Abstract

AbstractIn unanesthetized acute spinal cats an i.v. injection of 4, α‐dimethyl‐meta‐tyramine (H 77/77), which liberates noradrenaline (NA), depresses short‐latency transmission from the flexor reflex afferents (FRA) to motoneurones, ascending pathways and primary afferent terminals. The effect is similar to that produced by DOPA but the late flexor reflex evoked from the FRA after DOPA is not found after H 77/77. The effect by H 77/77 is reversed by the adrenergic α‐blockers phenoxybenzamine and chlorpromazine. H 77/77 has no effect in animals in which the stores of NA have been depleted by pretreatment with reserpine and a blocker of tyrosine hydroxylase. It is suggested that H 77/77 inhibits reflex transmission by transmitter liberation from noradrenergic terminals. H 77/77 also depresses short‐latency transmission from the FRA in chronic spinal cats after degeneration of the descending fibres. As a possible explanation it is suggested that the receptor sensitivity may have changed in the neurones deprived of NA terminals or that neighbouring glia cells may have taken over some of the functions of the NA terminals.

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