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Group I projections from intrinsic foot muscles to motoneurones of leg and thigh muscles in humans

2001; Wiley; Volume: 536; Issue: 1 Linguagem: Inglês

10.1111/j.1469-7793.2001.t01-1-00313.x

1469-7793

P. Marqué, Guillaume Nicolas, Véronique Marchand‐Pauvert, Julien Gautier, M. Simonetta‐Moreau, E. Pierrot‐Deseilligny,

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The Journal of PhysiologyVolume 536, Issue 1 p. 313-327 Free Access Group I projections from intrinsic foot muscles to motoneurones of leg and thigh muscles in humans Philippe Marque, Philippe Marque Neurophysiologie Clinique, Rééducation, Hôpital de la Salpêtrière, 47 boulevard de l'Hôpital, 75651 Paris cedex 13, FranceSearch for more papers by this authorGuillaume Nicolas, Guillaume Nicolas Neurophysiologie Clinique, Rééducation, Hôpital de la Salpêtrière, 47 boulevard de l'Hôpital, 75651 Paris cedex 13, FranceSearch for more papers by this authorVéronique Marchand-Pauvert, Véronique Marchand-Pauvert Neurophysiologie Clinique, Rééducation, Hôpital de la Salpêtrière, 47 boulevard de l'Hôpital, 75651 Paris cedex 13, FranceSearch for more papers by this authorJulien Gautier, Julien Gautier Neurophysiologie Clinique, Rééducation, Hôpital de la Salpêtrière, 47 boulevard de l'Hôpital, 75651 Paris cedex 13, FranceSearch for more papers by this authorMarion Simonetta-Moreau, Marion Simonetta-Moreau Neurophysiologie Clinique, Rééducation, Hôpital de la Salpêtrière, 47 boulevard de l'Hôpital, 75651 Paris cedex 13, FranceSearch for more papers by this authorEmmanuel Pierrot-Deseilligny, Corresponding Author Emmanuel Pierrot-Deseilligny Neurophysiologie Clinique, Rééducation, Hôpital de la Salpêtrière, 47 boulevard de l'Hôpital, 75651 Paris cedex 13, FranceCorresponding author E. Pierrot-Deseilligny: Rééducation, Hôpital de la Salpêtrière, 47 boulevard de l'Hôpital, F-75651 Paris cedex 13, France. Email: emmanuel.pierrot-deseilligny@chups.jussieu.frSearch for more papers by this author Philippe Marque, Philippe Marque Neurophysiologie Clinique, Rééducation, Hôpital de la Salpêtrière, 47 boulevard de l'Hôpital, 75651 Paris cedex 13, FranceSearch for more papers by this authorGuillaume Nicolas, Guillaume Nicolas Neurophysiologie Clinique, Rééducation, Hôpital de la Salpêtrière, 47 boulevard de l'Hôpital, 75651 Paris cedex 13, FranceSearch for more papers by this authorVéronique Marchand-Pauvert, Véronique Marchand-Pauvert Neurophysiologie Clinique, Rééducation, Hôpital de la Salpêtrière, 47 boulevard de l'Hôpital, 75651 Paris cedex 13, FranceSearch for more papers by this authorJulien Gautier, Julien Gautier Neurophysiologie Clinique, Rééducation, Hôpital de la Salpêtrière, 47 boulevard de l'Hôpital, 75651 Paris cedex 13, FranceSearch for more papers by this authorMarion Simonetta-Moreau, Marion Simonetta-Moreau Neurophysiologie Clinique, Rééducation, Hôpital de la Salpêtrière, 47 boulevard de l'Hôpital, 75651 Paris cedex 13, FranceSearch for more papers by this authorEmmanuel Pierrot-Deseilligny, Corresponding Author Emmanuel Pierrot-Deseilligny Neurophysiologie Clinique, Rééducation, Hôpital de la Salpêtrière, 47 boulevard de l'Hôpital, 75651 Paris cedex 13, FranceCorresponding author E. Pierrot-Deseilligny: Rééducation, Hôpital de la Salpêtrière, 47 boulevard de l'Hôpital, F-75651 Paris cedex 13, France. Email: emmanuel.pierrot-deseilligny@chups.jussieu.frSearch for more papers by this author First published: 01 October 2001 https://doi.org/10.1111/j.1469-7793.2001.t01-1-00313.xCitations: 33 Author's present address: M. Simonetta-Moreau: INSERM U 455, Toulouse, France. AboutSectionsPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Abstract 1 Group I projections from intrinsic plantar muscles to motoneurones (MNs) of human leg and thigh muscles were investigated. Changes in firing probability of single motor units (MUs) in the tibialis anterior (TA), peroneus brevis (Per brev), soleus (Sol), gastrocnemius medialis (GM), vastus lateralis (VL), semitendinosus (ST) and biceps (Bi) were studied after electrical stimuli applied to: (i) the tibial nerve (TN) at ankle level, (ii) the corresponding homonymous nerve, and (iii) the skin of the heel, to mimic the TN-induced cutaneous sensation. 2 Homonymous facilitation, attributable to monosynaptic Ia excitation, was found in all the sampled units. Early heteronymous excitation elicited by TN stimulation was found in many MUs. Later effects (3–5 ms central delay) were bigger and more frequently observed: excitation in most TA and Per brev MUs, and inhibition in most Sol, GM and Bi MUs and in many ST and VL MUs. The low threshold (∼0.5–0.6 × motor threshold) and the inability of a pure cutaneous stimulation to reproduce these effects (except the late excitation in TA MUs) indicate that they were due to stimulation of group I muscle afferents. 3 The early excitation was accepted to be monosynaptic when its central delay differed from that of the homonymous Ia excitation by less than 0.5 ms. Such a significant TN-induced monosynaptic Ia excitation was found in MUs belonging to all leg and thigh motor nuclei tested. Although its mean strength was relatively weak, it is argued that these monosynaptic connections might affect already depolarized MNs. 4 The late excitation found in TA and Per brev MUs is argued to be mediated through interneurones located rostral to MNs. 5 The late suppression, found in most Sol, GM and Bi MUs, and in many ST and VL MUs, was the dominant effect. It was accompanied by an inhibition of the Sol and quadriceps H reflexes at rest, and therefore reflects an inhibition directed to MNs. Its long latency is argued to reflect transmission by interneurones located rostral to MNs (the inhibitory counterpart of non-monosynaptic excitation). 6 The functional implications of these connections are discussed with respect to the requirements of the stance phase of human walking and running. In man, large stretch responses, due to activation of homonymous Ia and group II afferents, are elicited in the flexor digitorum brevis (FDB) by perturbation of stance (Schieppati et al. 1995; Corna et al. 1995; Schieppati & Nardone, 1997). The question then arises whether muscle spindle afferent discharges from intrinsic plantar muscles are confined to homonymous pathways or have more extensive projections through heteronymous monosynaptic connections of Ia afferents and/or interneurones co-activated by group I and group II afferents. Heteronymous monosynaptic Ia connections are indeed much more widespread in the human lower limb than in the cat (Eccles et al. 1957) or the baboon (Hongo et al. 1984) hindlimb; whereas in the latter species they mainly link motoneurones (MNs) of muscles acting synergistically at the same joint, transjoint Ia connections between ankle and knee muscles are almost the rule in humans (Meunier et al. 1993). This is probably to provide the more elaborate reflex assistance required in bipedal stance and gait. The first aim of the present study was therefore to investigate the extent to which such a broadening of transjoint monosynaptic Ia connections in humans also concerns projections from intrinsic plantar muscles. In addition, leg and thigh muscles in man are linked by an oligosynaptic group I excitation, which also has a very diffuse pattern of distribution, since stimulation of the femoral, the posterior tibial or the common peroneal nerve is able to elicit this effect in all leg and thigh muscles tested (Chaix et al. 1997). This oligosynaptic group I excitation is mediated through interneurones presumably located rostral to MNs (Chaix et al. 1997) and controlled by inhibitory interneurones facilitated by corticospinal volleys (Marchand-Pauvert et al. 1999). The second aim of the present investigation was to investigate: (i) the extent to which group I volleys from intrinsic plantar muscles elicit oligosynaptic facilitation–or suppression–in MNs supplying proximal muscles, as already shown for tibial nerve-induced inhibition- facilitation of gastrocnemius-soleus (GS) MNs (Abbruzzese et al. 1996); and (ii) in the case of suppression, whether it reflects a direct inhibition of MNs (inhibitory postsynaptic potentials (IPSPs) in MNs) or their disfacilitation (i.e. inhibition of pre-motoneurones mediating excitation to the MNs). METHODS The experiments were carried out on nine healthy subjects (aged 22–65 years), all of whom gave written informed consent (obtained according to the Declaration of Helsinki) to the experimental procedure, which was approved by the institutional ethics committee. The subjects were seated in an armchair and the examined leg was loosely fixed with the hip semi-flexed (120 deg), the knee slightly flexed (160 deg) and the ankle at 110 deg plantar flexion. Recording The EMG was recorded by surface electrodes 1 cm apart: either 0.8 cm2 silver plates or differential electrodes DE-2.3 (Delsys Inc., Boston, USA). They were secured to the skin over the corresponding muscle belly: quadriceps (Q; vastus lateralis (VL) and vastus intermedius (VI), 25–30 and 5–10 cm above the patella, on the lateral and anterior aspect of the thigh, respectively), biceps femoris (Bi), semitendinosus (ST), soleus (Sol), gastrocnemius medialis (GM), peroneus brevis (Per brev) and tibialis anterior (TA). Motor units (MUs) in flexor digitorum brevis (FDB) and flexor hallucis brevis (FHB) were also recorded to calculate the conduction velocity (CV) in the fastest Ia afferents in the tibial nerve. Subjects were instructed to perform a weak tonic voluntary contraction (strength below 5 % of maximal voluntary force) and to maintain it long enough (up to several hours in some experiments) to investigate changes in firing probability of the same MU with various stimulus intensities. Conditioning stimuli Electrical pulses of 1 ms duration were delivered through: (i) 1.5 cm diameter bipolar surface electrodes 1.5 cm apart (AG/AGCL, Niko, UK) to stimulate the tibial nerve (TN) at ankle level behind the medial malleolus, and the common peroneal nerve (CPN) at the level of the caput fibulae; (ii) half-ball electrodes 2 cm apart to stimulate the sciatic nerve at the upper part of the posterior aspect of the thigh; and (iii) unipolar electrodes to stimulate the femoral nerve (FN, active cathode in the femoral triangle, anode on the posterior aspect of the thigh) and the posterior tibial nerve (PTN, active cathode in the popliteal fossa, anode on the anterior aspect of the knee). The intensity of the nerve stimuli was expressed as multiples of the motor threshold (× MT). Cutaneous stimuli The cutaneous sensation (weak local and/or radiating paraesthesia) evoked by TN stimulation was mimicked by pure cutaneous stimuli to estimate the contribution of cutaneous afferents. The local sensation was reproduced by surface electrodes (AG/GCL) placed on the lateral and medial parts of the heel and the radiating paraesthesia by plate electrodes placed over the nerve projection area (big toe), allowance being made for the extra peripheral conduction time. The stimulus intensity was adjusted to imitate the sensation evoked by TN stimulation, and it was often impossible for the subject to make the distinction between the sensation elicited by TN stimulation and this pure cutaneous stimulation. Study of single motor units Method of post-stimulus time histogram (PSTH). The EMG potentials of single MUs recorded with surface electrodes were converted into standard pulses by a discriminator with variable trigger levels and these were fed to a computer which subsequently triggered the stimulators about once every 0.7 s. Stimuli were delivered in relation to the MU discharge to avoid the period of after-hyperpolarisation. PSTHs of MUs from various thigh (VL, Bi, ST) and leg (Sol, GM, TA, Per brev) muscles were constructed for the 20–90 ms following a conditioning stimulation (0.5 ms bin width). Histograms of the firing probability were constructed after the conditioning stimulus (□ in the left panels of 1-4) and in a control situation without stimulation (▪ in the left panels of 1-4). Figure 1Open in figure viewerPowerPoint Conduction velocity in tibial nerve Ia afferents between ankle and knee levels Post-stimulus time histograms (PSTHs, 0.2 ms bin width) of a flexor digitorum brevis (FDB) unit after stimulation of the tibial nerve (TN) at ankle level (1 × MT; A and B) and of the posterior tibial nerve (PTN) at knee level (0.7 × MT; C and D). The histograms in A and C show discharges of the voluntary activated MU under control conditions (▪) and after stimulation of the nerve (□). The differences between these two histograms, expressed as a percentage of the number of triggers, are plotted in B and D ( ) against the latency from the stimulation. Vertical dotted lines indicate the latency of the peaks. The difference between the latencies of the peak of excitation elicited by stimulation of the TN at ankle (B, 53.6 ms) and PTN at knee (D, 46.4 ms) levels was 7.2 ms. Distance between ankle and knee electrodes, 42 cm. Figure 2Open in figure viewerPowerPoint Changes in firing probability of a tibialis anterior MU after stimulation of the homonymous and heteronymous group I and cutaneous afferents Comparison of PSTHs (0.5 ms bin width) of a tibialis anterior (TA) MU after stimulation of the homonymous Ia afferents in the common peroneal nerve (CPN) at knee level (0.8 × MT; A and B), of the TN at ankle level at 1 × MT (C and D), 0.8 × MT (E and F), 0.6 × MT (G and H) and 0.4 × MT (I and J), and of the skin of the heel to mimic the cutaneous sensation elicited by the TN at 0.8 × MT (K and L). Abscissa and ordinate, and column symbols as in Fig. 1. Vertical dotted lines indicate the latency of the peaks: homonymous, 42 ms (P < 0.001; B); heteronymous, 48 ms (P < 0.001; D). Distance between ankle and knee stimulation sites and L2 vertebra: 97 and 70 cm, respectively. CV in the fastest Ia afferents in the CPN and TN: 68 and 60 m s−1, respectively. The vertical dashed line indicates the latency of the 'late' excitation (51 ms; D, F and H). Figure 3Open in figure viewerPowerPoint Changes in firing probability of a peroneus brevis MU after stimulation of the homonymous and heteronymous group I and cutaneous afferents Comparison of PSTHs (0.5 ms bin width) of a peroneus brevis (Per brev) MU after stimulation of the homonymous Ia afferents in the CPN at knee level (0.8 × MT; A and B), of the TN at ankle level at 1 × MT (C and D) and at 0.8 × MT (E and F), and of the skin of the heel, to mimic the cutaneous sensation elicited by the TN at 0.8 × MT (G and H). Abscissa and ordinate, and column symbols as in Fig. 1. Vertical dotted lines indicate the latency of the peaks: homonymous, 46.5 ms (P < 0.001; B); heteronymous, 53 ms (P < 0.01; D). Distance between ankle and knee stimulation sites and L2 vertebra: 97 and 65 cm, respectively. CV in the fastest Ia afferents in the CPN and TN: 68 and 60 m s−1, respectively. Same subject as in Fig. 2. The difference in latencies of heteronymous and homonymous peaks (53–46.5 = 6.5 ms) can be entirely explained by the difference in afferent conduction times (0.97/60–0.65/68 = 6.6 ms). Figure 4Open in figure viewerPowerPoint Changes in firing probability of a soleus MU after stimulation of the homonymous and heteronymous group I and cutaneous afferents Comparison of PSTHs (0.5 ms bin width) of a soleus (Sol) MU after stimulation of the homonymous Ia afferents in the PTN at knee level (0.7 × MT; A and B), of the TN at ankle level at 1 × MT (C and D) and at 0.8 × MT (E and F), and of the skin of the heel, to mimic the cutaneous sensation elicited by the TN at 0.8 × MT (G and H). Abscissa and ordinate, and column symbols as in Fig. 1. Distance between ankle and knee stimulation sites and L2 vertebra: 97 and 56 cm, respectively. CV in the fastest Ia afferents in the PTN and TN: 66 and 58 m s−1, respectively. Vertical dotted lines indicate the latency of the homonymous peak (38 ms, P < 0.001; B) and the estimated monosynaptic heteronymous latency (46 ms, 38 + 8 {0.97/58–0.56/66}; D and F). The vertical dashed line indicates the latency of the inhibition (49.5 ms). Organisation of the experiments. The control situation without stimulation, stimulation of the homonymous nerve (FN, sciatic, PTN or CPN), of the TN at ankle level and cutaneous stimulation mimicking the cutaneous sensation evoked by TN stimulation were randomly alternated in the same sequence so that the TN-induced changes in firing probability were always compared to those elicited by stimulation of the homonymous nerve and by stimulation of cutaneous afferents recorded under the same conditions. To clarify the differences between the results obtained in control and conditioned situations the control value in each bin was subtracted from that observed after conditioning stimulation ( in 1-6, in which the number of counts in each bin is expressed as a percentage of the total number of corresponding stimuli delivered during the sequence). The exceptional sequences in which a change in the control sequence significantly contributed to the differences seen between the two situations were not retained for further analysis. Figure 5Open in figure viewerPowerPoint Changes in firing probability of a gastrocnemius medialis MU after stimulation of the homonymous and heteronymous group I and cutaneous afferents Comparison of PSTHs (0.5 ms bin width) of a gastrocnemius medialis (GM) MU after stimulation of the homonymous Ia afferents in the PTN at knee level (0.7 × MT; A), of the TN at ankle level at 0.8 × MT (B), 0.5 × MT (C) and 0.4 × MT (D), and of the skin of the heel, to mimic the cutaneous sensation elicited by the TN at 0.8 × MT (E). Abscissa and ordinate as in Fig. 1. Only the differences between conditioned and control histograms are shown ( ). Vertical dotted lines indicate the latency of the peaks: homonymous, 35 ms (P < 0.001; A); heteronymous, 43 ms (P < 0.01; B). Distance between ankle and knee stimulation sites and L2 vertebra: 97 and 57 cm, respectively. CV in the fastest Ia afferents in the PTN and TN: 65 and 58 m s−1, respectively. Same subject as in Fig. 4. The difference in latencies of heteronymous and homonymous peaks (43–35 = 8 ms) can be entirely explained by the difference in afferent conduction times (0.97/58–0.57/65 = 8 ms). Figure 6Open in figure viewerPowerPoint Changes in firing probability of a vastus lateralis MU after stimulation of the homonymous and heteronymous group I and cutaneous afferents Comparison of PSTHs (0.5 ms bin width) of a vastus lateralis (VL) MU after stimulation of the homonymous Ia afferents in the femoral nerve (FN) at hip level (0.7 × MT, A), of the TN at ankle level at 0.8 × MT (B), 0.6 × MT (C) and 0.4 × MT (D), and of the skin of the heel, to mimic the cutaneous sensation elicited by the TN at 0.8 × MT (E). Abscissa and ordinate as in Fig. 1. Only the differences between conditioned and control histograms are shown ( ). Vertical dotted lines indicate the latency of the peaks: homonymous, 33 ms (P < 0.001; A); heteronymous, 48.5 ms (P < 0.05; B). Distance between TN and FN stimulation sites and L2 vertebra: 112 and 26 cm, respectively. CV in the fastest Ia afferents in the FN and TN: 60 and 58 m s−1, respectively. Same subject as in Fig. 1. The difference in latencies of heteronymous and homonymous peaks (48.5–33 = 15.5 ms) differed by only 0.5 ms from the difference in afferent conduction times (1.12/0.58–0.26/0.60 = 15 ms). Statistical analysis. The statistical analysis of changes in firing probability was confined to a window that (i) started with the time of arrival at MN level of the TN (or homonymous) fastest Ia volley (estimated from the CV in Ia afferents and the distance from the stimulation site to L2 vertebra, see below), and (ii) lasted for 12 ms to avoid contamination by the long-latency M2 response (see Marsden et al. 1983). Within this window of analysis, each group of consecutive bins exhibiting an increase (or a decrease) in firing probability was grouped together and tested with a χ2 test to determine the extent to which the distribution of firing probability after stimulation within this group differed from that in the control situation. A peak of excitation (or a trough of suppression) was accepted if there was a significant (at least P < 0.05) increase (or decrease) in firing probability in a group of adjacent bins (a single bin was admitted for the peak of monosynaptic Ia excitation, as in Fig. 5B). The latency of the first bin of the increased (or decreased) firing probability was taken to be the latency of the excitation (or inhibition) provided that the probability was significantly changed in this bin or in the first group of two or three adjacent bins. Although the relation between the amplitude of a peak (or a trough) in the PSTH and that of the underlying excitatory postsynaptic potential (EPSP) (or IPSP) is complex (see Gustafsson & McCrea, 1984), the larger the EPSP the higher the peak (and the more profound the IPSP the larger the trough). Thus, the size of the peak (or the trough) was estimated as the sum of the differences (conditioned–control counts) in the different consecutive bins with increased (or decreased) firing probability contributing to a given peak or trough, e.g. there was a peak of 10.5 % between 51 and 53.5 ms in Fig. 2D, or a trough of 10 % between 49.5 and 56.5 ms in Fig. 4D. Homonymous Ia facilitation. Changes in firing probability were always studied after stimulation of the nerve containing the afferents from the muscle investigated (referred to as the 'homonymous' nerve): FN for VL, sciatic nerve for ST and Bi, PTN for Sol and GM, and CPN for TA and Per brev. Stimulation of the 'homonymous' nerve at 1 × MT, or usually below in order not to elicit a compound H reflex, always evoked an early increase in firing probability. After correction for the trigger delay (delay between the real onset of the MU potential and the onset of the triggered pulse), the actual latency of this early peak was identical to that of the H reflex in the corresponding muscle, obtained at rest (Sol, VL) or during voluntary contraction. This early peak can therefore be attributed to the monosynaptic Ia EPSP (Mao et al. 1984). Procedure used to define coupling (mono- or oligosynaptic) of the heteronymous effects. The same procedure was used as in previous studies (Meunier et al. 1990, 1993). Latencies of the early facilitation evoked in the same MU by stimulation of the homonymous nerve and of the TN were compared. Since the efferent conduction times were identical (same MU), the difference between the two latencies must reflect the difference in the afferent conduction times and/or in the central (synaptic) delay of the Ia effects evoked by homonymous and heteronymous stimulation. If, like homonymous, heteronymous excitation is mediated through a monosynaptic pathway, the difference in latency between heteronymous and homonymous excitations should be entirely explained by the difference in afferent conduction times. Latency of non-monosynaptic events. This was measured from the heteronymous monosynaptic Ia latency. In MUs in which there was no heteronymous monosynaptic Ia peak, heteronymous latency was estimated as the following sum: homonymous monosynaptic Ia latency + the difference in afferent conduction times between TN and homonymous Ia volleys from stimulation sites to the spinal cord. Afferent conduction times. Differences in afferent conduction times for the fastest Ia homonymous and TN volleys were estimated from: (i) the distance from stimulation sites of the electrodes eliciting the afferent volleys (homonymous or TN) to the L2 vertebra (entrance in the spinal cord) measured on the skin of the lower limb, and (ii) the CV in Ia afferents. The CV in Ia afferents in the TN was calculated from the latency of the monosynaptic Ia peaks measured in the PSTH of the same FDB or FHB MU after stimulation of Ia afferents at knee and ankle levels using 0.2 ms bins (see Fig. 1, and Appendix in Hultborn et al. 1987). Those in the CPN, PTN, FN and sciatic nerve had been already and similarly calculated for most subjects from the latency of the monosynaptic Ia peaks measured in the PSTH of the same MU in the corresponding muscle after stimulation of homonymous Ia afferents (Meunier et al. 1993; Simonetta-Moreau et al. 1999). H reflex studies Experiments using the H reflex in Sol and Q (VI) muscles were performed to investigate whether results obtained with PSTH tests could also be obtained in the absence of voluntary contraction. This was particularly important in the case of a decrease in firing probability in PSTHs to distinguish between inhibition or disfacilitation of the MNs (see Discussion). The Sol and Q H reflexes were obtained by unipolar stimulation of the PTN and FN, respectively. Because the sensitivity of H reflexes of small size varies with the amplitude of the unconditioned reflex (Crone et al. 1990), the size of the unconditioned reflex was adjusted to between 15 and 30 % of the maximum M wave. The reflex responses were measured as the peak-to-peak amplitude of muscle action potentials. In each experimental run, 20 control and 20 conditioned reflexes were randomly alternated for each conditioning-test interval. Conditioned reflexes were expressed as a percentage of control reflexes. An F test (Scheffé's test) was used to determine whether the changes evoked by the conditioning stimulation were significant. RESULTS Conduction velocity of Ia afferents from intrinsic plantar muscles As explained in Methods, the evidence that heteronymous projections of Ia afferents from intrinsic plantar muscles to MNs supplying proximal muscles are monosynaptic relies on the fact that the difference between the latencies of the peaks of excitation elicited by stimulation of heteronymous Ia afferents in the TN at ankle level and of homonymous Ia afferents can be entirely explained by the difference in afferent conduction times of the two volleys. It was therefore necessary to assess the CV in Ia afferents in the TN. To that end, homonymous monosynaptic Ia projections to MNs of FDB and FHB were used. The latencies of the peaks of homonymous Ia excitation elicited in the same FDB or FHB MU by stimulation of Ia afferents in the TN at ankle level and in the PTN at knee level were therefore compared, using 0.2 ms bins. Given that the peak elicited by PTN stimulation was larger than that evoked by TN stimulation and that increasing the PTN stimulation invariably resulted in a H reflex in short flexors of the toes, it can be assumed that the PTN-induced peak was mainly due to stimulation of Ia afferents from intrinsic plantar muscles. An example of the results obtained in a FDB MU is shown in Fig. 1. The difference between the latencies of the peaks elicited by stimulation of the TN (Fig. 1A and B) and PTN (Fig. 1C and D) was 7.2 ms, and the distance between the electrodes was 42 cm. This gave a CV of 58 m s−1 (0.42/0.0072). Similar measurements were performed in 20 MUs (8 subjects). The mean value (±s.e.m.) was 58 ± 0.8 m s−1 (range, 53–60 m s−1) for the fastest Ia afferents in the TN, thus significantly less than the mean values found by Meunier et al. (1993) for the fastest Ia afferents in the PTN (65 m s−1) or the CPN (68 m s−1). It is of interest that in the baboon lower limb the CV in Ia afferents from intrinsic plantar muscles is similarly slower (Hongo et al. 1984). Early excitations compatible with a monosynaptic heteronymous Ia connection will be first considered. Early heteronymous excitation from intrinsic plantar foot muscles in single units Evidence for monosynaptic heteronymous Ia excitation of tibialis anterior MUs The effects elicited by various stimuli in a TA MU are illustrated in Fig. 2. Stimulation of the CPN (0.8 × MT) at knee level (in a distal position close to the tibial crest to favour stimulation of TA fibres) elicited a highly significant (P < 0.001) peak of homonymous Ia excitation at a latency of 42 ms (Fig. 2A and B). After correction for the trigger delay of the MU (5 ms, see Methods), this latency exactly corresponded to that of the TA H reflex of this subject (37 ms), and can therefore be attributed to a monosynaptic Ia EPSP (Mao et al. 1984). Heteronymous stimulation of the TN (1 × MT) at ankle level elicited a highly significant (P < 0.001) peak of excitation that occurred at a latency of 48 ms (Fig. 2C and D), i.e. 6 ms later than the peak of homonymous Ia excitation, and lasted for 2 ms. The distances from CPN and TN stimulation to the L2 vertebra were 70 and 97 cm, respectively. Given that, in this subject, the CV for the fastest Ia afferents in the CPN and TN were measured at 68 and 60 m s−1, respectively, the supplementary peripheral conduction time for the TN volley should be at least 5.87 ms (0.97/60–0.70/68). This entirely accounts for the 6 ms difference in the latency of the two peaks of excitation, and thus strongly suggests that the heteronymous and homonymous excitations had the same central delay, i.e. that the heteronymous connection also corresponds to a monosynaptic linkage. When the stimulus intensity was decreased to 0.8 × MT (Fig. 2E and F) and 0.6 × MT (Fig. 2G and H), a smaller but still significant (P < 0.01 and 0.05, respectively) TN-induced heteronymous excitation persisted within the window 48.5–50.5 ms, but disappeared at 0.4 × MT (Fig. 2I and J), attesting that the threshold of the heteronymous excitation was low (within the range found for human group I afferents; Meunier et al. 1990, 1993). Note that the decrease in the underlying EPSP, attested by the reduction of the peak, was then accompanied by an increase in the latency