Facilitation of H-reflex by homonymous Ia-afferent fibers in man.

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Abstract
The recovery curve of the H-reflex was studied with the simultaneous recording of the nerve potential in the sciatic nerve. The conditioning stimulus was subliminal for an H-reflex. The recovery curve showed an inhibiton in an interval between 1.5-3 ms and a subsequent facilitation up to 15 ms. The nerve potential consisted of 2 components. The 1st component was considered to be the afferent volley in group I fibers, the conduction velocity of which was 65-70 m/s. The 2nd component was considered to be the antidromic volley in the .alpha.-motor fibers, the conduction velocity of which was 55-59 m/s. When the conditioning stimulus was applied, the nerve potential showed a depression for 3 ms after the conditioning stimulus. Therefore, the inhibition of the H-reflex recovery curve before 3 ms was due to the refractoriness of the afferent nerve fibers. The test H-response before 3 ms was really facilitated. This facilitation was masked in the recovery curve by the depression of the afferent nerve volley due to refractoriness. The nerve potentials and H-responses showed an almost linear relationship with or without the conditioning stimulus. The test H-response was more facilitated as the time interval between the conditioning and the test stimuli was shortened. The refractoriness of the afferent nerve fibers was compensated from the linear relation between the nerve potential and the test H-response, and the compensated recovery curve was obtained. When the conditioning stimulus was just above the threshold for the nerve volley but subthreshold for the H-reflex, the compensated recovery curve showed a pure facilitation, the half-decay time of which was 2.6 ms. This pure facilitation was considered to be mainly Ia facilitation. When the conditioning stimulus was slightly enhanced, the compensated recovery curve showed a notch superimposed on the facilitation. Consideration was given to Ib inhibition and to autogenic Ia inhibition mediating the notch on the compensated recovery curve, but the research approach was not sufficient to elucidate exclusive central mechanisms.

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