The effects of high- and low-intensity percutaneous stimulation on nitric oxide levels and spike activity in the superficial laminae of the spinal cord.
Nitric oxide (NO) was measured using a new electrochemical method with a carbon fibre microelectrode at depths of up to 400 microm in the lumbar dorsal horn of the anaesthetised rat. The method allowed extracellular spike recording from single units together with the electrochemical recording at the same electrode. Thirty-six cells with low threshold cutaneous (brush/touch) or wide dynamic range receptive fields (brush/touch plus pinch) were studied. Adequate stimulation of the receptive fields did not alter the extracellular NO level for any cells. Percutaneous needle electrodes inserted into the receptive fields were used to stimulate the cells electrically. Twenty-one cells were stimulated using 10 mA current with 0.05 ms duration (low intensity) pulses to stimulate predominantly A-fibre afferents. Single shock stimuli gave short latency spike responses but no change in nitric oxide level. Tetanic bursts of stimuli (400 stimuli at 50 Hz) generated a burst of spikes (spike count 548+/-42) and a transient increase in NO (2.61+/-0.11 microM NO). Nitric oxide synthesis inhibition with N(G)-nitro-L-arginine methyl ester (L-NAME) nearly abolished the stimulus-evoked increase in nitric oxide and increased the response of the cells (spike count 694+/-34). However, the inhibition of nitric oxide synthesis had no effect on the receptive fields. Fifteen cells were stimulated with shocks using 5 ms pulses (high intensity), to recruit C-fibre afferents into the input volley. This more intense stimulation increased the evoked NO release to 3.63+/-0.15 microM and the spike response to 647+/-54 in control conditions. Following L-NAME, the evoked NO release was reduced and the evoked spike response was significantly decreased. These results show that tetanic activity in afferent fibres increases NO synthesis in the dorsal horn and that inhibition of nitric oxide synthesis may be associated with a selective attenuation of the spike responses to C-fibre inputs. NO may be necessary to maintain proper function of C-fibre afferent synapses when they are subjected to sustained or tetanic inputs.
Department of Anaesthesiology, University Hospital Eppendorf, Hamburg, Germany.
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D000200:Action Potentials / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D004305:Dose-Response Relationship, Drug; D004558:Electric Stimulation; D004563:Electrochemistry / Q000379:methods; D004566:Electrodes; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005465:Fluorocarbon Polymers / Q000494:pharmacology; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D009569:Nitric Oxide / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D013116:Spinal Cord / Q000033:anatomy & histology / Q000187:drug effects / Q000502:physiology*; D013997:Time Factors; D014443:Tyrosine / Q000494:pharmacology
D004791:Enzyme Inhibitors; D005465:Fluorocarbon Polymers; D009569:Nitric Oxide; C040402:perfluorosulfonic acid; D014443:Tyrosine; D019331:NG-Nitroarginine Methyl Ester