Responses of identified spinal neurones to acetylcholine applied by micro‐electrophoresis.

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Abstract
The responses of identified cells in the cat Clarke''s column and dorsal horn to micro-electrophoretically applied cholinomimetics and anticholinergic substances were investigated. Antidromically identified [DSCT (dorsal spinocerebellar tract) neurons] and synaptically activated neurons from the region of the Clarke''s column of the spinal cord were excited by ACh [acetylcholine]. The proportion of ACh excited cells was greater in units synaptically activated by ipsilateral dorsolateral funiculus stimulation (78%) than in DSCT neurons (50%). About 55% of neurons activated antidromically or synaptically by ipsilateral dorsal column stimulation were excited by ACh. In contrast to a relatively weak excitatory potency on the DSCT neurons (maximum firing frequency did not exceed 130% of the control level), ACh proved to be a more potent excitant of units synaptically activated by ipsilateral dorsolateral funiculus stimulation (maximum firing frequency reached 430% of the control level). ACh has a relatively quick and rapidly reversible excitatory effect on Clarke''s column neurons and some types of dorsal horn interneurons, also obtained with nicotine. Nicotine action is frequently delayed in onset and recovery. This excitatory action of ACh can be blocked or markedly depressed by dihydro-.beta.-erythroidine. These results and those obtained with acetyl-.beta.-methylcholine and atropine suggest that the receptors mediating excitation of the cholinoceptive spinal cells activated antidromically or synaptically by ipsilateral dorsolateral funiculus stimulation besides predominantly nicotinic have weak muscarinic properties. Desensitization with repeated applications of ACh and nicotine was observed in DSCT neurons and units antidromically activated. About 11% of units antidromically activated by ipsilateral dorsolateral funiculus stimulation were depressed by ACh. The depressant effect of ACh was more frequently encountered in the cells unresponsive to the dorsolateral funiculus or dorsal column stimulation. ACh depression was seen in units activated antidromically or synaptically by ipsilateral dorsal column stimulation. No units synaptically activated by the ipsilateral dorsolateral funiculus stimulation or spinal neurons receiving convergent peripheral inputs activated either antidromically or synaptically by ipsilateral dorsolateral or dorsal column stimulation were depressed by ACh. Apparently ACh depression of all tested DSCT neurons is blocked by atropine and readily evoked by acetyl-.beta.-methylcholine; this indicates that receptors mediating the effect are of muscarinic type.