Experimental investigations on the afferent fibres in muscle nerves

Abstract

Nerves to various muscles of the cat’s hind limb have been stimulated under conditions designed to give uniform distribution of current throughout the whole cross-section of the nerve, and the conducted action potentials have been recorded from the dorsal roots. Alterna­tively, stimuli have been applied to a dorsal root and the conducted action potentials recorded from the nerve to a muscle. Strong stimuli evoke a compound spike potential with a time distribution conforming with the standard fibre-calibre spectrum. Following the large group I spike there is usually a double spike attributable to group II fibres, and a very low group III spike. The stimulus strength has to be increased to about twice threshold in order to set up a maximum group I spike, but a group II spike is usually detectable when the stimulus is increased to 1.3 to 1.4 times group I threshold. Group II b fibres usually have a higher threshold than group II a , and a group III spike is not as a rule detectable until the stimulus is about three times group I threshold. The excitatory and inhibitory actions of an afferent volley from a muscle on the moto-neurones of that muscle or of a synergic muscle have been revealed by the change in mono­ synaptic reflex response to a later testing volley (maximal for group I fibres) either in that same afferent nerve (homosynaptic testing) or in the afferent nerve from a synergic muscle (heterosynaptic testing). The conditioning volley has been set up by stimuli whose strength has varied from threshold for group I fibres to m any times that value, and several standard testing intervals have been chosen. From the data so obtained it has been possible to deter­mine the reflex effects exerted by the different groups of afferent fibres. The group I afferent fibres in the nerve of a flexor or extensor muscle exert the well-known excitatory action on the motoneurones of that muscle (autogenetic excitation). Our methods have failed to reveal any autogenetic inhibitory action, though its existence is not thereby disproven. The group III impulses of extensor muscles have a powerful autogenetic inhibitory action, while the group II impulses either have no detectable action or are weak autogenetic inhibitors. On the contrary, with flexor muscles both group II and group III impulses exert an effective autogenetic excitatory action. In addition, the group I afferent impulses of both extensor and flexor muscles exert on moto­-neurones an autogenetic depressant action which is clearly distinguishable from autogenetic inhibition. It is observed at an interval of more than 10 msec, subsequent to an excitatory action which was too weak to generate a reflex discharge. Since, in contrast to inhibition, this depression is virtually restricted to a homosynaptic testing reflex, it is attributed to the subnormality associated with the positive after-potential of the activated subsynaptic areas of motoneurones, and has been called ‘subsynaptic depression’.