Studies on the ionic basis of primary afferent depolarization in the isolated mammalian spinal cord
Studies on the ionic basis of primary afferent depolarization in the isolated mammalian spinal cord
The isolated non-hemisected adult hamster spinal cord was shown to possess good electrical activity in its lumbar dorsal roots, remaining viable for many hours; spontaneous activity in the dorsal roots was shown to be maximal at temperatures between 23o and 25oC. Hypoxia was observed to produce a maximal rate of spontaneous dorsal root discharge (DRD) before the preparation became unviable, and the potassium channel antagonist 4-amino-pyridine potentiated the spontaneous DRD at a dose of 10μM.
Elevation of the extracellular chloride-ion concentration led to a concentration-dependent reduction in the rate of spontaneous dorsal root discharges. This event was shown not to be an osmotic artifact. Reduction of the extracellular chloride-ion concentration had no discernible effect on the observed rate of spontaneous dorsal root discharges. Spike train analysis, however, indicated an underlying increase in activity under these conditions. Elevation of the extracellular potassium-ion concentration had no observable effect on dorsal root activity. Tolbutamide had no discernible dose-dependent effects on dorsal root activity; it did however block the increase in spontaneous firing rate associated with hypoxia, indicating a role for K_ATP channels in the response to hypoxia.
A technique of terminal fibre excitability was developed as a more sensitive indicator of events within the dorsal horn and dorsal roots with which it was found that evoked dorsal root activity was blocked by the exchange of calcium for 2mM manganese in the acsf, thus demonstrating that evoked manifestations of PAD were of synaptic origin. High extracellular chloride-ion concentration reduced the excitability of the preparation, while low extracellular chloride enhanced the excitability. Nipecotic acid at 1mM was shown to enhance fibre excitability.
University of Southampton
1994
Tyler, Alan Wayne
(1994)
Studies on the ionic basis of primary afferent depolarization in the isolated mammalian spinal cord.
University of Southampton, Doctoral Thesis.
Record type:
Thesis
(Doctoral)
Abstract
The isolated non-hemisected adult hamster spinal cord was shown to possess good electrical activity in its lumbar dorsal roots, remaining viable for many hours; spontaneous activity in the dorsal roots was shown to be maximal at temperatures between 23o and 25oC. Hypoxia was observed to produce a maximal rate of spontaneous dorsal root discharge (DRD) before the preparation became unviable, and the potassium channel antagonist 4-amino-pyridine potentiated the spontaneous DRD at a dose of 10μM.
Elevation of the extracellular chloride-ion concentration led to a concentration-dependent reduction in the rate of spontaneous dorsal root discharges. This event was shown not to be an osmotic artifact. Reduction of the extracellular chloride-ion concentration had no discernible effect on the observed rate of spontaneous dorsal root discharges. Spike train analysis, however, indicated an underlying increase in activity under these conditions. Elevation of the extracellular potassium-ion concentration had no observable effect on dorsal root activity. Tolbutamide had no discernible dose-dependent effects on dorsal root activity; it did however block the increase in spontaneous firing rate associated with hypoxia, indicating a role for K_ATP channels in the response to hypoxia.
A technique of terminal fibre excitability was developed as a more sensitive indicator of events within the dorsal horn and dorsal roots with which it was found that evoked dorsal root activity was blocked by the exchange of calcium for 2mM manganese in the acsf, thus demonstrating that evoked manifestations of PAD were of synaptic origin. High extracellular chloride-ion concentration reduced the excitability of the preparation, while low extracellular chloride enhanced the excitability. Nipecotic acid at 1mM was shown to enhance fibre excitability.
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Published date: 1994
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Local EPrints ID: 462853
URI: http://eprints.soton.ac.uk/id/eprint/462853
PURE UUID: 48d852c0-a1d3-4bfb-8fde-a3f0706c1020
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Date deposited: 04 Jul 2022 20:16
Last modified: 04 Jul 2022 20:16
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Author:
Alan Wayne Tyler
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