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Joan N Abbott - One of the best experts on this subject based on the ideXlab platform.
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an electrophysiological method for measuring the Potassium Permeability of the nerve perineurium
Brain Research, 1997Co-Authors: Joan N Abbott, Kevin J Ward, Faruhana Abdullah, Gillian Mitchell, Christopher I H SmithAbstract:Abstract An electrophysiological method is described for measuring the Potassium Permeability ( P K ) of the perineurium of the sciatic nerve of the frog. The method is based on the principle of grease-gap recording, in which an insulating compartment separates two surface recording electrodes. The sciatic nerves of frogs Rana temporaria and R. pipiens were isolated and mounted across a five compartment chamber, with Vaseline grease seals on the partitions between compartments. Compartments #1, #2 and #5 contained frog Ringer solution, #4 was filled with Vaseline and formed the grease gap, and #3 was the test compartment in which solutions could be changed. The nerve was stimulated via platinum electrodes in compartments #1 and #2, and DC potentials and compound action potentials (CAP) were recorded between Ag/AgCl electrodes connected through Ringer-agar bridges to compartments #3 and #5. In nerves with undamaged perineurium, changing from normal Ringer to high [K + ] Ringer (100 mM, KCl replacing NaCl) for 2 min caused negligible change in DC potential or CAP, indicating that raised [K + ] was not reaching the axon surface, and hence that the perineurium was exerting a diffusional restriction on K + entry. In nerves damaged by stretching or drying, K + pulses caused a depolarising change in DC potential (ΔDC), and corresponding decline in CAP amplitude, consistent with a leaky perineurium allowing K + entry and axonal depolarisation. Ringer made hypertonic by the addition of 2.5 M sucrose or 5 M NaCl caused increased perineurial Permeability to K + . The method was calibrated by measuring the ΔDC in response to raised [K + ] in the range 5–100 mM [K + ] in desheathed nerves; from this calibration curve relating ΔDC to endoneurial [K + ] it was possible to calculate the change in endoneurial [K + ] occurring in intact preparations. The calculations showed that the undamaged perineurium had a P K of −7 cm·s −1 , similar to the value calculated for in situ nerves using radioisotopic techniques, but less than the value reported for isolated perineurial cylinders. The method gives real-time information on the K + Permeability of the nerve perineurium and its modulation by experimental treatments.
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effects of the bile salt sodium deoxycholate protamine and inflammatory mediators on the Potassium Permeability of the frog nerve perineurium
Brain Research, 1997Co-Authors: B A Todd, E M Sedgwick, Joan N AbbottAbstract:Abstract An electrophysiological method was used to measure the Potassium Permeability ( P K ) of the perineurium of the sciatic nerve of frogs Rana temporaria and R. pipiens . Isolated but intact nerves were mounted in a grease-gap chamber, and compound action potential and DC potential monitored. Change in the DC potential (ΔDC) in response to challenge with 100 mM [K + ] Ringer was used to assess the K + Permeability of the perineurium, since change in DC potential under these conditions reflected changes in the axonal resting potential. The Permeability of the perineurium was calculated from the published calibration curve relating ΔDC to bathing [K + ] in desheathed nerves of Abbott et al. (1997). In the control condition, P K was −6 cm·s −1 . The bile salt sodium deoxycholate (DOC, 1–4 mM) caused a dose-dependent increase in P K , which reached a maximum of 1.7×10 −5 cm·s −1 after 2-min exposure to 4 mM DOC, but access of K + to the endoneurial compartment was more restricted after DOC than after desheathing. Protamine phosphate (1 mM) and protamine sulphate (0.1–5 mg/ml equals 0.125–6.25 mM) had no effect on P K . Neither histamine (0.4–40 mg/ml), bradykinin (0.1–5 mg/ml) nor serotonin (5-hydroxytryptamine, 0.1–5 mg/ml) affected P K . The frog nerve perineurium appears to be relatively insensitive to chemical agents and inflammatory mediators, in contrast to the endothelial cells forming the endoneurial blood–nerve barrier and the blood–brain barrier.
B A Todd - One of the best experts on this subject based on the ideXlab platform.
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effects of the bile salt sodium deoxycholate protamine and inflammatory mediators on the Potassium Permeability of the frog nerve perineurium
Brain Research, 1997Co-Authors: B A Todd, E M Sedgwick, Joan N AbbottAbstract:Abstract An electrophysiological method was used to measure the Potassium Permeability ( P K ) of the perineurium of the sciatic nerve of frogs Rana temporaria and R. pipiens . Isolated but intact nerves were mounted in a grease-gap chamber, and compound action potential and DC potential monitored. Change in the DC potential (ΔDC) in response to challenge with 100 mM [K + ] Ringer was used to assess the K + Permeability of the perineurium, since change in DC potential under these conditions reflected changes in the axonal resting potential. The Permeability of the perineurium was calculated from the published calibration curve relating ΔDC to bathing [K + ] in desheathed nerves of Abbott et al. (1997). In the control condition, P K was −6 cm·s −1 . The bile salt sodium deoxycholate (DOC, 1–4 mM) caused a dose-dependent increase in P K , which reached a maximum of 1.7×10 −5 cm·s −1 after 2-min exposure to 4 mM DOC, but access of K + to the endoneurial compartment was more restricted after DOC than after desheathing. Protamine phosphate (1 mM) and protamine sulphate (0.1–5 mg/ml equals 0.125–6.25 mM) had no effect on P K . Neither histamine (0.4–40 mg/ml), bradykinin (0.1–5 mg/ml) nor serotonin (5-hydroxytryptamine, 0.1–5 mg/ml) affected P K . The frog nerve perineurium appears to be relatively insensitive to chemical agents and inflammatory mediators, in contrast to the endothelial cells forming the endoneurial blood–nerve barrier and the blood–brain barrier.
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Effects of the bile salt sodium deoxycholate, protamine, and inflammatory mediators on the Potassium Permeability of the frog nerve perineurium.
Brain research, 1997Co-Authors: B A Todd, E M Sedgwick, N Joan AbbottAbstract:An electrophysiological method was used to measure the Potassium Permeability (PK) of the perineurium of the sciatic nerve of frogs Rana temporaria and R. pipiens. Isolated but intact nerves were mounted in a grease-gap chamber, and compound action potential and DC potential monitored. Change in the DC potential (delta DC) in response to challenge with 100 mM [K+] Ringer was used to assess the K+ Permeability of the perineurium, since change in DC potential under these conditions reflected changes in the axonal resting potential. The Permeability of the perineurium was calculated from the published calibration curve relating delta DC to bathing [K+] in desheathed nerves of Abbott et al. (1997). In the control condition, PK was < 1.1 x 10(-6) cm.s-1. The bile salt sodium deoxycholate (DOC, 1-4 mM) caused a dose-dependent increase in PK, which reached a maximum of 1.7 x 10(-5) cm.s-1 after 2-min exposure to 4 mM DOC, but access of K+ to the endoneurial compartment was more restricted after DOC than after desheathing. Protamine phosphate (1 mM) and protamine sulphate (0.1-5 mg/ml equals 0.125-6.25 mM) had no effect on PK. Neither histamine (0.4-40 mg/ml), bradykinin (0.1-5 mg/ml) nor serotonin (5-hydroxytryptamine, 0.1-5 mg/ml) affected PK. The frog nerve perineurium appears to be relatively insensitive to chemical agents and inflammatory mediators, in contrast to the endothelial cells forming the endoneurial blood-nerve barrier and the blood-brain barrier.
S M Wilson - One of the best experts on this subject based on the ideXlab platform.
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The effect of a phorbol ester upon the cholinergic regulation of Potassium Permeability in the rat submandibular gland.
Cellular and Molecular Life Sciences, 1995Co-Authors: John D Pediani, S M WilsonAbstract:Acetylcholine releases calcium from cytoplasmic stores and permits an influx of calcium in salivary acinar cells. The resultant rise in [Ca2+]i causes an increase in Potassium Permeability which is an important part of the secretory response. We have investigated the effects of 12-0-tetradecanoyl phorbol-13-acetate, a potent activator of protein kinase C, upon this regulation of Potassium Permeability in superfused pieces of rat submandibular salivary gland. This compound inhibited the initial [Ca2+]o-independent component of the response of acetylcholine but had no effect upon the subsequent [Ca2+]o-dependent phase. This compound does not, therefore, appear to inhibit receptor-regulated calcium influx.
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The effect of removing external sodium upon the cholinergic regulation of Potassium Permeability in the rat submandibular gland in vitro
Comparative Biochemistry and Physiology Part C: Pharmacology Toxicology and Endocrinology, 1994Co-Authors: John D Pediani, H Y Elder, P.e. Mcewan, S M WilsonAbstract:Abstract Fragments of rat submandibular gland were loaded with 86 Rb + and superfused so that the rate of 86 Rb + -efflux could be quantified as an indicator of Potassium Permeability. Acetylcholine evoked an increase in Permeability consisting of a transient, calcium-independent response and a sustained, calcium-dependent. Total removal of external sodium significantly inhibited both phases of this response. The results thus confirm that the cholinergic regulation of Potassium Permeability is compromised by removal of external sodium but do not support the view that this is due, exclusively, to an effect on calcium influx.
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amiloride impairs the cholinergic regulation of Potassium Permeability in the human sweat gland but not in the rat submandibular gland
Cellular and Molecular Life Sciences, 1992Co-Authors: S M Wilson, John D Pediani, Mce D Jenkinson, H Y ElderAbstract:Potassium Permeability was monitored in human sweat glands and rat submandibular glands. Acetylcholine increased Permeability in both tissues and the responses consisted of transient, calcium-independent and sustained, calcium-dependent components. Amiloride, a drug which inhibits Na+−H+ countertransport, impaired the regulation of Potassium Permeability in sweat glands but not in the submandibular gland. It is suggested that the stimulus-Permeability coupling process in the sweat gland may be sensitive to the lowering of internal pH.
H Y Elder - One of the best experts on this subject based on the ideXlab platform.
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The effect of removing external sodium upon the cholinergic regulation of Potassium Permeability in the rat submandibular gland in vitro
Comparative Biochemistry and Physiology Part C: Pharmacology Toxicology and Endocrinology, 1994Co-Authors: John D Pediani, H Y Elder, P.e. Mcewan, S M WilsonAbstract:Abstract Fragments of rat submandibular gland were loaded with 86 Rb + and superfused so that the rate of 86 Rb + -efflux could be quantified as an indicator of Potassium Permeability. Acetylcholine evoked an increase in Permeability consisting of a transient, calcium-independent response and a sustained, calcium-dependent. Total removal of external sodium significantly inhibited both phases of this response. The results thus confirm that the cholinergic regulation of Potassium Permeability is compromised by removal of external sodium but do not support the view that this is due, exclusively, to an effect on calcium influx.
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amiloride impairs the cholinergic regulation of Potassium Permeability in the human sweat gland but not in the rat submandibular gland
Cellular and Molecular Life Sciences, 1992Co-Authors: S M Wilson, John D Pediani, Mce D Jenkinson, H Y ElderAbstract:Potassium Permeability was monitored in human sweat glands and rat submandibular glands. Acetylcholine increased Permeability in both tissues and the responses consisted of transient, calcium-independent and sustained, calcium-dependent components. Amiloride, a drug which inhibits Na+−H+ countertransport, impaired the regulation of Potassium Permeability in sweat glands but not in the submandibular gland. It is suggested that the stimulus-Permeability coupling process in the sweat gland may be sensitive to the lowering of internal pH.
E M Sedgwick - One of the best experts on this subject based on the ideXlab platform.
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effects of the bile salt sodium deoxycholate protamine and inflammatory mediators on the Potassium Permeability of the frog nerve perineurium
Brain Research, 1997Co-Authors: B A Todd, E M Sedgwick, Joan N AbbottAbstract:Abstract An electrophysiological method was used to measure the Potassium Permeability ( P K ) of the perineurium of the sciatic nerve of frogs Rana temporaria and R. pipiens . Isolated but intact nerves were mounted in a grease-gap chamber, and compound action potential and DC potential monitored. Change in the DC potential (ΔDC) in response to challenge with 100 mM [K + ] Ringer was used to assess the K + Permeability of the perineurium, since change in DC potential under these conditions reflected changes in the axonal resting potential. The Permeability of the perineurium was calculated from the published calibration curve relating ΔDC to bathing [K + ] in desheathed nerves of Abbott et al. (1997). In the control condition, P K was −6 cm·s −1 . The bile salt sodium deoxycholate (DOC, 1–4 mM) caused a dose-dependent increase in P K , which reached a maximum of 1.7×10 −5 cm·s −1 after 2-min exposure to 4 mM DOC, but access of K + to the endoneurial compartment was more restricted after DOC than after desheathing. Protamine phosphate (1 mM) and protamine sulphate (0.1–5 mg/ml equals 0.125–6.25 mM) had no effect on P K . Neither histamine (0.4–40 mg/ml), bradykinin (0.1–5 mg/ml) nor serotonin (5-hydroxytryptamine, 0.1–5 mg/ml) affected P K . The frog nerve perineurium appears to be relatively insensitive to chemical agents and inflammatory mediators, in contrast to the endothelial cells forming the endoneurial blood–nerve barrier and the blood–brain barrier.
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Effects of the bile salt sodium deoxycholate, protamine, and inflammatory mediators on the Potassium Permeability of the frog nerve perineurium.
Brain research, 1997Co-Authors: B A Todd, E M Sedgwick, N Joan AbbottAbstract:An electrophysiological method was used to measure the Potassium Permeability (PK) of the perineurium of the sciatic nerve of frogs Rana temporaria and R. pipiens. Isolated but intact nerves were mounted in a grease-gap chamber, and compound action potential and DC potential monitored. Change in the DC potential (delta DC) in response to challenge with 100 mM [K+] Ringer was used to assess the K+ Permeability of the perineurium, since change in DC potential under these conditions reflected changes in the axonal resting potential. The Permeability of the perineurium was calculated from the published calibration curve relating delta DC to bathing [K+] in desheathed nerves of Abbott et al. (1997). In the control condition, PK was < 1.1 x 10(-6) cm.s-1. The bile salt sodium deoxycholate (DOC, 1-4 mM) caused a dose-dependent increase in PK, which reached a maximum of 1.7 x 10(-5) cm.s-1 after 2-min exposure to 4 mM DOC, but access of K+ to the endoneurial compartment was more restricted after DOC than after desheathing. Protamine phosphate (1 mM) and protamine sulphate (0.1-5 mg/ml equals 0.125-6.25 mM) had no effect on PK. Neither histamine (0.4-40 mg/ml), bradykinin (0.1-5 mg/ml) nor serotonin (5-hydroxytryptamine, 0.1-5 mg/ml) affected PK. The frog nerve perineurium appears to be relatively insensitive to chemical agents and inflammatory mediators, in contrast to the endothelial cells forming the endoneurial blood-nerve barrier and the blood-brain barrier.