Summary.
The fungal toxin cytochalasin D as well as endogenous gelsolin depolymerize filamentous actin which may induce dynamic uncoupling of membrane ion channels. In vitro application of cytochalasin D reduced NMDA-induced [3H]noradrenaline release from mouse brain neocortical slices by 38%. In gsn deficient neocortical synaptosomes [Ca2+]i increase in response to K+ (30 mM) depolarization was 33% higher than in wild-type. After transient focal cerebral ischemia K+-induced [Ca2+]i increase in neocortical synaptosomes was 56% lower than in synaptosomes prepared from the non-ischemic contralateral hemisphere. After in vivo pretreatment with cytochalasin D 10 min before MCA occlusion K+-induced [Ca2+]i increase in synaptosomes in vitro prepared 1 h after reperfusion from the ischemic hemisphere was only 25% lower than in contralateral synaptosomes, while cytochalasin D pretreatment in vivo did not reduce K+-induced [Ca2+]i increase in vitro. Hence, presynaptic Ca2+ influx and subsequently neuronal vulnerability are attenuated by increased and are aggravated by decreased F-actin depolymerization.
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Received June 29, 2001 Accepted August 6, 2001 Published online August 9, 2002
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Fink, K., Paehr, M., Djoufack, P. et al. Effects of cytoskeletal modi?cations on Ca2+ in?ux after cerebral ischemia. Amino Acids 23, 325–329 (2002). https://doi.org/10.1007/s00726-001-0145-z
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DOI: https://doi.org/10.1007/s00726-001-0145-z