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J Neurophysiol 90: 2964-2972, 2003. First published July 16, 2003; doi:10.1152/jn.00172.2003
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Membrane Potential of CA3 Hippocampal Pyramidal Cells During Postnatal Development

Roman Tyzio1,*, Anton Ivanov1,*, Cristophe Bernard1, Gregory L. Holmes2, Yehezkiel Ben-Ari1 and Roustem Khazipov1,2

1 Institut de la Neurobiologie de la Méditterranée-Institute National de la Santé et de la Recherche Médicale U29, Marseille, France; 2 Division of Neurology, Neuroscience Center at Dartmouth, Dartmouth Medical School, Lebanon, New Hampshire 03756

Submitted 25 February 2003; accepted in final form 12 June 2003

A depolarized resting membrane potential has long been considered to be a universal feature of immature neurons. Despite the physiological importance, the underlying mechanisms of this developmental phenomenon are poorly understood. Using perforated-patch, whole cell, and cell-attached recordings, we measured the membrane potential in CA3 pyramidal cells in hippocampal slices from postnatal rats. With gramicidin perforated-patch recordings, membrane potential was –44 ± 4 (SE) mV at postnatal days P0–P2, and it progressively shifted to –67 ± 2 mV at P13–15. A similar developmental change of the membrane potential has been also observed with conventional whole cell recordings. However, the value of the membrane potential deduced from the reversal potential of N-methyl-D-aspartate channels in cell-attached recordings did not change with age and was –77 ± 2 mV at P2 and –77 ± 2 mV at P13–14. The membrane potential measured using whole cell recordings correlated with seal and input resistance, being most depolarized in neurons with high, several gigaohms, input resistance and low seal resistance. Simulations revealed that depolarized values of the membrane potential in whole cell and perforated-patch recordings could be explained by a shunt through the seal contact between the pipette and membrane. Thus the membrane potential of CA3 pyramidal cells appears to be strongly negative at birth and does not change during postnatal development.


Address for reprint requests and other correspondence: R. Khazipov, Div. of Neurology, Dartmouth Medical School, One Medical Center Dr., Lebanon, NH 03756 (E-mail: roustem.khazipov{at}dartmouth.edu).




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