Input Resistance Of Motoneurons Research Articles

Rapid activity-dependent modulation of the intrinsic excitability through up-regulation of KCNQ/Kv7 channel function in neonatal spinal motoneurons.

Activity-dependent changes in the properties of the motor system underlie the necessary adjustments in its responsiveness on the basis of the environmental and developmental demands of the organism. Although plastic changes in the properties of the spinal cord have historically been neglected because of the archaic belief that the spinal cord is constituted by a hardwired network that simply relays information to muscles, plenty of evidence has been accumulated showing that synapses impinging on spinal motoneurons undergo short- and long-term plasticity. In the brain, brief changes in the activity level of the network have been shown to be paralleled by changes in the intrinsic excitability of the neurons and are suggested to either reinforce or stabilize the changes at the synaptic level. However, rapid activity-dependent changes in the intrinsic properties of spinal motoneurons have never been reported. In this study, we show that in neonatal mice the intrinsic excitability of spinal motoneurons is depressed after relatively brief but sustained changes in the spinal cord network activity. Using electrophysiological techniques together with specific pharmacological blockers of KCNQ/Kv7 channels, we demonstrate their involvement in the reduction of the intrinsic excitability of spinal motoneurons. This action results from an increased M-current, the product of the activation of KCNQ/Kv7 channels, which leads to a hyperpolarization of the resting membrane potential and a decrease in the input resistance of spinal motoneurons. Computer simulations showed that specific up-regulations in KCNQ/Kv7 channels functions lead to a modulation of the intrinsic excitability of spinal motoneurons as observed experimentally. These results indicate that KCNQ/Kv7 channels play a fundamental role in the activity-dependent modulation of the excitability of spinal motoneurons.

Control of motor activity, via motoneuron excitability and sensory-motor integration, by the steroid hormone 20-hydroxyecdysone in crayfish

We studied the effects of the molting hormone 20-hydroxyecdysone (20E) on leg sensory-motor networks of the red swamp crayfish, Procambarus clarkii. The hormone was injected in isolated crayfish and network activity was analyzed 3 days after injection using electrophysiology on an in vitro preparation of the leg locomotor network. This 20E treatment deeply reduced motor activity, by affecting both intrinsic motoneuron (MN) properties and sensory-motor integration. Indeed, we noticed a general decrease in motor nerve tonic activities, principally in depressor and promotor nerves. Moreover, intracellular recordings of depressor MNs confirmed a decrease of MN excitability due to a drop in input resistance. In parallel, sensory inputs originating from a proprioceptor, which codes joint movements controlled by these MNs, were also reduced. The shape of excitatory post-synaptic potentials (PSPs) triggered in MNs by sensory activity of this proprioceptor showed a reduction of polysynaptic components, whereas inhibitory PSPs were suppressed, demonstrating that 20E acted also on interneurons relaying sensory to motor inputs. Consequently, 20E injection modified the whole sensory-motor loop, as demonstrated by the alteration of the resistance reflex amplitude. These locomotor network changes induced by 20E were consistent with the decrease of locomotion observed in a behavioral test. In summary, 20E controls locomotion during crayfish premolt by acting on both MN excitability and sensory-motor integration. Among these cooperative effects, the drop of input resistance of MNs seems to be mostly responsible for the reduction of motor activity.

Cystic fibrosis transmembrane conductance regulator modulates synaptic chloride homeostasis in motoneurons of the rat spinal cord during neonatal development

Cystic fibrosis transmembrane conductance regulator (CFTR) is a cAMP-regulated Cl(-) channel functional in neonatal rat spinal motoneurons. The present study investigated the developmental (P1-P8) expression of CFTR, its impact on motoneuron excitability and Cl(-) homeostasis in relation to canonical Cl(-) transporters. The Cl(-) outward transporter KCC2 gene was upregulated in females over males and increased from P1 to P8. The gene activities of the Cl(-) inward transporter NKCC1 and CFTR were positively correlated and grew between P1 and P8. P1 motoneuronal somata were immunopositive for CFTR whose expression later (P8) extended to cell processes. KCC2 immunopositivity outlined somata and cell processes at P1 and P8. Electrophysiological recording with sharp electrodes showed that the CFTR blocker glibenclamide increased motoneuron input resistance, suggesting functional CFTR in P1-P8 motoneurons. Whole cell patch-clamping of spinal motoneurons to study CFTR contribution to postnatal synaptic Cl(-) regulation indicated that glibenclamide or the selective CFTR blocker diphenylamine-2,2'-dicarboxylic acid produced a negative shift in GABA/glycine reversal potential (E(GABA/Gly) ) of spontaneously occurring synaptic events measured after block of excitatory transmission. A similar effect on E(GABA/Gly) was induced by the NKCC1 inhibitor bumetanide. A 3D reconstructed motoneuron model suggested that CFTR activity contributes to set the E(GABA/Gly) positive to the resting potential. The functional outcome of these Cl(-) mediated synaptic events depended not only on the postnatal age of the animal but also on their timing with respect to the excitatory synaptic signals. We propose that CFTR operated together with NKCC1 to produce depolarizing GABA/glycine mediated synaptic events.

Principles governing recruitment of motoneurons during swimming in zebrafish

Locomotor movements are coordinated by a network of neurons that produces sequential muscle activation. Different motoneurons need to be recruited in an orderly manner to generate movement with appropriate speed and force. However, the mechanisms governing recruitment order have not been fully clarified. Using an in vitro juvenile/adult zebrafish brainstem-spinal cord preparation, we found that motoneurons were organized into four pools with specific topographic locations and were incrementally recruited to produce swimming at different frequencies. The threshold of recruitment was not dictated by the input resistance of motoneurons, but was instead set by a combination of specific biophysical properties and the strength of the synaptic currents. Our results provide insights into the cellular and synaptic computations governing recruitment of motoneurons during locomotion.

Intramuscular AAV delivery of NT‐3 alters synaptic transmission to motoneurons in adult rats

We examined whether elevating levels of neurotrophin-3 (NT-3) in the spinal cord and dorsal root ganglion (DRG) would alter connections made by muscle spindle afferent fibers on motoneurons. Adeno-associated virus (AAV) serotypes AAV1, AAV2 and AAV5, selected for their tropism profile, were engineered with the NT-3 gene and administered to the medial gastrocnemius muscle in adult rats. ELISA studies in muscle, DRG and spinal cord revealed that NT-3 concentration in all tissues peaked about 3 months after a single viral injection; after 6 months NT-3 concentration returned to normal values. Intracellular recording in triceps surae motoneurons revealed complex electrophysiological changes. Moderate elevation in cord NT-3 resulted in diminished segmental excitatory postsynaptic potential (EPSP) amplitude, perhaps as a result of the observed decrease in motoneuron input resistance. With further elevation in NT-3 expression, the decline in EPSP amplitude was reversed, indicating that NT-3 at higher concentration could increase EPSP amplitude. No correlation was observed between EPSP amplitude and NT-3 concentration in the DRG. Treatment with control viruses could elevate NT-3 levels minimally resulting in measurable electrophysiological effects, perhaps as a result of inflammation associated with injection. EPSPs elicited by stimulation of the ventrolateral funiculus underwent a consistent decline in amplitude independent of NT-3 level. These novel correlations between modified NT-3 expression and single-cell electrophysiological parameters indicate that intramuscular administration of AAV(NT-3) can exert long-lasting effects on synaptic transmission to motoneurons. This approach to neurotrophin delivery could be useful in modifying spinal function after injury.

Early electrophysiological abnormalities in lumbar motoneurons in a transgenic mouse model of amyotrophic lateral sclerosis

Amyotrophic lateral sclerosis is a lethal, adult-onset disease characterized by progressive degeneration of motoneurons. Recent data have suggested that the disease could be linked to abnormal development of the motor nervous system. Therefore, we investigated the electrical properties of lumbar motoneurons in an in-vitro neonatal spinal cord preparation isolated from SOD1(G85R) mice, which is a transgenic model of amyotrophic lateral sclerosis. The study was performed on young animals at the beginning of their second week, between postnatal days 6 and 10. Measurements of resting membrane potential and action potential characteristics of motoneurons were similar in wild-type and SOD1(G85R) mice. However, the input resistance of motoneurons from transgenic mice was significantly lower than that of wild-type animals, whereas their membrane capacitance was increased, strongly suggesting larger SOD1(G85R) motoneurons. Furthermore, the slope of the frequency-intensity curve was steeper in motoneurons from wild-type pups. Interestingly, the input resistance as well as the slope of the frequency-intensity curves of other spinal neurons did not show such differences. Finally, the amplitude of dorsal root-evoked potentials following high-intensity stimulation was significantly smaller in SOD1(G85R) motoneurons. The superoxide dismutase 1 mutation thus induces specific alterations of the functional properties of motoneurons early in development.

Serotonin enhances the resistance reflex of the locomotor network of the crayfish through multiple modulatory effects that act cooperatively.

Serotonin (5HT) is an endogenous amine that modifies posture in crustacea. Here, we examined the mechanisms of action of 5HT on the resistance reflex in crayfish legs. This reflex, which counteracts movements imposed on a limb, is based on a negative feedback system formed by proprioceptors that sense joint angle movements and activate opposing motoneurons. We performed intracellular recordings from depressor motoneurons while repetitively stretching and releasing a leg joint proprioceptor in a resting in vitro preparation (i.e., a preparation that lacks spontaneous rhythmic activity). 5HT increased the amplitude of the depolarization during the release phase of the proprioceptor (corresponding to an upward movement of the leg) and the discharge frequency of the motoneurons. The 5HT-induced increase in the resistance reflex is caused, to a large extent, by polysynaptic pathways because it was very attenuated in the presence of high divalent cation solution. In addition to this activation of the polysynaptic pathways, 5HT also has postsynaptic effects that enhance the resistance reflex. 5HT causes a tonic depolarization, as well as an increase in the time constant and input resistance of motoneurons. We developed a simple mathematical model to describe the integrative properties of the motoneurons. The conclusion of this study is that the input frequency and the decay time constant of the EPSPs interact in such a way that small simultaneous changes in these parameters can cause a large effect on summation. Therefore, the conjunction of presynaptic and postsynaptic changes produces a strong cooperative effect on the resistance reflex response.

Low micromolar concentrations of 4-aminopyridine facilitate fictive locomotion expressed by the rat spinal cord in vitro

Upregulating the operation of spinal locomotor networks is one mechanism to restore, at least partially, lesion-impaired locomotion. We investigated if the K + channel blocker 4-aminopyridine (4-AP) could facilitate spinal locomotor networks in addition to its well-known effect on motor nerve conduction. Fictive locomotor patterns were recorded from ventral roots (VRs) of the isolated spinal cord of the neonatal rat. 4-AP (0.1–50 μM) produced synchronous VR oscillations which did not develop into fictive locomotion. These oscillations had network origin, required intact glutamatergic transmission and were probably amplified via electrotonic coupling because of their depression by the selective gap junction blocker carbenoxolone. 4-AP (5 μM) slightly increased input resistance of lumbar motoneurons without affecting their action or resting potentials. Dorsal root (DR) evoked synaptic responses were enhanced (217±65%) by 5 μM 4-AP without changes in axon conduction. 4-AP (5 μM) accelerated fictive locomotion induced by N-methyl- d-aspartate (NMDA) and serotonin (5-HT) without altering cycle amplitude and facilitated the onset of fictive locomotion in the presence of sub-threshold concentrations of NMDA and 5-HT. Furthermore, in the presence of 4-AP, weak DR stimuli, previously insufficient to activate locomotor patterns, generated alternating VR discharges. Thus, although 4-AP per se could not directly activate the locomotor network of the spinal cord, it could strongly facilitate the locomotor program initiated by neurochemicals or electrical stimuli. These data suggest that the reported improvement by 4-AP in locomotor activity of spinal-injury patients may include activation of locomotor networks when low concentrations of this drug are administered in coincidence with appropriate stimuli.

Motoneurons Have Different Membrane Resistance during Fictive Scratching and Weight Support

The passive membrane properties of motoneurons may be affected in a behavior-specific manner because of differences in synaptic drive during different motor behaviors. To explore this possibility, the changes in input resistance (R(in)) and membrane time constant (tau(m)) of single extensor motoneurons were compared during two different types of motor activities: fictive scratching and fictive weight support. These two activities were selected because the membrane potential of extensor motoneurons follows a very different trajectory during fictive scratching (multiphasic, mostly rhythmic trajectory) and fictive weight support (monophasic, tonic trajectory). The intracellular recordings were performed in vivo in the immobilized, decerebrate cat using QX-314-containing microelectrodes to block action potentials. The R(in) and tau(m) at rest (control) were reduced substantially during all phases of fictive scratching. In contrast, R(in) and tau(m) changed only little during fictive weight support. Such a differential effect on the membrane resistance was observed even in motoneurons in which the peak voltage of the rhythmic depolarization during scratching was similar to the peak voltage of the tonic depolarization during weight support. The differential effect was attributed mainly to a difference in synaptic drive and, in particular, to a larger amount of inhibitory synaptic activity during fictive scratching. The present study demonstrates how the same motoneuron can have a different membrane resistance while participating in two different behaviors. Such tuning of the membrane resistance may provide motoneurons with behavior-specific integrative capabilities that, in turn, could be used advantageously to increase motor performance.

Denervation causes changes in electrophysiological properties in rat phrenic motoneurons

Thirty-nine male adult rats were divided into a control group and a denervation group that had been subjected to phrenicotomy 4 weeks earlier. Electrophysiological membrane properties (input resistance and rheobase) of phrenic motoneurons were measured from intracellular recordings made with glass microelectrodes. Under anesthetized and artificially ventilated conditions, the recorded motoneurons were divided into recruited (spike discharge) and non-recruited (depolarization only) types. There was a significant inverse relationship between the rheobase and input resistance in the control rats, but not in the denervated rats. In the control rats, the mean value of rheobase in the non-recruited motoneurons was significantly higher than that in the recruited motoneurons. In denervated rats, however, the mean value of rheobase in the recruited motoneurons was identical to that in the non-recruited motoneurons. The results indicated that phrenicotomy induced a de-differentiation of electrophysiological properties of the phrenic motoneurons, and that these changes might be restricted to the motoneurons innervating fast-twitch, low fatigue resistance muscle fibers.

Time-dependent changes in input resistance of rat hypoglossal motoneurons associated with whole-cell recording.

The effect of cellular dialysis associated with whole-cell recording was studied in 24 developing hypoglossal motoneurons in a rat brainstem slice preparation. In all cases, establishing whole-cell continuity with the electrode solution resulted in an increase in the input resistance measured in current clamp. The mean magnitude of this increase was 39.7% and the time course of the maximum effect was quite variable. There was no correlation found between the time to maximum effect and the magnitude of the increase in resistance. These data indicate that the passive membrane properties are not constant during whole-cell recording in mammalian motoneurons.

Developmental attenuation of Manduca pre-ecdysis behavior involves neural changes upstream of motoneurons and relay interneurons.

Each molt in the hawkmoth, Manduca sexta, culminates in the shedding of the old cuticle at ecdysis. Prior to each larval ecdysis, the old cuticle is loosened by pre-ecdysis behavior, which includes rhythmic, synchronous compressions in all abdominal segments. Prior to ecdysis to the pupal stage, pre-ecdysis behavior and its underlying motor pattern are markedly attenuated. A single pair of interneurons located in the terminal abdominal ganglion, the IN-402s, drives compression motoneuron activity during the pre-ecdysis motor pattern via monosynaptic excitatory connections. The present study tested the hypotheses that (1) changes in intrinsic properties (resting membrane potential, spike threshold, input resistance and excitability) of compression motoneurons, or (2) changes in the strength of synaptic connections from IN-402s to compression motoneurons, underlie the developmental attenuation of the pre-ecdysis motor pattern. Membrane potential was slightly more hyperpolarized in prepupal as compared to larval motoneurons, but no other findings supported the tested hypotheses. These results suggest that developmental weakening of the pre-ecdysis motor pattern results from changes upstream of the compression motoneurons and their synaptic connections from IN-402s.

Phase-dependent presynaptic modulation of mechanosensory signals in the locust flight system.

In the locust flight system, afferents of a wing hinge mechanoreceptor, the hindwing tegula, make monosynaptic excitatory connections with motoneurons of the elevator muscles. During flight motor activity, the excitatory postsynaptic potentials (EPSPs) produced by these connections changed in amplitude with the phase of the wingbeat cycle. The largest changes occurred around the phase where elevator motoneurons passed through their minimum membrane potential. This phase-dependent modulation was neither due to flight-related oscillations in motoneuron membrane potential nor to changes in motoneuron input resistance. This indicates that modulation of EPSP amplitude is mediated by presynaptic mechanisms that affect the efficacy of afferent synaptic input. Primary afferent depolarizations (PADs) were recorded in the terminal arborizations of tegula afferents, presynaptic to elevator motoneurons in the same hemiganglion. PADs were attributed to presynaptic inhibitory input because they reduced the input resistance of the afferents and were sensitive to the gamma-aminobutyric acid antagonist picrotoxin. PADs occurred either spontaneously or were elicited by spike activity in the tegula afferents. In summary, afferent signaling in the locust flight system appears to be under presynaptic control, a candidate mechanism of which is presynaptic inhibition.

Naloxone reduces the amplitude of IPSPs evoked in lumbar motoneurons by reticular stimulation during carbachol-induced motor inhibition

During active sleep or carbachol-induced motor inhibition, electrical stimulation of the medullary nucleus reticularis gigantocellularis (NRGc) evoked large amplitude, glycinergic inhibitory postsynaptic potentials (IPSPs) in cat motoneurons. The present study was directed to determine whether these IPSPs, that are specific to the state of active sleep, are modulated by opioid peptides. Accordingly, intracellular recordings were obtained from lumbar motoneurons of acute decerebrate cats during carbachol-induced motor inhibition while an opiate receptor antagonist, naloxone, was microiontophoretically released next to the recorded cells. Naloxone reversibly reduced by 26% the mean amplitude of NRGc-evoked IPSPs (1.9±0.2 mV (S.E.M.) vs. 1.4±0.2 mV; n=11, control and naloxone, respectively, p<0.05), but had no effect on the other waveform parameters of these IPSPs (e.g., latency-to-onset, latency-to-peak, duration, etc.). The mean resting membrane potential, input resistance and membrane time constant of motoneurons following naloxone ejection were not statistically different from those of the control. These data indicate that opioid peptides have a modulatory effect on NRGc-evoked IPSPs during carbachol-induced motor inhibition. We therefore suggest that endogenous opioid peptides may act as neuromodulators to regulate inhibitory glycinergic synaptic transmission at motoneurons during active sleep.

Electrical properties and morphology of motoneurons developing in dissociated unpurified co-culture of the embryonic rat brainstem, spinal cord, and hindlimb tissues

Experimental measurements of the input resistance were performed using a whole-cell patch-clamp recording technique of presumed motoneurons in unpurified co-culture of the dissociated prenatal rat brainstem, spinal cord, and hindlimb muscle tissues at different terms of thein vitro development. The recorded neurons were then labelled with Neurobiotin. Morphology of 21 completely stained cells was reconstructed and quantified in 3-D space. To estimate the size of the neurons, their total membrane areas and terminal tip numbers were computed. Computer models based on the reconstructed forms were used to evaluate the impact of cell morphology on the input resistance of motoneurons. The membrane resistivity was assumed as passive, uniform, and constant (12,000 Ω·cm2) at all ages studied. We found that changes in the measured input resistance paralleled those in dendritic morphology at all stages of the development, and that computed values correlated well with measured data. Therefore, we conclude that changes in geometry of the neuron may themselves account for evolution of its input resistance during development.

Comparison of corticomotoneuronal EPSPs and macro-MUPs in amyotrophic lateral sclerosis.

We correlated the size of the corticomotoneuronal excitatory postsynaptic potential (CM-EPSP) arising in a single spinal motor neuron with the function of the target motor unit as measured by conventional and macro EMG in early amyotrophic lateral sclerosis (ALS). Macro motor unit potentials (macro-MUPs) were recorded from a surface electrode after spike-triggered averaging in the extensor digitorum communis muscle. The size of the CM-EPSP projecting to the same motor unit was measured from changes in the firing probability of single motor units induced by transcranial magnetic stimulation using peristimulus time histograms. In controls, the amplitudes of CM-EPSPs and macro-MUPs correlated inversely, probably reflecting a lower input resistance of larger spinal motoneurons. In ALS the amplitude of macro-MUPs did not correlate with that of CM-EPSPs and one third of normal ALS motor units had a reduced or temporally dispersed CM-EPSP. The findings indicate primary dysfunction of the corticomotoneuronal projection system in ALS that is independent of functional changes of spinal motoneurons.

Modulation of inspiratory drive to phrenic motoneurons by presynaptic adenosine A1 receptors

The involvement and mechanisms of adenosine A1 receptors in regulating bulbospinal synaptic transmission of inspiratory drive to phrenic motoneurons were investigated. The adenosine analog N6-cyclopentyladenosine (CPA) induced a dose-dependent decrease of both inspiratory-modulated activity of C4 ventral roots and synaptic currents of phrenic motoneurons in an in vitro brainstem/spinal cord preparation from neonatal rats. No significant changes were observed in steady-state membrane current (during the expiratory phase). The depressant action of CPA on inspiratory drive was blocked by the selective A1 receptor antagonist 8-cyclopentyltheophylline (CPT). The adenosine receptor antagonist 3-isobutyl-1-methylxanthine (IBMX) induced varying degrees of enhancement of inspiratory-modulated synaptic current, as did CPT. This suggests a role of endogenous adenosine in synaptic transmission of respiratory drive to phrenic motoneurons. The relative contribution of pre- and postsynaptic adenosine receptors was examined by looking at the effects of CPA on postsynaptic membrane properties and on spontaneous or miniature excitatory postsynaptic currents (EPSCs). CPA had no detectable effect on the input resistance of phrenic moto-neurons. Moreover, the inward currents of phrenic moto-neurons in response to exogenously applied glutamate were not affected by adenosine-related compounds. On the other hand, CPA produced a significant decrease in the frequency of spontaneous and of miniature EPSCs. We conclude that adenosine can modulate transmission of inspiratory drive from bulbospinal neurons to phrenic motoneurons via presynaptic A1 receptors.

Dendritic properties of uropod motoneurons and premotor nonspiking interneurons in the crayfish Procambarus clarkii Girard

Dendritic properties of uropod motoneurons and premotor nonspiking interneurons of crayfish have been studied using intradendritic recording and current injection. The input resistance of phasic motoneurons (5.20 ± 0.5 MΩ; mean ± standard error) measured by injecting constant hyperpolarizing current was significantly lower than that of tonic motoneurons (10.3 ± 2.6 MΩ; 0.02 0.05). In response to intracellular injection of sinusoidally oscillating current, phasic motoneurons showed one or two spikes per depolarization period irrespective of oscillating frequency ranging from 1 to 16 Hz. Tonic motoneurons showed larger numbers of spikes per stimulus period at lower frequencies. Nonspiking interneurons also showed phase-locked effects on the motoneuron spike activity. The effective frequency range over which injected oscillating current could modulate motoneuron spike activity was similar for tonic motoneurons and nonspiking interneurons.

Analysis of Ia-inhibitory synaptic input to cat spinal motoneurons evoked by vibration of antagonist muscles

1. Steady-state inhibitory postsynaptic potentials (IPSPs) were evoked in tibialis anterior and extensor digitorum longus motoneurons of the cat by using tendon vibration to activate Ia-afferent fibers from the antagonist medial gastrocnemius muscle. 2. The effective synaptic currents (IN) underlying the steady-state IPSPs were measured by the use of a modified voltage-clamp technique. The amplitudes of the effective synaptic currents (1.62 +/- 0.66 nA, mean +/- SD; n = 20) extended over a fivefold range (0.5-2.7 nA) but were not correlated with the intrinsic properties of the motoneurons or with putative motor unit type. 3. We calculated the synaptic conductance (GS) underlying the steady-state Ia IPSPs from measurements of motoneuron input conductance during the activation of the Ia synaptic input. As was expected from Ohm's law, the Ia-inhibitory GS and IN were correlated (r = 0.49; P less than 0.05). Like IN, GS (175 +/- 202 nS, mean +/- SD; n = 20) was not correlated with the intrinsic properties of the motoneurons. 4. As has been reported previously for transient Ia IPSPs, the amplitudes of the steady-state IPSPs were correlated with motoneuron input resistance (r = 0.74; P less than 0.001) and homonymous Ia excitatory postsynaptic synaptic potential (EPSP) amplitude (r = 0.72; P less than 0.001). 5. The amplitudes of the steady-state Ia IPSPs and the homonymous Ia EPSPs were plotted on logarithmic axes. The slope (0.59) was significantly less than 1, which indicates that the gradient of Ia inhibition across the motoneuron pool is less steep than that of Ia excitation.(ABSTRACT TRUNCATED AT 250 WORDS)

Distribution of effective synaptic currents underlying recurrent inhibition in cat triceps surae motoneurons

1. Steady-state recurrent (Renshaw) inhibitory postsynaptic potentials (RIPSPs) were evoked in cat triceps surae motoneurons by stimulating the heteronymous muscle nerve at 100 Hz after dorsal root section. The effective synaptic currents (i.e., the net synaptic current measured at the soma, IN) underlying these inhibitory potentials were measured with a modified voltage-clamp technique. 2. The average value of the effective synaptic currents measured in medial gastrocnemius (MG) motoneurons was 0.4 nA. There was no significant correlation between the IN measured in individual cells and motoneuron input resistance (RN), rheobase (IR), duration of the spike afterhyperpolarization (AHPt1/2), or putative motor-unit type, although the steady-state inhibitory post-synaptic potential (IPSP) amplitudes were correlated with all of these parameters. 3. Steady-state recurrent inhibition was accompanied by a small (3.5%, on average) decrease in the resting input resistance of the motoneurons. The small magnitude of this measured change supports the hypothesis of Burke et al. that the site of synaptic contact between Renshaw cells and motoneurons is somewhat distal to the cell soma. 4. The absence of a differential distribution of the effective synaptic currents generated by Renshaw cells within the MG pool does not support the idea that recurrent inhibition mediates a selective reduction of the firing of small, low-threshold motoneurons by large, high-threshold motoneurons. The small amplitude of the effective synaptic currents we measured suggests that the contribution of recurrent inhibition to the direct modulation of motoneuron firing rate is subtle and that it is perhaps principally involved in the fine control and smooth production of muscle force.