PMID- 14519494
OWN - NLM
STAT- MEDLINE
DCOM- 20031216
LR  - 20190901
IS  - 0165-3806 (Print)
IS  - 0165-3806 (Linking)
VI  - 145
IP  - 1
DP  - 2003 Oct 10
TI  - Muscarinic calcium mobilization in the regenerating retina of adult newt.
PG  - 61-9
AB  - 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.
FAU - Ohmasa, Motoko
AU  - Ohmasa M
AD  - Institute of Biological Sciences, The University of Tsukuba, Tsukuba, Ibaraki, 
      305-8572, Japan.
FAU - Saito, Takehiko
AU  - Saito T
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Brain Res Dev Brain Res
JT  - Brain research. Developmental brain research
JID - 8908639
RN  - 0 (Calcium Channel Blockers)
RN  - 0 (Cholinergic Agents)
RN  - 0 (Muscarinic Agonists)
RN  - 0 (Receptors, Muscarinic)
RN  - 660YQ98I10 (Potassium Chloride)
RN  - 7T101UWZ5W (Muscarine)
RN  - SY7Q814VUP (Calcium)
RN  - TSN3DL106G (Fura-2)
SB  - IM
MH  - Aging
MH  - Animals
MH  - Calcium/*metabolism
MH  - Calcium Channel Blockers/pharmacology
MH  - Cholinergic Agents/pharmacology
MH  - Drug Interactions
MH  - Fura-2/metabolism
MH  - In Vitro Techniques
MH  - Muscarine/*pharmacology
MH  - Muscarinic Agonists/*pharmacology
MH  - Nerve Regeneration/drug effects/*physiology
MH  - Potassium Chloride/pharmacology
MH  - Receptors, Muscarinic/*metabolism
MH  - Retina/cytology/drug effects/*physiology
MH  - Salamandridae
EDAT- 2003/10/02 05:00
MHDA- 2003/12/17 05:00
CRDT- 2003/10/02 05:00
PHST- 2003/10/02 05:00 [pubmed]
PHST- 2003/12/17 05:00 [medline]
PHST- 2003/10/02 05:00 [entrez]
AID - S0165380603002141 [pii]
AID - 10.1016/s0165-3806(03)00214-1 [doi]
PST - ppublish
SO  - Brain Res Dev Brain Res. 2003 Oct 10;145(1):61-9. doi: 
      10.1016/s0165-3806(03)00214-1.