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[Abstract Title]. - Society for Neuroscience

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Hippocampal astrocytes were electrophysiologically identified by the large resting K + currents<br />

which dominated the current pattern of these cells beyond postnatal (p) day 3. These currents<br />

were sensitive to Ba 2+ at submillimolar concentration but were not pH-sensitive up to a pH of<br />

6.5. By using single cell RT-PCR, the subunit Kir4.1 was encountered in all cells while Kir5.1,<br />

another glial Kir subunit that co-assembles with Kir4.1, was co-expressed scarcely. In some<br />

cells, co-expression of Kir2 transcripts was detected. In Kir4.1-deficient mice, astrocytes were<br />

almost devoid of Ba 2+ -sensitive currents and lacked negative resting potentials, suggesting that<br />

Kir4.1 is mainly responsible <strong>for</strong> astroglial Kir currents in the hippocampus.<br />

A developmental up-regulation of Kir4.1 expression was found both on the mRNA and protein<br />

levels. Semi-quantitative real-time RT-PCR revealed a strong rise in the amount of Kir4.1<br />

mRNA between the p3 and p10, both in tissue from the stratum radiatum of the CA1 region as<br />

well as in single astrocytes. Quantification of grey levels of Kir4.1 tetramers in respect to the<br />

loading control of b-actin by Western blot analysis showed a 13-fold increase of Kir4.1 protein<br />

between p3 and p10. Electrophysiological analysis confirmed expression of Ba 2+ sensitive Kir<br />

currents in p3 astrocytes, but the amplitudes per cell surface area amounted to only 25%<br />

compared to astrocytes at p10. This increase in astroglial Kir4.1 channel density parallels a<br />

significant drop of the extracellular volume fraction of the developing hippocampus, suggesting<br />

an important role of Kir4.1 in extracellular K + buffering.<br />

Disclosures: G. Seifert , None; C. Hartmann, None; D.K. Binder, None; K. Hüttmann,<br />

None; A. Wyczynski, None; C. Steinhäuser, None.<br />

Poster<br />

242. Glial Neuronal Interactions: Glutamate and Calcium<br />

Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm<br />

Program#/Poster#: 242.2/H9<br />

Topic: B.11.c. In vivo approaches<br />

Support: NHMRC<br />

<strong>Title</strong>: Role of ATP in memory <strong>for</strong>mation<br />

Authors: *D. N. BOWSER 1 , M. E. GIBBS 2 ;<br />

1 Howard Florey Inst., Parkville, Australia; 2 Anatmoy and Cell Biol., Monash Univ., Melbourne,<br />

Australia<br />

<strong>Abstract</strong>: The nucleotide ATP is recognized as a neurotransmitter and amongst its various roles,<br />

is involved in neural-glial interactions in the brain. It functions both as an extracellular signalling<br />

molecule and as a gliotransmitter and it has been suggested to have a pivotal role in learning and

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