Influence of Discharge of Motoneurons upon Excitation of Neighboring Motoneurons

SOME spinal motoneurons are equipped with recurrent collaterals which arise from the axon near its origin and terminate in association with other neurons of the ventral horn (cf. Cajal, 1909). An impulse that sweeps over the motor axon must also invade its collaterals. Does it then affect the excita-bility of the neurons in association with which the collaterals terminate? Miiller (1835) could produce no muscular contractions by stimulating the central end of a cut motor root. Others have likewise failed to find evidence that an antidromic volley produces either a centrifugal discharge in motor axons or activity in other nerve tracts In the absence of known excitatory effects it has been suggested that impulses in recurrent collaterals might lead to inhibition of the activity in the neurons to which they pass (Graham Brown, 1914; Gesell, 1940). The collaterals would then be an important part of the mechanism for reciprocal innervation. Forbes and his collaborators (1933) put the suggestion of Graham Brown to a careful experimental test. They found that a contralaterally evoked reflex discharge into the tibia1 nerve is not conditioned by antidromic volleys arriving at the cord in the motor axons of the peroneal nerve. The present experiments show that the antidromic activation of certain groups of motoneurons does condition the reflex discharges of other moto-neurons. The conditioning effect is often inhibitory. It is then neither preceded by facilitation nor delayed; inhibition is present when the antidromic volley reaches the cord approximately simultaneously with an afferent volley which fires the testing motoneurons directly after a single synaptic delay. The inhibition must then be caused by events occurring during the synaptic delay at the motoneurons-a period of only 0.9 msec. or less (Lorente de No, 1938; Renshaw, 1940). The conditioning volley cannot have fired either the tested motoneurons or premotor interneurons in time for the refractori-ness (subnormality) which follows activity to mediate the response deficit (cf. Gasser, 1937a, b; Lorente de No, 1936). In a discussion of this phenomenon it would be misleading to focus attention only upon the possible role of recurrent collaterals. It is not necessary to infer from the early onset of inhibition that a specific inhibitory action is produced by the arrival of impulses at the synapses made by the recurrent collaterals with other neurons. As Grundfest (1940) has pointed out, an alternative explanation for findings of this sort is suggested by the fact that