1,272 research outputs found
Astrocytes Modulate Thapsigargin-induced Changes in Calcium Concentration and Neuronal Survival
No full textFavourable outcome in a pregnancy with concomitant maternal and fetal osteogenesis imperfecta associated with a novel COL1A2 mutation
No full textRoles of Thapsigargin-Sensitive Ca2+ Stores in the Survival of Developing Cultured Neurons
No full textMode of Inhibitory Action of Zn2+, Hg2+ and UO22+ on 5'-Nucleotidase of Mouse Hepatic Microsomes
No full textEffect of Sulbactam on the Antibacterial Activity of Ampicillin Against Various Clinical Isolates from NTUH
No full textMutagenicity of Dipyridyl and Their Methylated Derivtives in Salmonella Typhimurium/Rat Liver Microsome System
No full textSuramin Inhibits the Toxic Effects of Presynaptic Neurotoxins at the Mouse Motor Nerve Terminals
No full textClinically available chemical antagonists of snake neurotoxins still await to be identified. In this study, we demonstrate that an anti- trypanosomiasis agent, suramin, is an effective inhibitor of -bungarotoxin isolated from the venom of Formosan Krait snake. Following intraperitoneal injection (12 ng/g) of -bungarotoxin in mice, the time to paralysis (loss a limb withdrawal reflex, 21.8±3.4 h, n=4) was significantly prolonged after intravenous injection (16 g/g) of suramin ( 35.9±4.0 h, n=4, P<0.05). The mechanism of this inhibitory effect of suramin was analyzed at the mouse nerve terminals. -Bungarotoxin (1 g/ml) produces an irreversible blocking effect of nerve-evoked muscle contractions of mouse phrenic nerve–diaphragm (blocking time 135±6 min, n=6). Pretreatment with suramin (0.3 mM) significantly prolonged the blocking time by three-fold. This selective inhibitory effect of suramin was further confirmed when suramin was shown to delay the neuromuscular blocking effect of another presynaptic neurotoxin, crotoxin (from American rattlesnake venom), but not that of the postsynaptic neurotoxin, - bungarotoxin. Furthermore, suramin inhibited -bungarotoxin in blocking transmitter release as revealed by prolonging the time to abolish the end- plate potential amplitude (with suramin, 391±8 min; without treatment, 141±5 min). K+ current was measured in the mouse triangularis sterni preparation; suramin (0.3 mM) had no significant effect on -bungarotoxin in inhibiting K+ current (77±3% of control; with suramin 75±3% of control, respectively). These findings clearly show that suramin is an inhibitor of presynaptic neurotoxins, mediated by interrupting the toxins in blocking the releasing mechanism of transmitter at the motor nerve terminals. The implication of these findings is that suramin and related compounds can become useful agents in management of snakebites
Enhanced Spontaneous Transmitter Release at Murine Motor Nerve Terminals with Cyclosporine
No full textCyclosporine, a calcineurin inhibitor, significantly enhances spontaneous acetylcholine release after a brief tetanus and potentiates the effect of phorbol 12,13- dibutyrate. Both actions are prevented by the protein kinase C inhibitor, bisindolylmaleimide iodide. Protein kinase C and calcineurin thus play important roles in the balance between phosphorylation and dephosphorylation regulating spontaneous transmitter release at motor nerve terminals
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