Group Ia Fibers Research Articles

Afferent-mediated modulation of the soleus muscle activity during the stance phase of human walking

The aim of this study was to investigate the contribution of proprioceptive feedback to the amplitude modulation of the soleus muscle activity during human walking. We have previously shown that slow-velocity, small-amplitude ankle dorsiflexion enhancements and reductions applied during the stance phase of the step cycle generate, respectively, increments and decrements on the ongoing soleus activity. We have also shown that the increments in soleus activity are at least partially mediated by feedback from group Ia fibres. In the present study, we further investigated the afferent-mediated contribution from muscle group II afferents, cutaneous and proprioceptive afferents from the foot, and load-sensitive afferents to the soleus EMG. Slow-velocity, small-amplitude ankle trajectory modifications were combined with the pharmaceutical depression of group II polysynaptic pathways with tizanidine hydrochloride, anaesthetic blocking of sensory information from the foot with injections of lidocaine hydrochloride, and modulation of load feedback by increasing and decreasing the body load. The depression of the group II afferents significantly reduced the soleus response to the ankle trajectory modifications. Blocking sensory feedback from the foot did not have an effect on the soleus muscle activity. Changes in body load affected the ongoing soleus activity level; however, it did not affect the amplitude of the soleus EMG responses to the ankle trajectory modifications. These results suggest that the feedback from group II afferents, and possibly from load-sensitive afferents, contribute to the amplitude modulation of the soleus muscle activity during the stance phase of the step cycle. However, feedback from cutaneous afferents and instrinsic proprioceptive afferents from the foot does not seem to contribute to this muscle activation.

Discharge of group Ia fibers innervating tail muscles during passive tail movements in cats.

Discharge of group Ia fibers innervating tail muscles during passive tail movements in cats.

Effects of transcranial magnetic stimulation to the reciprocal Ia inhibitory interneurones in the human wrist.

In humans, which neural volleys strongly activate the reciprocal Ia inhibitory interneurones have not been clarified via the corticospinal tract or from the muscle spindles. We examined the inhibition from the corticospinal tract and antagonist group Ia fibres to alpha motoneurone pools using the combined method of transcranial magnetic stimulation (TMS) and the standard H-reflex technique. The test stimulus for the forearm H-reflex and the conditioning stimulus to antagonist muscle afferents were applied to the median and radial nerves, respectively. The transcranial magnetic stimulation was applied noninvasively over the left motor cortex. The radial nerve conditioning strongly suppressed the H-reflex rather than the transcranial magnetic stimulation. Transcranial magnetic stimulation-induced inhibition was disinhibited by the conditioning stimulus applied to the median nerve. To estimate the subliminal inhibition produced by the transcranial magnetic stimulation, we used the following method: the radial nerve conditioning was altered among several different intensities, while transcranial magnetic stimulation intensity was fixed at that for which transcranial magnetic stimulation-induced inhibition was observable. A minor subliminal inhibition was observed. These results suggest that the corticospinal excitatory inputs to reciprocal Ia inhibitory interneurones in the human wrist are very weak relative to those of the originating group I muscle afferents.

The complex role of spindle afferent input, as evidenced by the study of posture control in normal subjects and patients

This report reviews recent findings from our laboratory on the connectivity of the group II spindle afferent input and the role played by these afferents in the control of quiet and perturbed human stance. At variance with group Ia fibres, which subserve the monosynaptic stretch reflex, the group II fibres, after having entered the spinal cord, make synamptic contacts with a short chain of interneurons which impinge on homonymous motoneurons. Analysis of the short- and medium-latency responses evoked in foot and leg muscles by perturbations of upright stance under different experimental conditions has revealed a role of group II fibres in the production of the medium-latency response. The conduction velocity of group II spindle afferent fibres and their central delay have also been estimated. Furthermore, data from normal subjects and from neuropathic and hemiparetic patients are in favour of a prevailing role of the input from group II fibres in the afferent control of quiet and perturbed stance. Since Ia fibres innervate receptors more sensitive to the veolocity of muscle stretch, and II fibres innervate receptors more sensitive to the absolute value of muscle length, it is hypothesised that the major role of the latter in the reflex control of stance reflects the slow velocity and amplitude of sway during quiet upright posture. Indirect evidence supports the conclusion that, also in humans, monoaminergic descending pathways from brainstem nuclei modulate the excitability of the circuits mediating the group II input.

The effect of fatigue caused by electrical induction or voluntary contraction on Ia inhibition in human soleus muscle

A comparison of the effect of fatigue caused by electrical induction or voluntary contraction on Ia inhibition in human soleus muscle was investigated in fourteen healthy male subjects. The Hoffmann reflex (H reflex) was employed to elucidate the contribution of fatigue induced contraction to the Ia inhibition. A statistically significant difference ( P < 0.05) in H reflex amplitude between the intermittent stimulation at 15 Hz and voluntary contraction was observed. Our study suggested that Ia inhibition in human soleus muscle, caused by electrically induced or voluntary contraction, induced differences in the number of impulses in the group Ia fibers, between the two conditions.

An in vivo pharmacological study of single group Ia fibre contacts with motoneurones in the cat spinal cord.

1. Direct experimental evidence was obtained on the spatial distribution of active synaptic contacts from single Ia muscle afferents on the dendrites of lumbosacral motoneurones in anaesthetized cats. 2. An extracellular micropipette was used to pressure eject the AMPA/kainate receptor antagonists 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) or 2,3-dihydroxy-6-nitro-7-sulphamoyl-benzo(F)quinoxaline (NBQX) in close proximity to the intracellular recording site, in order to create an extracellular concentration gradient of the antagonist. The effect of antagonist ejection on the time course and amplitude of excitatory postsynaptic potentials (EPSPs) evoked in motoneurones by impulses in single group Ia fibres was examined. 3. Pressure ejection of NBQX resulted in a complete block of the monosynaptic group Ia EPSP in two cells, and a significant reduction to 23-57% of control EPSP peak amplitudes in a further six cells (mean, 27%; n = 8). These effects were not associated with changes in membrane potential or membrane time constant. 4. The reduction in amplitude of these single group Ia fibre EPSPs following ejection of NBQX was usually accompanied by a pronounced slowing in the time course of the EPSPs. On average, the EPSP rise times and half-widths were increased by 269 and 37%, respectively. This is most probably due to a considerable spatial spread of the synaptic contacts along the dendrites of motoneurones, with the most proximal synaptic contacts (producing the briefest synaptic potentials) subjected to a greater reduction in amplitude due to a higher local antagonist concentration. 5. An equivalent dendritic cable model of the motoneurone was used to interpret the observed changes in the time course of single fibre EPSPs. The time course of control single fibre EPSPs examined in the present study could be well matched using the cable model and assuming a single location for synaptic input. The observation of a slowed EPSP time course following antagonist ejection indicated that this assumption was not correct and that there was in fact considerable spatial spread in the synaptic contacts arising from these single afferent fibres. These results provide direct evidence that spatial spread of synaptic input may not be detected using the time course of a synaptic potential in conjunction with a neuronal cable model of the postsynaptic cell.

Crossed and uncrossed projections to cat sacrocaudal spinal cord: II. Axons from muscle spindle primary endings

The terminal fields of primary afferent fibers from tail muscle spindle primary endings were mapped within cat sacrocaudal spinal cord (S3-Ca7), using intra-axonal recording and horseradish peroxidase staining techniques. We sought to determine the ipsilateral and contralateral projection patterns and to relate these to the fibers' muscles of origin. Fifty-three group Ia fibers were successfully stained. Segmental collaterals originated from either the ascending or descending branch within the dorsal columns. Collaterals coursed rostromedially within the dorsal columns and traversed the medial aspect of the dorsal horn. Ipsilateral terminations were similar for all fibers. Within the ventral horn, boutons were consistently observed in the medial or central portions of lamina VII. In lamina VIII, a variable number of boutons was seen on fine branches emerging from larger fibers coursing ventrally. Clusters of terminals were plentiful in the regions of motoneurons, i.e., lamina IX and the nucleus commissuralis. Terminals were found in the adjacent white matter. In addition to ipsilateral terminations, some group Ia fibers (20 of 53) had collateral branches that crossed ventrally to the central canal, terminating within the midline ventral gray commissure and/or the contralateral ventral horn. Crossed projections always originated in medial (dorsal or ventral), but not lateral, muscles of the tail. These data suggest that ipsilateral projections of group Ia fibers make connections on sacrocaudal motoneurons, on neurons mediating segmental reflex functions and on neurons conveying ascending information. It is speculated that crossed and uncrossed connections between group Ia fibers from medial muscles and bilateral dendritic trees of motoneurons subserve synchronized co-contraction of synergistic muscles located on the two sides of the body, such as with dorsal or ventral flexion of the tail. Group Ia projections from lateral muscles, that are entirely ipsilateral, would be involved with lateral movements of the tail.

Cutaneous nerve-evoked cholinergic inhibition of monosynaptic reflex in the neonatal rat spinal cord: Involvement of M 2 receptors and tachykininergic primary afferents

The mechanisms of a cutaneous nerve-evoked inhibition of monosynaptic reflex were investigated in an isolated spinal cord-peripheral nerve preparation of the neonatal rat. Conditioning stimulation of the saphenous nerve, with five pulses at 50 Hz and a strength sufficient to activate C fibers, evoked an inhibition lasting about 20 s of the monosynaptic reflex that was elicited by stimulation of the nerve branch to quadriceps femoris muscle and recorded from the L3 ventral root. This inhibition of monosynaptic reflex was potentiated by an anticholinesterase, edrophonium, and mostly blocked by atropine. Application of acetylcholine, muscarine, bethanechol, carbachol, arecoline and oxotremorine induced an inhibition of monosynaptic reflex. From the effects of muscarinic antagonists, pirenzepine, AF-DX 116, and 4-diphenylacetoxy- N-methylpiperidine on the agonist-evoked and primary afferent-evoked inhibition of monosynaptic reflex it was concluded that the muscarinic receptors involved in the cutaneous nerve-evoked inhibition of monosynaptic reflex are of M 2 type. When monosynaptic reflexes were evoked by two successive stimuli with intervals of 15 ms to 1 s, the second response was smaller than the first. This depression of monosynaptic reflex became less pronounced when the reflex was reduced by application of oxotremorine or arecoline or by conditioning stimulation of primary afférents, suggesting that the inhibition of monosynaptic reflex is presynaptic in nature. The late phase of the cutaneous nerve-evoked inhibition of monosynaptic reflex (5–20 s after conditioning stimulation) was markedly depressed by a tachykinin antagonist, spantide. Perfusion of the spinal cord with capsaicin (1 μM) for 1 h also abolished the late phase of the inhibition. Application of capsaicin or substance P to the spinal cord induced an inhibition of monosynaptic reflex, and the inhibition was antagonized by spantide and atropine. Measurements of acetylcholine content in the perfusate of isolated rat spinal cords demonstrated that bath-applied substance P evoked a release of acetylcholine from spinal neurons. These results suggest that tachykininergic primary afferent C fibers excite cholinergic spinal neurons and the released acetylcholine inhibits the monosynaptic reflex by acting on the presynaptic muscarinic receptors on group Ia fibers.

Carbonic anhydrase activity in the peripheral nervous system of rat: the enzyme as a marker for muscle afferents

The distribution of carbonic anhydrase (CA) activity was determined histochemically using Hansson's cobalt phosphate method in cross-sections of peripheral nerves from rats. As the studied nerves contain either efferent, proprioceptive or exteroceptive myelinated fibres, our survey particularly focused on the question whether CA-reactive nerve fibres are functionally related. Intense CA activity was detected in all large diameter (8–12 μm) muscle afferents. The amount of similarly reactive cutaneous afferents was negligibly low (3.6%). Efferent fibres displayed only weak CA activity, which was confined to the small myelinated fibres (3–6 μm). Moderate staining could be assessed in medium-sized (4–11 μm) proprioceptive fibres. The same reactivity occurred in a sizeable percentage (11.4%) of exteroceptive afferents. Their diameters ranged from 4 to 11 μm. These results indicated, that high enzyme activity is found predominantly in large-calibre proprioceptive afferents, which according to Hunt's classification were identified as group IA and IB fibres. Further confirmation for our observations was obtained by demonstrating high levels of enzyme activity in primary nerve endings of muscle spindles (IA fibres) and in axon terminals of Golgi tendon organs (IB fibres) constantly. Finally possible functions for neuronal CA are discussed with respect to its high activity in a functionally related subpopulation of nerve fibres.

Modulation of EPSP amplitude during high frequency stimulation depends on the correlation between potentiation, depression and facilitation

High frequency bursts were delivered every 2 s to single group Ia fibers in anesthetized cats. The modulation of EPSP amplitude in target motoneurons was determined. Changes in EPSP amplitude during the high frequency stimulation (facilitation or depression) were correlated with those occurring 2 s after the burst (potentiation). Connections displaying high levels of potentiation exhibited more depression resulting in a net negative modulation. Negative amplitude modulation was greatest at connections on low rheobase (‘small’) motoneurons that develop large EPSPs. Positive modulation occurred at a subset of connections on high rheobase (‘large’) motoneurons that exhibit small EPSPs. We suggest that these synaptic properties permit the appropriate amount of depolarization to be delivered to the heterogenous elements of the motoneuron pool during high frequency Ia fiber activity characteristic of the step cycle.

PAD patterns of physiologically identified afferent fibres from the medial gastrocnemius muscle.

Intracellular recordings were made in the barbiturate-anesthetized cat from single afferent fibres left in continuity with the medial gastrocnemius muscle to document the transmembrane potential changes produced in functionally identified fibres by stimulation of sensory nerves and of the contralateral red nucleus (RN). Fifty five fibres from muscle spindles had conduction velocities above 70 m/s and were considered as from group Ia. Stimulation of group I afferent fibres of the posterior biceps and semitendinosus nerve (PBSt) produced primary afferent depolarization (PAD) in 30 (54%) Ia fibres. Stimulation of the sural (SU) nerve produced no transmembrane potential changes in 39 (71%) group Ia fibres and dorsal root reflex-like activity (DRRs) in 16 (29%) fibres. In 17 out of 28 group Ia fibres (60.7%) SU conditioning inhibited the PAD generated by stimulation of the PBSt nerve. Facilitation of the PBSt-induced PAD by SU conditioning was not seen. Repetitive stimulation of the RN had mixed effects: it produced PAD in 1 out of 8 fibres and inhibited the PAD induced by PBSt stimulation in 2 other fibres. Nine fibres connected to muscle spindles had conduction velocities below 70 m/s and were considered to be group II afferents. No PAD was produced in these fibres by SU stimulation but DRRs were generated in 5 of them. In 23 out of 31 fibres identified as from tendon organs group I PBSt volleys produced PAD. However, stimulation of the SU nerve produced PAD only in 3 out of 34 fibres, no transmembrane potential changes in 30 fibres and DRRs in 1 fibre. The effects of SU conditioning on the PAD produced by PBSt stimulation were tested in 19 Ib fibres and were inhibitory in 12 of them. In 9 of these fibres SU alone produced no transmembrane potential changes. Repetitive stimulation of the RN produced PAD in 3 out of 9 Ib fibres. SU conditioning inhibited the RN-induced PAD. The present findings support the existence of an alternative inhibitory pathway from cutaneous to Ib fibres, in addition to the well known excitatory pathway producing PAD. Possible functional implications of inhibitory actions of cutaneous fibres with the pathways mediating the PAD of group Ia and Ib fibres are discussed.

Amplitude modulation of EPSPs in motoneurons in response to a frequency- modulated train in single la afferent fibers

In anesthetized cats, single group Ia fibers were activated with a train of 52 stimuli whose interspike intervals were obtained from the discharge of a group Ia fiber in a walking cat (courtesy of Dr. G. E. Loeb, NIH). The EPSPs recorded in motoneurons to which the afferents projected were averaged in register (EPSP1, EPSP2, ..., EPSP52) in response to multiple presentations of the train at a rate (0.77 Hz) similar to the stepping rate of the cat. Amplitudes of these averaged EPSPs were found to be highly variable, depending both on afferent discharge rate and history of activation. The initial EPSP was generally potentiated, and EPSPs in the high-frequency (greater than 200 Hz) middle portion of the train were generally reduced in amplitude. Connections at which the first EPSP was most potentiated tended to be those which showed the most depression of EPSP amplitude during the high-frequency portion of the train. Thus, at some connections, modulation of EPSP amplitude during the frequency-modulated train was much greater than at other connections. In general, the extent of modulation was greater on low-rheobase motoneurons than on high-rheobase motoneurons. We suggest that these differences in transmission permit type S (i.e., low-rheobase) motoneurons, which on average generate the largest EPSPs, to reach threshold at low levels of input (size principle) but prevent excessive depolarization due to temporal summation during high-frequency stimulation.

Prolonged activation of alpha-motoneurons following electrical stimulation of group Ia fibres in anemically decerebrated cats

Prolonged activation of alpha-motoneurons following electrical stimulation of group Ia fibres in anemically decerebrated cats

Specific and nonspecific mechanisms involved in generation of PAD of group Ia afferents in cat spinal cord.

In the spinal cord of the anesthetized cat, we measured the changes in extracellular concentration of potassium ions [K+]e and the negative DC shifts produced by stimulation of muscle, cutaneous and mixed afferent nerves, together with alterations in the threshold of single group Ia fibers that were tested at the same site as the potassium measurements. This approach provided information on the extent to which the excitability changes of single Ia-fibers can be correlated with the changes in [K+]e occurring at the same site. Stimulation of the tibial (TIB) nerve and of the cutaneous sural (SU), and superficial peroneous (SP) nerve (100-Hz trains lasting 30-60 s) with stimulus strengths of 10-15 times threshold increased the concentration of [K+]e in the dorsal horn by 2-5 mmol/l above the resting value of 3 mmol/l. This was in clear contrast with the very small [K+]e increases produced at the same site during stimulation of muscle nerves, such as the posterior biceps and semitendinosus (PBSt), gastrocnemius soleus (GS), and deep peroneus (DP), which were generally smaller than 0.25 mmol/l. Stimulation of the PBSt and GS muscle nerves did produce small, but clear, increases of [K+]e (up to 0.3 mmol/l) in the region of the intermediate nucleus, where these fibers synapse with second order cells. These changes were nevertheless smaller than those produced at the same site by stimulation of the TIB, SU, and SP nerves. The peak amplitudes of the [K+]e transients produced by long-lasting 100-Hz trains applied to cutaneous and/or to muscle nerves showed a linear relationship with the amplitudes of the slow negative DC shifts, which were simultaneously recorded from the NaCl barrel of the potassium electrode assembly. Stimulus trains (100 Hz) applied to group I muscle afferents (PBSt and DP) very effectively reduced the threshold for intraspinal activation of individual group I GS fibers but produced negligible negative DC shifts at the same site. On the other hand, 100-Hz stimulus trains applied to the SU and SP nerves produced large negative DC shifts, even with low-stimulus strengths (2 X T, where T is threshold), but had much smaller effects on the threshold of group Ia GS fibers. Increasing the intensity of the stimuli applied to cutaneous and mixed nerves above 2 X T strength further reduced the threshold of the Ia-fibers.(ABSTRACT TRUNCATED AT 400 WORDS)

Sites of action of segmental and descending control of transmission on pathways mediating PAD of Ia- and Ib-afferent fibers in cat spinal cord.

The present series of investigations was aimed to disclose the possible sites of action of excitatory and inhibitory inputs on tho-interneuron pathway mediating the primary afferent depolarization (PAD) of group I afferents of extensor muscles in the cat spinal cord. To this end we compared the effects produced by stimulation of segmental and descending pathways on the PAD generated either by stimulation of group I fibers of flexor muscles or by intraspinal microstimulation. It was assumed that under the appropriate conditions the PAD produced by intraspinal microstimulation results from the activation of the last-order interneurons in the PAD pathway and may, therefore, allow detection pathway. The PAD of single group I afferent fibers was determined in barbiturate-anesthetized preparations by measuring the test stimulus current required to maintain a constant probability of antidromic firing. This was achieved by means of a feedback system that continuously adjusted the test stimulus current to the required values. The PAD of individual group Ia gastrocnemius soleus (GS) fibers that is produced by activation of the low-threshold afferents of the posterior biceps and semitendinosus nerve was found to be inhibited by conditioning stimulation of the relatively low-threshold cutaneous fibers and also by stimulation of supraspinal structures such as the ipsilateral brain stem reticular formation, the contralateral red nucleus, and the contralateral pyramidal tract. In contrast, the PAD of group Ia fibers produced by microstimulation applied in the intermediate nucleus could be inhibited only by stimulation of the brain stem reticular formation but not by stimulation of the other descending inputs presently tested or by stimulation of cutaneous nerves. PAD of group Ia fibers was produced also by microstimulation applied within the motor nucleus. However, in most fibers the resulting PAD could not be inhibited either by stimulation of the brain stem reticular formation, the red nucleus, the pyramidal tract, or cutaneous nerves. Stimulation of cutaneous and of flexor muscle nerves of the brain stem reticular formation, the red nucleus, and the pyramidal tract all produced PAD of the group Ib GS fibers.(ABSTRACT TRUNCATED AT 400 WORDS)

Specific and potassium components in the depolarization of the Ia afferents in the spinal cord of the cat

In the cat spinal cord, primary afferent depolarization (PAD) of group Ia fibers of extensor muscles is produced by high-frequency stimulation (100 Hz) of group I muscle flexor afferents without significant increases in extracellular potassium. On the other hand, the PAD produced by stimulation of mixed and pure cutaneous nerves correlates well with increases in potassium ions. We conclude that the PAD produced by group I muscle afferents results from the activation of specific pathways making axo-axonic synapses with the Ia fiber terminals. The PAD of Ia fibers resulting from activation of cutaneous nerves involves instead unspecific accumulation of potassium ions.

Synaptic linkage of masseter muscle afferents to masseteric motoneurones in the cat

The synaptic linkage of masseter muscle afferents to masseteric motoneurones was investigated under blockage of soma-dendritic invasion of antidromic spikes by passing constant inward current across the cell membrane. A monosynaptic latency for excitatory postsynaptic potentials produced by group Ia afferents was measured as 1.3 ms and no group lb component was obtained. Inhibitory postsynaptic potentials with latencies of 5.5 ms were produced at a stimulus strength of 4.5 times the threshold of group Ia fibers. On the basis of stimulus strength, muscle afferents activated at 4.5 times the threshold and producing inhibitory postsynaptic potentials in masseteric motoneurones are probably group II afferents. The same reversal point was obtained in both the lingually induced and the group II IPSPs, indicating that the group II inhibitory postsynaptic potential is dependent on an increased permeability to Cl ions. The inhibitory postsynaptic potentials produced by stimulation of the high threshold muscle afferents were the composite of a strychnine-sensitive and strychnine-insensitive inhibitory postsynaptic potential. The latency of the inhibitory postsynaptic potentials caused by the high threshold muscle afferents was about 10 ms.

Role of Ia afferents in the soleus motoneurones. Inhibition during a tibialis anterior voluntary contraction in man.

Variations of the soleus H-reflex were studied during voluntary isometric or anisometric contractions of the tibialis anterior in man. At the onset of isometric contractions there was a weak inhibition of the soleus H-reflex, which was not related to the force of the tibialis anterior contraction. 110 msec after the onset of the EMG activity, the inhibition became secondarily more marked and was then related to the force of the contraction. This secondary potentiation of the H-reflex inhibition is brought about by group I fibres activity, since it was markedly reduced during ischemia of the leg. It persisted during local muscular fatigue, this indicating that Ib fibres from tibialis anterior are not involved and that, by the process of elimination, group Ia fibres must be responsible for the supplementary secondary inhibition. It is concluded that the early inhibition is only due to suprasegmental activity, whereas during the secondary part of the inhibition there is a supplementary inhibitory action brought about by Ia fibres from tibialis anterior. The secondary potentiation of the inhibition is therefore likely to be produced via the gamma loop.

Monosynaptic excitation of motoneurones from secondary endings of muscle spindles.

SINCE Lloyd's original work on the myotatic unit more than 30 yr ago1, it has been assumed that the monosynaptic excitation of motoneurones from receptor nerve fibres derives entirely from the Group Ia afferents, which terminate as primary endings in the muscle spindles. Group Ib afferents from tendon organs are thought to exert their inhibitory actions2 over di- or trisynaptic pathways3, while Group II and III fibres, which include those from the secondary endings of muscle spindles, form part of the flexor reflex afferent (FRA) system4, the synaptic actions of which are thought also to be mediated polysynaptically5. Whereas the monosynaptic excitation of motoneurones by Group Ia fibres has been directly confirmed in terms of unitary synaptic potentials evoked by single, stretch excited primary endings6, knowledge of the synaptic actions of fibres innervating secondary endings is known only indirectly from electrical stimulation of Group II fibres and is not without controversy7.

Distributed feedback systems for muscle control

Responses of single neurones in motor cortex to passive stretches of the contralateral extensor digitorum communis muscle were studied in regionally anaesthetized, paralyzed cats. Parameters of stimulation could be adjusted to activate either only group Ia afferents, or a combination of group Ia, group II and group Ib afferents from muscle. Cooling of the ipsilateral cerebellar cortex or underlying nuclei was done to ascertain the role of the cerebellum in the feedback system from muscle to motor cortex. Activation of only group Ia fibres by this natural stimulation resulted in short latency (11 msec) responses in a well circumscribed region of pericruciate cortex. This region corresponded to the output region for this muscle as determined by electrostimulation in previous experiments of Asanuma and Sakata. These fast responses were usually unaffected by cerebellar cooling and were probably mediated by lemniscal pathways. Other cells in the same spatial region of motor cortex responded at a longer latency (18 msec) to higher threshold inputs from the same muscle. These latter responses were strongly influenced by cooling of the intermediate part of the anterior lobe of the cerebellar cortex or of interpositus nucleus. It was therefore concluded that this transcerebellar pathway was responsible for a significant portion of these higher threshold responses. Cells responding to the lemniscal system activation with an early response were found only in layers III and IV of motor cortex. In contrast, neurones responding to activation of the transcerebellar pathway were found in all layers of the same region of cortex, including layer V. The results are consistent with the view that proprioceptive information from single muscles controlling limb position is relayed over multiple parallel channels, including lemniscal and transcerebellar channels, to that region of motor cortex which directly controls the output of the muscle from which the feedback arises.