Send to

Choose Destination
See comment in PubMed Commons below
Neurosci Lett. 2004 Jul 29;365(3):167-70.

Switch of K+ buffering conditions in rabbit retinal Müller glial cells during postnatal development.

Author information

Department of Neurophysiology, Paul Flechsig Institute of Brain Research, University of Leipzig, D-04109 Leipzig, Germany.


Although spatial buffering of excess extracellular K+ by K+ channels is a main function of retinal glial (Müller) cells, there are severe limitations to long distance K+-spatial buffering that have been predicted for (immature) glial cells: (i) a lack of inwardly rectifying K+ (Kir) channels [Glia 21(1997) 46]; and (ii) high internal resistance of outgrowing (cable like) processes [W. Rall, Handbook of Physiology, Section 1, vol. 1, Part 1, American Physiological Society, Bethesda, 1977, pp. 39-97]. In order to determine if changes in developing Müller cells improve or worsen their capability of carrying K+ spatial buffering currents, we compared the whole-cell currents of acutely isolated Müller cells at 5, 11 and 28 postnatal days of rabbits. Both K+-spatial buffer limitations described above were found in early postnatal stage (5 days), however, the cells overcome these limitations shortly after 11 days. During the period of 11-28 days, rabbit Müller cells simultaneously increase stalk axial conductance and express Kir channels. Both processes take place during the critical stage of retinal maturation, and should dramatically improve "cable" K+-spatial buffering.

[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center