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Fig. 6 | Acta Neuropathologica Communications

Fig. 6

From: Astrocytes respond to a neurotoxic Aβ fragment with state-dependent Ca2+ alteration and multiphasic transmitter release

Fig. 6

Involvement of CX hemichannels in Ca2+-independent glutamate release. a Glutamate release prior to the Ca2+ elevation (top, CTR) was reduced by the CX hemichannel blocker CBX (100 µM; present throughout the recording; n = 8–13 cells per condition). b During the Aβ application phase, Ca2+-independent glutamate release was blocked by another CX hemichannel blocker Gap26 peptide (200 µM). The inactive scramble peptide of Gap26 showed no effect (n = 8–10 cells per condition). c A more pronounced inhibition effect of Gap26 was observed when applying it throughout the entire imaging period (i.e., pre-, during- and post-Aβ; n = 12–14 per condition). d Chelating astrocytic Ca2+ with BAPTA AM isolated Ca2+-independent astrocytic glutamate release, which was inhibited by CX hemichannel blocker Gap26 (n = 8–10 per condition)

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