Activity Of Renshaw Cells Research Articles

Activity of Renshaw cells during fictive scratch reflex in the cat.

The experiments were performed on decerebrate curarized cats with a hindlimb either completely deafferented or partly deefferented. Through tactile stimulation of the pinna, a fictive scratch reflex was evoked and activity in muscle efferents was then observed, similar to that in actual scratching. The duration of the cycle was about 250 ms, with extensor activity during a short period of about 50 ms (S phase) and flexor activity during a much longer one (about 200 ms; L phase). Appearance of rhythmic bursts of discharges was preceded by tonic flexor activity (tonic phase of scratching). Discharges of Renshaw cells were recorded extracellularly during these three phases, in parallel with discharges in the gastrochemius-soleus nerve. During the tonic phase of the scratch reflex, some Renshaw cells with input from flexors decreased their activity while others increased. No change in Renshaw cell activity with input from extensors was then observed. During the rhythmic phases of the scratch reflex a majority of Renshaw cells was phasically active. They usually responded once per cycle, with a burst of 1–30 impulses of 50–100 ms duration, most often occurring at the end of the L phase and during the S phase. Bursts of Renshaw cells with input from flexors and of extensors, respectively, overlapped to a high degree. However, maximal firing of extensor-coupled Renshaw cells occurred somewhat later than that of flexor-coupled cells. Flexor-coupled Renshaw cells discharged mainly at the end of the L phase and during the S phase, i.e. when the flexor moto-neurones terminated their activity. Extensor-coupled Renshaw cells reached maximal activity during the S phase, i.e. when the extensor motoneurones were recruited. After spinal transection at C1 level, Renshaw cells responded with an increased number of spikes but without change in timing of the discharges during the scratch cycle. Most of the contralaterally located Renshaw cells studied were also phasically active during the scratch reflex. The role of motoneurones and spinal interneurones in determining the timing of Renshaw cell activity and the role of the latter in control of posture and rhythmic movements are discussed.

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.

Modulation of renshaw cell activity during scratching

The activity of the Renshaw cells was recorded during fictitious scratching in 7 decerebrated and 1 spinal curarized cats. The flexor and extensor Renshaw cells were identified according to the responses induced by orthodromic stimulation of muscle nerves. Before the beginning of rhythmical oscillations, the background activity of the flexor Renshaw cells was inhibited. When the rhythmical generation began, both flexor and and extensor cells generated short bursts of spikes at the end of the flexor phase and at the extensor phase of the cycle. The activity of flexor cells began and terminated earlier in the cycle than that of the extensor cells. The results show that the flexor Renshaw cells are active reciprocally with flexor motoneurons, while the extensor cells are coactivated with extensor motoneurons.

Contribution of single motoneurons to renshaw cell activity

Single spinal alpha motoneurons driven by injected current are shown to increase the activity of Renshaw cells. This fact is a necessary condition for the validity of hypotheses concerning the functional significance of recurrent inhibition which are based on the conception that individual motoneurons can interact with each other.

Recurrent inhibition of individual Ia inhibitory interneurones and disinhibition of their target alpha-motoneurones during muscle stretches.

The effects of ramp stretches applied to triceps surae muscle on the discharge patterns of single Ia inhibitory interneurones, monosynaptically invaded from various nerves, were studied in either decerebrate or anesthetized cats. Interneurones which received direct excitatory Ia input from the stretched muscle exhibited augmented activity both during the dynamic and static phase of stretch, which was, however, interrupted by a transient inhibitory influence during the dynamic phase of stretch. The influences on Ia inhibitory interneurones, monosynaptically invaded from hamstring or tibial nerve, were exclusively inhibitory. These stretch-induced inhibitions were better demonstrable in decerebrate than in anesthetized preparations. The timing of the discharge patterns of additionally recorded Renshaw cells during stretch, and the disappearance or reduction of the above described inhibitory effects after administration of DHE, strongly support the idea that these inhibitory actions are caused by Renshaw inhibition. In Ia inhibitory interneurones, monosynaptically activated from the antagonistic peroneal nerve, stretch induced also pronounced inhibitory effects, which were most probably caused by mutual inhibition between Ia inhibitory interneurones. The suppression of agonistic Ia inhibitory interneurone activity below the tonic resting activity corresponded to an enhancement of the monosynaptic reflex amplitude of the antagonistic motoneurone pool. The findings suggest that normal orthodromic activation of Renshaw cells, and consequently the recurrent inhibition of the Ia inhibitory interneurones, is predominantly linked with rapid phasic, rather than slow tonic, motoneuronal firing. The functional role of this mechanism for the performance of rapidly alternating movements and the damping of ballistic agonist contractions is discussed.

The relative sensitivity of Renshaw cells to orthodromic group Ia volleys caused by static stretch and vibrations of extensor muscles.

1. Activity of Renshaw cells monosynaptically excited by ventral root stimulation and disynaptically excited by electric stimulation of the group Ia afferents in the gastrocnemius-soleus (GS) nerve, was recorded in precollicular decerebrate cats. The response of these units to prolonged vibration applied longitudinally to the deefferented GS muscle was then compared with that elicited by static stretch of the homonymous muscle, for comparable frequencies of discharge of the group Ia afferents. 2. Small-amplitude vibration of the GS muscle at 200/sec for one second produced a sudden increase in the discharge rate of Renshaw cells, which gradually decreased within the first 100 msec of vibration to reach steady albeit lower level than that obtained during the first part of vibration. The response of the Renshaw cells during the first 100 msec of vibration (phasic response) and that elicited during the last 500 msec of vibration (tonic response) were evaluated for different frequencies of sinusoidal stretch. The mean increase in the firing frequency per imp./sec in the Ia afferents was also calculated using the total one-second period. 3. The response of Renshaw cells to muscle vibration increased with the frequency of vibration and, over the value of 10/sec, appeared to be linearly related to the frequency of the input, at least up to the frequency of 150/sec. Since vibration was of sufficient amplitude to produce driving of all the primary endings of muscle spindles, the responses were expressed as mean increases in the discharge rate of Renshaw cells per average impulse/sec in the Ia afferents. The discharge of the Renshaw cell increased on the average by 2.90 and 1.08 imp./sec per each imp./sec in the Ia afferents during the phasic and the tonic component of the response respectively, while the response calculated during the whole period of vibration corresponded on the average to 1.45 imp./sec per each imp./sec in the Ia afferents. 4. The Renshaw cells tested above responded also with increasing frequencies of discharge to increasing levels of static extension of the GS muscle. In particular the discharge frequency of Renshaw cells was on the average linearly related to muscle extension, at least for values ranging from 0 to 8 mm. The mean increase in discharge rate as a function of the static extension corresponded on the average to 0.89 imp./sec/mm. Since the discharge rate of the primary endings of muscle spindles recorded from the deefferented GS muscle increased by 2.62 imp./sec/mm, it appears that the mean increase in the discharge rate of Renshaw cells as a function of static extension corresponded to 0.34 imp./sec per each imp./sec in the Ia afferents.

Effect of differential blocking of motor axons on antidromic activation of Renshaw cells in the cat.

Attempts were made to study differences in the relative effectiveness of different size ranges of motor axons to Renshaw cells by differential blocking of larger fibers of the gastrocnemius nerve in cats anesthetized with Nembutal. 1. Differential blocking of larger fibers in the nerve was successfully obtained by applying trapezoid wave current to the nerve. 2. It was shown that more than half (58.1%) of the Renshaw cells receive homogeneous inputs from a motor axon collaterals, 25.8% of the cell receive collateral inputs from a certain group of fibers, and 12.5% of the Renshaw cells were activated by “γ range” fibers.

Antidromic activation of Renshaw cells and their axonal projections.

AbstractAntidromic invasion of Renshaw cells following stimulation of their axons was found always to produce only a single spike in contrast to repetitive synaptic discharges. A systematic exploration of the spinal cord in a search for sites from which single Renshaw cells could be activated antidromically revealed that their axons: 1) can project to distances over 12 mm, 2) run in the ventral funiculus. 3) are likely to terminate both within motor nuclei (mainly at short distances) and in an area dorso‐medial and medial to them, and 4) have a maximal conduction velocity of about 30 mls.

Antagonism of pyrithinol-HCl to ethyl alcohol at a spinal cholinergic synapse.

Pyrithinol-HCl (40 mg/kg i.v.) decreased in cats the activity of individual Renshaw cells in the spinal ventral horn which are known to be excited via typically cholinergic motor axon collaterals. On the other hand this substance prevented the excitatory action which ethyl alcohol (0.8–1.6 g/kg i.v.) normally exerts upon the Renshaw cells. No protective effect of pyrithinol-HCl was found against the alcohol induced depression of gamma motoneurones. It is assumed from the results that pyrithinol-HCl exerts its protective action specifically upon cholinergic systems.

Morphine and the synaptic activation of Renshaw cells

Morphine administered electrophoretically prolonged the latencies of action potentials of Renshaw cells evoked by maximal and submaximal stimulation of ventral roots, without reducing the sensitivity of these neurones to electrophoretically administered acetylcholine. Such an effect was not observed when spikes were evoked by dorsal root stimuli, suggesting that morphine impairs the release of acetylcholine from motoneurone axon collaterals. High concentrations of morphine had a direct excitant action on Renshaw cells, and a procaine-like effect on action potentials and the sensitivity to both acetylcholine and dl-homocysteate. Morphine administered i.v. in doses (10 mg/kg) which substantially reduce the recurrent inhibition of motoneurones did not alter the latencies of Renshaw cell firing in response to submaximal ventral root stimuli. The effect of the alkaloid on the recurrent inhibition of spinal motoneurones occurs predominantly at Renshaw cell-motoneurone inhibitory synapses.

The action of ethyl alcohol on the activity of individual Renshaw cells

Ethyl alcohol (0.16–2.4 g/kg i.v.) causes a marked increase in Renshaw cell activity as tested by antidromic stimulation of motor nerve fibres in cats. Ethanol decreases the threshold, enhances the frequency of the early discharge and prolongs the firing rate, and induces or increases spontaneous activity. This activating effect is present in anesthetized as well as in unanesthetized decerebrated or spinalized cats. The effects of ethanol on the cholinergic Renshaw cells correspond well with its known facilitating effect on the cholinergic neuromuscular junction.

Pentylenetetrazol and Renshaw cell activity.

The evoked and spontaneous activity of Renshaw cells in unanesthetized spinal cats was studied with metal microelectrodes before and after pentylenetetrazol (40 mg/kg). The drug did not prolong the discharge of Renshaw cells following dorsal root or ventral root stimulation. In addition, several cells were examined for the effects of the drug on spontaneous activity. Pentylenetrazol did not produce consistent changes in the rate of discharge.

The synaptic excitation of Renshaw cells

An analysis has been made in spinal cats anaesthetised with pentobarbitone of the firing of Renshaw cells induced by stimulation of ventral roots or by volleys entering the spinal cord via dorsal root fibres. The response to maximal ventral root stimulation consisted of an early high frequency discharge which was blocked by dihydro-β-erythroidine (nicotinic receptors), a depression of spontaneous firing and a subsequent late firing which was specifically depressed by atropine (muscarinic receptors). The intervening depression or pause was associated with a non-specific depression of the sensitivity of these neurones to both acetylcholine and excitant amino acids. It is proposed that these responses may be the consequence of the action of acetylcholine released simultaneously from all of the axon collateral endings upon a Renshaw cell and that the late response may have no functional role. Other possibilities are discussed. The spontaneous activity of these neurones appears to involve muscarinic receptors. The activation of Renshaw cells by dorsal root volleys, which is independent of the prior discharge of motoneurones, does not involve cholinergic mechanisms.

Chloralose and the activity of renshaw cells

Renshaw cells in the lumbosacral region of the spinal cord in anesthetized or decerebrate cats were examined with multibarrelled micropipettes, testing their responses to ventral root volleys and iontophoretic applications of glutamate and ACh. The intravenous administration of one or more doses of chloralose (20–80 mg/kg) did not alter specifically the sensitivity to ACh, nor were there any consistent changes in the responses to ventral root stimulation, so long as the blood supply remained adequate. From these results it is concluded that chloralose does not cause a general block of the release of ACh from central cholinergic nerve endings. It is suggested that chloralose depresses the recurrent inhibition of motoneurons by inactivating spinal inhibitory synapses.

CENTRAL EFFECTS OF CENTRIPETAL IMPULSES IN AXONS OF SPINAL VENTRAL ROOTS

CENTRAL EFFECTS OF CENTRIPETAL IMPULSES IN AXONS OF SPINAL VENTRAL ROOTS