Abstract
ALTHOUGH many factors need to be considered before a chemical compound can be identified as a synaptic transmitter substance within the nervous system1, it is essential that, when administered to the appropriate subsynaptic receptors, it evokes the same response of the particular neurones as does the synaptically released transmitter. The demonstration of such a postsynaptic action is, however, insufficient by itself to warrant the assumption that an agent is a transmitter. Thus the conclusion that acetyl-choline is an excitatory transmitter of Renshaw cells is based not only on the excitatory action of this substance but also on the very close similarity between the pharmacology of this excitation, the pharmacology of the synaptic excitation of these neurones by volleys in motor axon collaterals and the pharmacology of the mammalian neuromuscular junction2–3. Recently, the sensitivity of neurones in the cerebral cortex to electrophoretically administered acetylcholine4,5 has led to the suggestion that such cells may be activated synaptically by cholinergic fibres5. However, no details have been given of the effect of pharmacological agents on the synaptic excitation of these neurones; moreover, the reported pharmacology of the excitation by acetylcholine differs in certain respects from that of the excitation of Renshaw cells by this choline ester.
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References
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CURTIS, D., ANDERSEN, P. Acetylcholine: a Central Transmitter?. Nature 195, 1105–1106 (1962). https://doi.org/10.1038/1951105a0
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DOI: https://doi.org/10.1038/1951105a0
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