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Brain Res Dev Brain Res. 2003 Oct 10;145(1):61-9.

Muscarinic calcium mobilization in the regenerating retina of adult newt.

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Institute of Biological Sciences, The University of Tsukuba, Tsukuba, Ibaraki, 305-8572, Japan.


We used optical recording with a Ca(2+)-sensitive dye, fura2, in living slice preparations from the newt retina at different stages of regeneration. ACh produced the most pronounced [Ca2+]i rise in progenitor cells and premature ganglion cells of the earlier stage of retinal regeneration, but less pronounced Ca2+ response in ganglion cells just before, or at the beginning of, synaptogenesis. The [Ca2+]i rise to ACh was mediated by mAChRs. This was shown by inhibition of the ACh-induced Ca2+ response with a preincubation of the mAChR antagonist atropine as well as with direct stimulation of the [Ca2+]i rise by the mAChR agonist muscarine. This muscarine-induced [Ca2+]i rise was more greatly suppressed by the M1 and/or M3 preferring mAChR antagonists than by the M2 preferring mAChR antagonist. The [Ca2+]i rise due to muscarine was not suppressed in the absence of extracellular Ca2+, but suppressed in part in the presence of the L-type voltage-gated Ca2+ channel blockers, verapamil or nicardipine. Furthermore, thapsigargin (TG), a Ca-ATPase inhibitor, abolished the muscarine-induced [Ca2+]i rise in the absence of extracellular Ca2+. These results suggest that the mAChR-mediated [Ca2+]i rise is mainly a result of a release of Ca2+ from intracellular stores. TG produced a slow rise in the resting level of [Ca2+]i. This [Ca2+]i raise was suppressed as extracellular Ca2+ was omitted, whereas a rapid rise in [Ca2+]i occurred when extracellular Ca2+ was reintroduced, suggesting the occurrence of the capacitative Ca2+ influx in the progenitor cells and premature ganglion cells of the regenerating newt retina.

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