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  • Title: The H reflex recovery curve reinvestigated: low-intensity conditioning stimulation and nerve compression disclose differential effects of presumed group Ia fibres in man.
    Author: Rossi A, Mazzocchio R, Schieppati M.
    Journal: Hum Neurobiol; 1988; 6(4):281-8. PubMed ID: 3350708.
    Abstract:
    The recovery curve of the soleus H reflex, evoked by stimulation of the tibial nerve in the popliteal fossa, was studied by applying an electrical conditioning stimulus to the inferior soleus nerve. Under these conditions a long-latency facilitatory phase could be superimposed on a long-lasting inhibition, the excitability cycle being therefore similar to that obtained by means of a paired shock to the tibial nerve. In order to identify the afferent fibres responsible for the effects observed, various conditioning stimulus strengths and nerve compression were used. A low-intensity stimulus induced only a facilitatory phase, while the inhibition promptly ensued on increasing stimulus strength, which remained however subliminal for activation of group II fibres. During calf compression exerted by a sphygmomanometer cuff placed between the conditioning and test stimuli, the facilitatory effects disappeared within 10 to 15 min, and the inhibitory ones disappeared within 25 to 30 min from the onset of compression. Tonic voluntary contraction enhanced both the inhibition and the facilitation. In a subject with complete spinal section, both inhibitory and facilitatory phases could be demonstrated on low-intensity stimulation. The present data, and previous results of ours, allow the following conclusions. (1) Facilitation and inhibition are produced by fibres likely belonging to group Ia spindle afferents. (2) Both effects are of spinal origin. (3) The spinal circuits mediating the effects may be modulated by descending commands. (4) The facilitation is sustained by tonic supraspinal influences while the inhibition is independent of it. Arguments are proposed against the hypotheses that the inhibition be due to transmitter depletion or to presynaptic mechanisms.
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