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The inhibitory action of noradrenaline and other monoamines on spinal neurones
Author(s) -
Engberg I.,
Ryall R. W.
Publication year - 1966
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1966.sp007988
Subject(s) - inhibitory postsynaptic potential , excitatory postsynaptic potential , renshaw cell , chemistry , depolarization , acetylcholine , monoamine neurotransmitter , neuroscience , hyperpolarization (physics) , biophysics , spinal cord , serotonin , pharmacology , biology , biochemistry , stereochemistry , receptor , nuclear magnetic resonance spectroscopy
1. L ‐Noradrenaline (NA), 5‐hydroxytryptamine (5‐HT) and acetylcholine (ACh) were administered micro‐electrophoretically to feline lumbar neurones while recording their spike potentials extracellularly. 2. There was no evidence to suggest that NA acts as an excitatory transmitter in the spinal cord. 3. NA had potent inhibitory effects on some interneurones as revealed by a depression of spontaneous and synaptic firing and on the firing to a local application of an excitant amino acid. The effects on Renshaw cells and motoneurones were less marked. 4. The depressant actions of 5‐HT were less marked than those of NA. ACh and carbamylcholine had depressant effects on some NA‐sensitive interneurones but were invariably far less potent and on other NA‐sensitive cells were completely inactive. 5. NA had no detectable effect on the normal spike amplitude but when the action potentials were reduced by excessive depolarization then both NA and synaptic inhibition increased the spike amplitude; this effect could be due to a hyperpolarization of the cell membrane. 6. There was a correlation between the distribution of NA‐sensitive cells and the relative densities of NA‐containing terminals in various layers of the grey matter. 7. It was postulated that NA acts as an inhibitory transmitter released from the terminals of descending pathways in the spinal cord. Other possible mechanisms were discussed but lacked experimental support.