Renshaw Cell Discharges Research Articles

Renshaw cell responses to intra-arterial injection of muscle metabolites into cat calf muscles

Metabolites released during fatiguing muscle contractions excite group III–IV muscle afferents which might inhibit skeleto-motoneuron firing, hypothetically via Renshaw cells. This was tested, in decerebrated, spinalized cats, by recording changes in Renshaw cell spontaneous discharges and responses to antidromic electrical stimulation of motor axons when small-diameter calf muscle afferents were excited by intra-arterially injected bradykinin, serotonin, lactic acid and KCl. Whenever such injections had an effect, it transiently raised or lowered the spontaneous firing rate and almost always decreased the antidromic response to motor axon stimulation. Injection of bradykinin and serotonin commonly decreased the blood pressure and concomitantly the spinal blood flow (as measured using laser Doppler flowmetry), which could have indirectly influenced Renshaw cell firing. But in general, blood pressure and flow changed after the Renshaw cell discharge did, which thus, appears to be modulated independently by group III–IV afferents. These results suggest that the Renshaw cell-mediated effects of neurochemically excited afferents would predominantly disinhibit rather than inhibit motoneurons.

Renshaw cells and recurrent inhibition: Comparison of responses to cyclic inputs

Spinal recurrent inhibition influences the discharge patterns of motoneurons and spinal interneurons. The precise pattern of this influence depends on the static and dynamic characteristics of this feedback system. It is thus of importance to quantify its characteristics as well as possible. We here compare nonlinear features (hysteresis) in Renshaw cells and recurrent inhibition in response to cyclic stimulation of motor axons. In pentobarbitone-anaesthetized or decerebrate cats, intracellular recordings were obtained from 26 hindlimb muscle nerves skeleto-motoneurons and extracellular recordings from nine Renshaw cells. Various hindlimb muscle nerves (dorsal roots cut) or ventral roots (dorsal roots intact) were prepared for electrical stimulation to elicit recurrent inhibition in motoneurons or discharges in Renshaw cells. Stimulus patterns consisted of repetitive pulse trains whose rates varied cyclically between around 10 pulses/s and several tens of pulses/s, at modulation frequencies between 0.1 and 1.0 Hz, in one of two waveforms: triangular or sinusoidal. Recurrent inhibitory potentials in motoneurons and discharge patterns of Renshaw cells were averaged with respect to triggers (cycle-triggers) marking a fixed phase in the stimulation cycle. In another two experiments, motor axons to hindlimb muscles (soleus and medial gastrocnemius) were stimulated with sinusoidal and distorted temporal patterns to show their effects on force production. Most often the cycle-averaged motoneuron membrane potential changed in a temporally asymmetrical way, i.e. it fairly rapidly hyperpolarized early in the stimulus cycle (during increasing rate) and then depolarized more slowly throughout the rest.(ABSTRACT TRUNCATED AT 250 WORDS)

Distribution of recurrent inhibition within a motor nucleus. II. Amount of recurrent inhibition in motoneurones to fast and slow units.

The maximal recurrent inhibition was studied by intracellular recording from 43 triceps surae motoneurones (tentatively type-identified by the biophysical properties of the neurones) and from 67 medial gastrocnemius motoneurones (type-identified by the muscle unit properties; fast fatiguing, FF; fatigue resistant, FR and slow, S). Maximal homonymous recurrent IPSP (RIPSP) and input resistance (RN) were measured at 'resting' membrane potential and close to firing threshold. The 'synaptic current' at the peak of the RIPSP was estimated (RIPSP/RN). At 'resting' membrane potential the RIPSPs increased in the order FF less than FR less than S (0.9, 1.4, and 2.5 mV, respectively). This order was preserved when the 'current' (RIPSP/RN) rather than voltage was considered, although the overall range was much reduced. When investigated close to firing threshold there were no significant differences in synaptic 'current'. This apparent paradox may be explained by systematic differences in firing threshold between motor unit types; it increased in the order S less than FR less than FF (4.6, 8.9 and 13.5 mV, respectively).

Distribution of recurrent inhibition within a motor nucleus. I. Contribution from slow and fast motor units to the excitation of Renshaw cells.

The relation between the size of a monosynaptic reflex (MSR) to triceps surae and the resulting Renshaw cell discharge was used to evaluate the contribution from slow and fast motor units to the excitation of Renshaw cells. It is, however, difficult to interpret these results in terms of excitation contributed by slow and fast motor units because of the following reasons. First, the size of the MSR recorded in ventral roots is not linearly related to the number of recruited motor units, since larger motor axons contribute more to the size of the MSR than smaller ones. Second, the number of spikes evoked in a Renshaw cell burst is not linearly related to the excitatory input because Renshaw cell discharge saturates in the case of large responses. The contribution of small, early-recruited motoneurones to Renshaw cell excitation is consequently overestimated. Procedures were introduced to deal with these problems. It is concluded that the last-recruited motor units (probably 'fast twitch, fast fatiguing') on average contribute four times as much excitation to Renshaw cells as the first recruited ('slow twitch') motor units.

Time constants of facilitation and depression in Renshaw cell responses to random stimulation of motor axons.

In 9 adult anaesthetized cats, 22 lumbosacral Renshaw cells recorded with NaCl-filled micropipettes were activated by random stimulation of ventral roots or peripheral nerves. The stimulus patterns had mean rates of 9.5-13 or 20-23 or 45 pulses per second and were pseudo-Poisson; short intervals below ca. 5 ms (except in two cases) were excluded. The Renshaw cell responses were evaluated by two kinds of peristimulus-time histograms (PSTHs). "Conventional" PSTHs were calculated by averaging the Renshaw cell discharge with respect to all the stimuli in a train. These PSTHs showed an early excitatory response which was often followed by a longer-lasting slight reduction of the discharge probability. These two response components were positively correlated. "Conditional" PSTHs were determined by averaging the Renshaw cell discharge with respect to the second ("test") stimulus in pairs of stimuli which were separated by varied intervals, delta. The direct effect of the first "conditional" response was subtracted from the excitation following the second ("test") stimulus so as to isolate the effect caused by the second stimulus per se. After such a correction, the effect of the first "conditioning" stimulus showed pure depression, pure facilitation or mixed facilitation/depression. Analysis of such conditioning curves yielded two time constants of facilitation (ranges: ca. 4-35 ms and 93-102 ms) and two of depression (ranges: ca. 7-25 ms and 50-161 ms). It is concluded that these time constants are compatible with processes of short-term synaptic plasticity known from other synapses. Other processes such as afterhyperpolarization and mutual inhibition probably are of less importance.

Central drive on Renshaw cells coupled with phrenic motoneurons

In anesthesized spontaneously breathing cats (C4–C5 deafferentation), recurrent inhibition of phrenic motoneurons was analyzed by studying either recurrent IPSPs in phrenic motoneurons, or Renshaw cell discharges evoked by C5 phrenic nerve stimulation. Of 90 intracellularly recorded phrenic motoneurons, 7 motoneurons showed evoked recurrent IPSPs with stimulation of C5 phrenic axons subthreshold for eliciting antidromic activation of the motoneuron from which intracellular recording was done. These IPSPs could be reversed by imposed hyperpolarization of the motoneuron, and were of greater amplitude during inspiration than during expiration. Within the phrenic nucleus, interneurons were classified as Renshaw cells if they responded to C5 phrenic axon stimulation with a typical high frequency burst of potentials. Reactivity of these Renshaw cells was related to the respiratory cycle, number of spikes in the burst being greater during inspiration than during expiration. Injection of a nicotinic cholinergic blocker (mecamylamine) decreased responses of Renshaw cells but the respiratory modulation was still present. Some Renshaw cells (18/33) were spontaneously active during inspiration. Their activity was generally maximal during the last third of inspiration. Since: (1) spontaneous activity of Renshaw cells is related to the respiratory drive; (2) persists after C7 spinal transection and after mecamylamine poisoning of the axonal recurrent pathway; and (3) might appear before sustained phrenic activity, the assumption of a central respiratory drive impinging on the Renshaw cells has to be retained.

Recurrent inhibition of intercostal motoneurones in the cat.

1. The external and internal intercostal nerves of a single intercostal space were stimulated in anaesthetized paralysed cats with dorsal roots cut in the corresponding spinal cord segment. 2. Extracellular recording in the ventral horn revealed single units which fired short high frequency bursts of spikes at short latency to stimulation of either or both of the two nerves at stimulus strengths appropriate to the activation of alpha motor axons. These units were deduced to be Renshaw cells. 3. Small (0.1-0.2 mV) hyperpolarizing potentials of duration up to 50 msec were recorded intracellularly in both inspiratory and expiratory motoneurones of the same segment. Latencies and thresholds were appropriate for disynaptic i.p.s.p.s evoked by collaterals of alpha motor axons. 4. The changes in probability of firing following the stimuli were examined for inspiratory alpha motoneurones by constructing post-stimulus histograms of efferent discharges recorded from filaments of the external intercostal nerve of the segment stimulated and from other segments. 5. A period of reduced probability of firing of up to 24 msec duration, corresponding in all respects to disynaptic inhibition from alpha motor axon collaterals, was seen in the segment stimulated and up to three segments distant, though declining in intensity with distance. Either nerve could evoke such inhibition although that evoked from the internal intercostal nerve was stronger, as were the intensities of the Renshaw cell discharges. 6. We conclude that recurrent inhibition, via Renshaw cells which have axons up to 30 mm in length, is present for intercostal motoneurones. Arguments are adduced to show that although the effects from stimulating any one segmental nerve may be relatively weak, the over-all effect resulting from the widely spread projections of the Renshaw cells concerned is an inhibition comparable intensity with that seen in many hind limb motor nuclei.

Electrophysiological studies on the specific benzodiazepine antagonist Ro 15-1788.

This is an electrophysiological study in cats and rats of the imidazobenzodiazepinone derivative, Ro 15-1788, the first representative of specific benzodiazepine antagonists. (1) In unanaesthetized spinal cats, 1-10 mg kg-1 Ro 15-1788 i.v. did not affect segmental dorsal root potentials (DRPs), polysynaptic ventral root reflexes (VRRs), Renshaw cell responses to antidromic ventral root volleys and spontaneous gamma-motoneurone activity. However, at 1 mg kg-1 i.v., it antagonized the enhancement of DRPs as well as the depression of polysynaptic VRRs, Renshaw cell discharges and gamma-motoneurone activity induced by meclonazepam (0.1 mg kg-1 i.v.), diazepam (0.3 mg kg-1 i.v.) or zopiclone (1 mg kg-1 i.v.). The same dose of Ro 15-1788 failed to reduce similar effects of phenobarbital (10 mg kg-1 i.v.) on spinal cord activities. (2)In unanaesthetized "encéphale isole" rats, 3 mg kg-1 Ro 15-1788 i.v. abolished the decrease induced by 5 mg kg-1 midazolam i.v. of spontaneous multiunit activity (MUA) in the substantia nigra pars compacta, nucleus raphé dorsalis, nucleus locus coeruleus and the CAl area of the hippocampus dorsalis, but not the decrease produced by 10mg kg-1 pentobarbital i.v. Ro 15-1788 (12mg kg-1 i.v.) by itself did not affect MUA in the substantia nigra, but slightly depressed MUA in the other 3 areas. (3) In intact immobilized rats, the increase of power induced by 1 mg kg-1 flunitrazepam i.v. in the 0.5-48 Hz range of the electrocorticogram as well as in the 0.5-8 Hz, 8-32 Hz and 32-48 Hz frequency bands was transiently abolished by 5 mg kg-1 Ro 15-1788 i.v. (4) In unrestrained cats, 5 mg kg-1 Ro 15-1788 i.p. had no effect on the electrical threshold for eliciting a rage reaction evoked by electric hypothalamic stimulation, but abolished the threshold increase caused by 1 mg kg-1 diazepam i.p. These results are in line with biochemical and behavioural findings and support the selective antagonism by Ro 15-1788 of central effects of benzodiazepines through an interaction at benzodiazepine receptors.

Caffeine antagonizes several central effects of diazepam

In spinal cats, caffeine (3–30 mg·kg −1 i.v.) reduced the increase of dorsal root potentials (DRPs) caused by diazepam (0.1–1 mg·kg −1 i.v.) without affecting the prolongation of DRPs evoked by phenobarbitone (10–20 mg·kg −1 i.v.). Caffeine antagonized the depression by diazepam, but not that by phenobarbitone, of the ventral root-evoked Renshaw cell discharge. In unrestrained cats, 50 mg·kg −1 caffeine i.p. abolished the elevation induced by 1 mg·kg −1 diazepam i.p. of the threshold for eliciting a rage reaction by stimulation of the lateral hypothalamus, but was ineffective against the threshold increase caused by 20 mg·kg −1 phenobarbitine i.p. In the horizontal wire test in mice, caffeine was more potent in reversing the depression of performance induced by diazepam that that by phenobarbitone (ED50 1.8 mg·kg −1 and 139 mg·kg −1 p.o., respectively). The reduction of skeletal muscle tone in mice produced by diazepam was antagonized by low doses of caffeine (ED50 0.53 mg·kg −1 p.o.). While caffeine at low doses (0.3-3 mg·kg −1 p.o.) abolished the anticonflict effect of diazepam in rats, high doses (ED50 160 mg·kg −1 p.o.) were necessary to antagonize the anticonvulsant effect of diazepam on pentylene-tetrazole-induced seizures in mice. The interaction between caffeine and diazepam is not due to a competition at the benzodiazepine receptors but may involve purinergic mechanisms.

Renshaw cell discharge at the beginning of muscular contraction and its relation to the silent period

Renshaw cell activity was recorded simultaneously with the motoneuronal discharge during vibration or stretch of the triceps muscles. Both the monosynaptic reflex responses and the phasic discharge of Renshaw cells elicited by the first stroke of the vibrator or by the onset of muscle extension were followed by a period of silence in their electrical recordings. The Renshaw cell burst, recorded at the onset of both stimuli, coincided with the early part of the silent period in motoneuronal discharge. It preceded the onset of muscle contraction and ended within 30 to 40 ms after the silent period began. The silent period could still persist after the pause in the discharge of the primary endings of muscle spindles had completely disappeared. On the basis of these findings, the view that recurrent inhibition could contribute to the early part of the silent period is strongly favored.

Input‐output relations in the pathway of recurrent inhibition to motoneurones in the cat.

1. The output from Renshaw cells caused by a phasic motor volley was investigated when these neurones were submitted to a background firing secondary to a tonic motor discharge elicited by a repetitive stimulation of muscle group I afferents. It was invariably found in individual Renshaw cells that tonic excitation produced an increase in the additional ouput caused by the phasic motor volley. The curves displaying this increase exhibited a significant 'jump' when the output resulting from the combined tonic and phasic motor discharges ranged between 2 and 5 spikes during the first 10 msec following the phasic volley. 2. The whole pool of Renshaw cells was also considered by assessing the amount of recurrent inhibition in motoneurones following a phasic motor volley. Similarly it was found that additional recurrent inhibition elicited by a phasic motor volley was enhanced when the Renshaw cells received a tonic excitatory input. 3. The Renshaw cell discharges elicited by stimulation of two different nerves were compared when a conditioning stimulus was previously applied to only one of them. The results strongly suggest that a preceding volley caused a decrease in synaptic efficacy at the terminals of the recurrent collaterals. 4. The firing produced by current injected through the recording micro-electrode was investigated in one intracellularly recorded Renshaw cell. It was found that the current-frequency curve was linear for 'steady-state' firing but displayed a clearcut sigmoid shape for the earliest intervals before the final adaptation. 5. It is demonstrated that this sigmoid input-output relation in individual Renshaw cells is sufficient to explain how the controls acting on these neurones may change the gain in the recurrent pathway when Renshaw cells are fired by a phasic motor discharge. When Renshaw cells are fired by a longlasting tonic motor discharge the linear input-output relation in individual cells should not cause any modifications of the gain in the recurrent pathway. A change in this gain secondary to the effects of segmental and supraspinal control systems is, however, possible if the motor discharge creates a subliminal fringe within the pool of Renshaw cells.

Contribution of Different Size Motoneurons to Renshaw Cell Discharge During Stretch and Vibration Reflexes

Publisher Summary The contribution of motoneurons of different size to Renshaw cell discharge can be understood by considering the organization of autogenetic reflex pathways. Two basic mechanisms of autogenetic inhibition tend to reduce excitation of extensor motoneurons elicited by the corresponding Ia pathway. The first is a mechanism of presynaptic inhibition due to primary afferent depolarization (PAD) of both the homonymous and heteronymous Ia afferents. Muscle vibration was particularly effective in producing PAD of the Ia pathway, while static stretch was apparently inoperative in this respect. The second is a mechanism of postsynaptic inhibition due to recurrent excitation of Renshaw cells. It has shown that Renshaw cells are mainly sensitive to dynamic changes in muscle length, as produced by muscle vibration, but less sensitive to static muscle stretch. It has been hypothesized that static stretch and vibration of the gastrocnemius-soleus (GS) muscle activate small and large motoneurons in different proportions in the two experimental conditions, and that axon collaterals of large phasic motoneurons, on the average, make more powerful excitatory connections onto Renshaw cells than do those drginating from small tonic motoneurons.

The relative dependence of the activity of Renshaw cells on recurrent pathways during contraction of the triceps muscle.

Renshaw cell activity was recorded simultaneously with motoneuronal unit discharge during vibration and tetanic stimulation of triceps muscles in decerebrated cats. The experiments confirm that, in this preparation, the motoneurones are the main source of Renshaw cell firing during muscle stretch and vibration and when motoneuronal discharge was induced through the gamma loop. However they also show that a discharge of Renshaw cells, monosynaptically coupled with triceps motoneurones through their recurrent collaterals, could be elicited during contraction of the muscle at the time when the discharge of these motoneurones had been silenced. The recording of the stretch receptors and motoneuronal unit discharge during stretch, vibration, and ventral root stimulation gave evidence of the contribution of the withdrawal of excitation by primary endings to the occurrence of the silent period during tetanic contraction of the muscle. The measurements of the critical firing level in motoneuronal units responding reflexly to held stretch and vibration of the muscles, and silencing their discharge during muscle shortening, showed that these cells are amongst the lowest ranking in the pool For these reasons, these data suggest that Renshaw cell firing during vibration and tetanic contraction of the muscle cannot be attributed only to the alpha motoneurone excitation by the Ia fibres.

Dynamic properties of Renshaw cells: frequency response characteristics.

The dynamic properties of Renshaw cells located in the lumbar spinal cord of intercollicular decerebrate cats were measured. The responses of these interneurones were recorded extracellularly, while the ventral root was stimulated with sinusoidally frequency-modulated trains of electrical pulses. The frequency of the Renshaw cell discharges resulting from such stimulation varied sinusoidally. The amplitude of modulation about the average (or "carrier") rate of discharge exhibited a linear dependence on the modulation amplitude of the stimulus pulse train. Renshaw cells were able to follow modulated stimulus trains in the entire range of modulation frequencies (0.2 to 80 Hz) encompassed by the present study. Above modulation frequencies between 20 and 50 Hz, the amplitude of modulation of the responses declined. Frequency responses measured at low average frequencies of the stimulus pulse train (centre frequencies 30 and 40 Hz) showed comparatively little dependence on modulation frequency. The higher the centre frequency, however, the greater was the enhancement of the modulation amplitudes at high modulation frequencies compared with those observed at low modulation frequencies. Some aspects of the functional implications of these results are considered and an approximate formula for the transfer function of Renshaw cells is presented.

Reflex effects and postsynaptic membrane potential changes during epileptiform activity induced by penicillin in decapitate spinal cords

The administration of a convulsant dose of penicillin enhanced the transmission of monosynaptic reflexes in spinal cords in which reflex transmission was feeble before the drug treatment, but it had little effect in cords where monosynaptic reflexes were powerful to begin with. Post-tetanic potentiation was not altered by penicillin. Polysynaptic reflexes were invariably enhanced by convulsant amounts of penicillin. Postsynaptic (“direct”) inhibition was not affected in the seizure-free intervals in spinal cords treated with penicillin, but it seemed to be suppressed during tonic seizures. The disability of reflex inhibition during ictal discharges may be due to presynaptic depolarization of inhibitory terminals. Recurrent inhibition was partially suppressed in spinal cords treated with penicillin. Neurons in the dorsal and intermediate gray matter were sometimes excited, sometimes inhibited, and sometimes unaffected by seizure activity of their segment. Motoneurons in the ventral horns invariably participated in the interictal and ictal activity. The timing of clonic seizure sequences coincided with bursts of Renshaw cell discharges. Action potential of abnormal amplitude and configuration were frequently observed in convulsing motoneurons. Paroxysmal depolarizing shifts (PDSs) of motoneurons were similar to those observed by other investigators in neurons in experimental epileptic foci of the cerebral cortex, except that spinal PDSs were not followed by hyperpolarizing waves.

The Relative Sensitivity of Renshaw Cells to Static and Dynamic Changes in Muscle Length

Publisher Summary This chapter discusses that Renshaw cells, which belong to the monosynaptic reflex pathway made by the Ia afferents from the gastrocnemius-soleus (GS) muscle on the homonymous motoneurons, may respond to both static stretch and vibration of the homonymous muscle. However, the Renshaw cell discharge induced by vibration of the GS muscle is much higher than that elicited during static stretch of the same muscle for comparable frequencies of discharge of the primary endings of the muscle spindles. The possible factors responsible for this difference are considered at length in the chapter. The experiments are performed on precollicular decerebrate cats, operated under ether anesthesia. Results show that Renshaw cells disynaptically excited by the orthodromic group I volleys induced by low-threshold electrical stimulation of the intact GS nerve responds to vibration applied longitudinally to the de-efferented GS muscle. Even in this instance, the Renshaw cells fire with a latency that is compatible with the disynaptic origin of the response, indicating that excitation of the Renshaw cells depend upon monosynaptic reflex discharge of the GS motoneurons following the stimulation of the Ia afferents. An analysis of the stimulus-response relationship, evaluated by measuring the discharge rate of the Renshaw cells as a function of the amplitude of vibration, clearly indicates that this response depends upon the activation of the primary endings of the muscle spindles.

Response of Renshaw cells to sinusoidal stretch of hindlimb extensor muscles.

1. Renshaw cells responding disynaptically to electrically induced group I volleys in the intact gastrocnemius-soleus (GS) nerve, were submitted to small-amplitude, high-frequency vibration applied longitudinally to the deefferented GS muscle in precollicular decerebrate cats. 2. Vibration of the GS muscle at 200/sec, 180 mu peak-to-peak amplitude for 80-100 msec produced a sudden increase in the discharge rate of Renshaw cells, which gradually decreased within 25-50 msec to reach a steady level higher than that recorded in the absence of vibration. 3. Excitation of Renshaw cells appeared at a threshold amplitude of vibration (at 200-250/sec) of 5-20 mu and increased to a maximum value for amplitudes of about 70-80 mu, i.e., when all the primary endings of the spindles from the GS muscle had been driven by the stimulus. Recruitment of the secondary endings of the muscle spindles, due to large amplitude muscle vibration, did not modify the response of the Renshaw cells to the mechanically induced group Ia volleys. 4. These findings were obtained with the GS muscle pulled at 8 mm of initial extension. A threshold response of Renshaw cells to vibration appeared at 4 mm of static stretch, while maximal responses occurred at 8 mm. No further increase and actually a slight decrease in the response appeared for initial extensions of the muscle of 10-12 mm. 5. For a given vibration amplitude, the response of the Renshaw cells increased with increasing frequencies of vibration to reach the maximum at frequencies of 150-250/sec. Bursts of Renshaw cell discharges synchronous to each stroke of vibrator occurred only for low frequencies of stimulation (less than 25/sec). 6. It is concluded that vibration of the GS muscle represents a very effective method in exciting the Renshaw cells and that this response depends upon selective stimulation of homonymous motoneurons monosynaptically excited by the orthodromic volleys originating from the primary endings of the corresponding muscle spindles.

A quantitative analysis of Renshaw cell discharges caused by stretch and vibration reflexes

A quantitative analysis of Renshaw cell discharges caused by stretch and vibration reflexes

Renshaw cell activity in man.

The H-reflex elicited in triceps surae by percutaneous stimulation of the posterior tibial nerve was conditioned by stimuli applied through the same electrode. The differential sensitivity of motor and sensory fibres to duration of the stimulus pulse made it possible to condition the H-reflex with either a motor or a sensory stimulus. With both types of conditioning, the H-reflex was inhibited at conditioning-test intervals of 2-3 msec and was then facilitated, the peak of facilitation occurring at 5-8 msec with motor conditioning and 6-10 msec with sensory conditioning. The phase of facilitation was followed by further inhibition. We have concluded (1) that the effects of motor conditioning on the H-reflex result from the discharge of Renshaw cells activated by the antidromic volley in the motor axons, and (2) that the effects of sensory conditioning (at the times used in these experiments) are largely due to the activation of Renshaw cells secondary to the discharge of alpha motoneurones by the conditioning volley.

Quantitative relation of Renshaw cell discharges to monosynaptic reflex height

If Renshaw cells are fired by monosynaptically excited motoneurons the number of repetitive discharges of the interneurons increases in direct proportion to the height of the monosynaptic reflex, i.e., to the number of motoneurons in the discharge zone. The average slope is 10.6±2.9.