title: Microsphere embolism-induced changes in presynaptic function of the cerebral cortex in rats.
abstract: The present study was undertaken to elucidate pathophysiological changes in the cortical presynaptic function, K(+)-stimulated calcium influx, noradrenaline release and noradrenaline uptake, on the 1st and 3rd days after microsphere embolism in rats. Voltage-dependent calcium channels were characterized pharmacologically using three types of calcium channel blockers, L-type (nifedipine and diltiazem), N-type (omega-conotoxin GVIA), and P-type channel (omega-agatoxin IVA) blockers. K(+)-stimulated calcium influx of the normal rat synaptosome was inhibited by 100 nM omega-agatoxin IVA, but not by 10 microM nifedipine, 10 microM diltiazem and 100 nM omega-conotoxin GVIA. Calcium influx of the cortical nerve terminals of the right hemisphere was decreased on the 1st and 3rd days after the embolism. Noradrenaline release and uptake were also decreased on the 1st and 3rd days after the embolism. However, the percent release of noradrenaline was not altered. The results suggest that P-type channels are predominant in the cerebrocortical nerve terminals in rats and that calcium influx, noradrenaline release and uptake in the cerebrocortical nerve terminals are decreased by microsphere embolism. The decrease in noradrenaline release may be mainly due to a reduction in the activity of noradrenaline uptake in cerebrocortical nerve terminals of the microsphere-embolized rat.
authors.affiliation: Department of Pharmacology, Tokyo University of Pharmacy and Life Science, Hachioji, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Hayashi
authors.forename: N
authors.initials: N
authors.lastname: Takagi
authors.forename: N
authors.initials: N
authors.lastname: Kamimoto
authors.forename: S
authors.initials: S
authors.lastname: Takeo
mesh_terms: D000818:Animals; D002545:Brain Ischemia / Q000503:physiopathology; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000502:physiology; D002540:Cerebral Cortex / Q000098:blood supply* / Q000503:physiopathology*; D004110:Diltiazem / Q000494:pharmacology; D004617:Embolism / Q000503:physiopathology*; D015640:Ion Channel Gating / Q000502:physiology; D008297:Male; D008863:Microspheres; D008978:Mollusk Venoms / Q000494:pharmacology; D009543:Nifedipine / Q000494:pharmacology; D009638:Norepinephrine / Q000378:metabolism; D010455:Peptides / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D017729:Presynaptic Terminals / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D013111:Spider Venoms / Q000494:pharmacology; D013574:Synaptosomes / Q000737:chemistry / Q000187:drug effects; D013997:Time Factors; D014662:Vasoconstrictor Agents / Q000378:metabolism; D020867:omega-Agatoxin IVA; D020866:omega-Conotoxin GVIA
chemical_list: D002121:Calcium Channel Blockers; D015220:Calcium Channels; D008978:Mollusk Venoms; D010455:Peptides; D013111:Spider Venoms; D014662:Vasoconstrictor Agents; D020867:omega-Agatoxin IVA; D020866:omega-Conotoxin GVIA; D004110:Diltiazem; D009543:Nifedipine; D011188:Potassium; D002118:Calcium; D009638:Norepinephrine