Recently, we described a downregulation of the K
+ conductance of Müller cells during ischemia-reperfusion of the rat retina.
41 However, there are significant differences between Müller cells from postischemic rat and rabbit retinas: (1) The K
+ current downregulation in rat cells was accompanied by a significant increase in the inward rectification of the K
+ currents due to an almost complete absence of K
+ outward currents.
41 However, in rabbit cells, the inward rectification remained largely unaltered
(Fig. 3C) . (2) In contrast to Müller cells of the postischemic rat retina, which showed the strongest downregulation of the K
+ conductance in perisomatic membrane domains,
41 the cells of the postischemic rabbit retina decreased their conductance at all membrane domains to a similar degree and showed, similar to the cells from control retinas, their highest conductance at the end foot membrane
(Fig. 4B) . A similar rather uniform downregulation of the K
+ conductance at all membrane domains has been found recently in rabbit Müller cells during experimental rhegmatogenous detachment (Pannicke T, unpublished observation, 2004). Although the reasons for these species differences are unclear, they may be explained by the dominant expression of K
+ channels in cell membrane domains that surround retinal vessels in the case of rat cells,
41 whereas rabbit Müller cells seem to express their K
+ channels more evenly in the whole cell membrane,
49 with the exception of a pronounced expression at the end foot membrane.
46 Furthermore, Müller cells from rat and rabbit retinas may express different subtypes of K
+ channels. Rodent Müller cells express both weakly rectifying Kir4.1 channels and strongly rectifying K
+ channels (e.g., Kir2.1),
50 whereas in rabbit cells, the virtually exclusive expression of the weakly rectifying Kir4.1 channel subtype in the entire cell membrane has been suggested.
49 However, such a difference in the patterns of Kir4.1 protein expression between rat and rabbit Müller cells remains to be demonstrated unequivocally, as well as the proposed specific downregulation of the Kir4.1 (but not of the Kir2.1) protein in rat Müller cells.