抄録
Astrocytes play an essential role in the two-way glial-neuronal communication by forming an elaborate network with neurons. Glutamate is known to be a key mediator for the glia-neuron interaction. Recent studies showed that significant permeability of some anion channels to organic molecules, such as taurine, glutamate and ATP. Thus, there is a possibility that glutamate release from glial cells is mediated by some anion channels. An enzymatic assay showed that release of glutamate from mouse astrocytes in primary culture was small under normal conditions but greatly increased upon a hypotonic challenge or under chemical ischemia. Patch-clamp experiments showed that both maneuvers activated maxi-anion channels in cell-attached patches. This channel was conductive to glutamate with a permeability ratio of PGlu/PCl=0.20±0.01. Sensitivity of glutamate release to NPPB, SITS, arachidonate and Gd3+ was very similar to that of glutamate-permeable maxi-anion channel. Neither blocker of gap-junction hemi-channels (carbenoxolone or 1-octanol) nor inhibitor of exocytosis (brefeldin A) affected glutamate release from astrocytes. Thus, our data suggest that the maxi-anion channel serves as a major pathway for glutamate release under hypotonic or ischemic conditions. [Jpn J Physiol 54 Suppl:S141 (2004)]
