Simon R. Stapleton
St George's Hospital
12 Papers
142 Citations
Simon R. Stapleton is an academic researcher from St George's Hospital. The author has contributed to research in topics: Patch clamp & Spider toxin. The author has an hindex of 6, co-authored 10 publications.
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Papers
Aspects of calcium-activated chloride currents : a neuronal perspective
TL;DR: The whole cell ICl(Ca) can be identified by sensitivity to increased Ca2+ buffering capacity of the cell, anion substitution studies and reversal potential measurements, as well as by the actions of Cl- channel blockers, and can be used as a physiological index of intracellular Ca 2+ close to the cell membrane.
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Effects of metabolic blockers on Ca2+-dependent currents in cultured sensory neurones from neonatal rats
TL;DR: The whole cell recording technique with cultured neurones under conditions which produce a degree of metabolic stress as reflected by prolonged Ca2+‐activated Cl− tail currents is combined to conclude that some agents used to induce chemical hypoxia, such as carbonyl cyanide p‐trifluoromethoxyphenylhydrazone and sodium cyanide, are not appropriate for use in studying disturbed neuronal Ca2+.
20
Regional heterogeneity of benzodiazepine binding sites in rat brain.
TL;DR: Ethyl-beta-carboline-3-carboxylate (beta CCE) and CL 218,872 displaced [ 3H]PrCC more potently than [3H]FNM and were more potent in the cerebellum than the hippocampus and more potent with BZ1 than BZ2 sites.
15
Craniotomy for recurrent glioblastoma: Is it justified? A comparative cohort study with outcomes over 10 years.
TL;DR: This first large prospective comparative cohort study of rGBM demonstrates that repeat resection confers a small but significant benefit in survival and quality of life over non-operative treatment.
12
Palmitoyl-DL-carnitine has calcium-dependent effects on cultured neurones from rat dorsal root ganglia.
TL;DR: It is concluded that palmitoyl‐dl‐carnitine reduced the efficiency of intracellular Ca2+ handling in cultured dorsal root ganglion neurones and resulted in enhancement of Ca2-‐dependent events including inactivation of voltage‐activated Ca 2+ currents.
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