Differential expression of KCC2 accounts for the differentialGABA responses between relay and intrinsic neuronsin the early postnatal rat olfactory bulbIonization Mass Spectrometry

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The rat olfactory bulb is anatomically immature at birth and considerableneurogenesis and synaptogenesis are known to take place postnatally. In addition,significant physiological changes have also been reported in this period. Forexample, granule cell-mediated inhibition following electrical stimulations to thelateral olfactory tract is robust during the first postnatal week, then subsequentlyand abruptly decreases after the second week. However, the mechanism(s)underlying this enhanced inhibition remains to be elucidated. To know the cause ofthis phenomenon, we investigated the expression patterns of cation-Clcotransporters(KCC1, KCC2, and NKCC1) mRNAs, that are responsible for theregulation of [Cl-]i. In addition, GABA responses were measured bygramicidin-perforated patch-clamp recordings and Ca2+ imaging using fura-2. Wefound that, in the early postnatal period, mitral cells expressing KCC2 mRNA wereinhibited by GABA, while granule cells lacking KCC2 mRNA expression weredepolarized or excited by GABA. These results indicate that transientGABA-mediated excitation on granule cells might be the main cause of theenhanced inhibition onto mitral cells, and suggest that this differential GABAresponses between relay and intrinsic neurons play pivotal roles in the earlypostnatal rat olfactory bulb.
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