RCMI International Symposium on Health Disparities
November 12-15, 2000
San Juan, Puerto Rico

Oral Presentations

KIR 6.1, PORE-FORMING SUBUNIT OF KATP-CHANNELS, ARE RESTRICTED TO GLIAL CELLS, NOT TO NEURONS IN HIPPOCAMPUS AND RETINA

S.N. Skatchkov1, M.J. Eaton1, A. Thomzig2, A. Bringmann3, B. Biedermann3, R.K. Orkand4*, R. W. Veh2 and A. Reichenbach3. 1Center for Molec. and Behav. Neurosci., Univ. Central del Caribe, PR 00960,USA, 2Inst. for Anatomy, Humboldt Univ., Berlin, FRG, 3Paul Flechsig Inst. for Brain Research, Leipzig Univ., FRG, 4Inst. of Neurobiology, Univ. of Puerto Rico, PR 00901, USA.

Polyamine-sensitive inwardly rectifying potassium (Kir) channels are the dominant K+ channels in glial cells and polyamines are predominantly localized in these cells (Glia (1997) 19:171-179; Glia (1998) 23:209-220; Glia (2000) 31:84-90). The Kir 6.0 family is regulated by three endogenous substances: ATP, polyamines and H+ (EMBO J. (1999) 18:847-853), which, in turn, are found in glial cells. We examined: (i) the localization of Kir 6.1 and 6.2 and (ii) ATP and spermine (SPM) dependence of K+ currents. Hippocampus and retinae were prepared for immunocytochemical visualization of Kir 6.1 and 6.2 subunits. Surprisingly, Kir 6.1 immunoreactivity was restricted to glial cells, whereas Kir 6.2 was found solely in neurons. The endfeet of astrocytes attached to blood vessels were densely stained by Kir 6.1 antibody in hippocampus. In both avascular and vascular retinae of amphibians (frog, toad) and mammals (rat, guinea pig, human), Kir 6.1 was found in Müller (glial) cells and Kir 6.2 in neurons. During electrophysiological recording when there was no ATP and SPM in the patch pipette, a strong increase of K+ currents and relief of inward rectification was observed in Müller cells. We suggest that in traumatic conditions when ATP and SPM are decreased in glia (ex. ischemia, gliotoxins; Physiol. Research,Vol.48, suppl. 1:S87), Kir 6.1channels open to shunt excess potassium from brain extracellular fluid to blood vessels. This may help protect neurons from spreading depression caused by potassium accumulation. [Supported NIH-RCMI G12RR03035, NINDS, DFG Ve-187/1-2 and BMB+F (01KS 9504-Project-5)]