suggest that they might represent two different subtypes of CA1 pyramidal neurons.
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