Group Ia Muscle Spindle Afferents Research Articles

Diet-induced obesity decreases rate-dependent depression in the Hoffmann's reflex in adult mice.

Obesity is associated with balance and motor control deficits. We have recently shown that Group Ia muscle spindle afferents, the sensory arm of the muscle stretch reflex, are less responsive in mice fed a high‐fat diet. Here we test the hypothesis that reflex excitability to sensory information from Group Ia muscle spindle afferents is altered in a mouse model of diet‐induced obesity. We measured the anesthetized Hoffmann’s or H‐reflex, the electrical analog of the muscle stretch reflex. Adult mice of both sexes were fed a control diet (CD; 10% kcal from fat) or a high‐fat diet (HFD; 60% kcal from fat) for 5, 10, or 15 weeks. We used three quantitative measures of H‐reflex excitability: (1) H‐reflex latency; (2) the percentage of motor neurons recruited from electrical stimulation of Group Ia muscle spindle afferents (Hmax/Mmax); and (3) rate‐dependent depression (RDD), the decrease in H‐reflex amplitude to high frequency stimulation (20 stimuli at 5 Hz). A HFD did not significantly alter H latency (P = 0.16) or Hmax/Mmax ratios (P = 0.06), but RDD was significantly lower in HFD compared to CD groups (P < 0.001). Interestingly, HFD males exhibited decreased RDD compared to controls only after 5 and 10 weeks of feeding, but females showed progressive decreases in RDD that were only significant at 10 and 15 weeks on the HFD. These results suggest that high‐fat feeding increases H‐reflex excitability. Future studies are needed to determine whether these changes alter muscle stretch reflex strength and/or balance and to determine the underlying mechanism(s).

Spindle model responsive to mixed fusimotor inputs and testable predictions of beta feedback effects.

Skeletofusimotor (beta) motoneurons innervate both extrafusal muscle units and muscle fibers within muscle spindle stretch receptors. By receiving excitation from group Ia muscle spindle afferents and driving the muscle spindle afferents that excite them, they form a positive feedback loop of unknown function. To study it, we developed a computationally efficient model of group Ia afferent behavior, capable of responding to multiple fusimotor inputs, that matched experimental data. This spindle model was then incorporated into a simulation of group Ia feedback during ramp/hold and triangular stretches with and without closure of the beta loop, assuming that gamma and beta fusimotor drives of the same type (static or dynamic) have identical effects on spindle afferent firing. The effects of beta feedback were implemented by driving a fusimotor input with a delayed and filtered fraction of the spindle afferent output. During triangular stretches, feedback through static beta motoneurons enhanced Ia afferent firing during shortening of the spindle. In contrast, closure of a dynamic beta loop increased Ia firing during lengthening. The strength of beta feedback, estimated as a "loop gain" was comparable to experimental estimates. The loop gain increased with velocity and amplitude of stretch but decreased with increased superimposed gamma fusimotor rates. The strongest loop gains were seen when the beta loop and the gamma bias were of different types (static vs. dynamic).

Amplification and Linear Summation of Synaptic Effects on Motoneuron Firing Rate

The aim of this study was to measure the effects of synaptic input on motoneuron firing rate in an unanesthetized cat preparation, where activation of voltage-sensitive dendritic conductances may influence synaptic integration and repetitive firing. In anesthetized cats, the change in firing rate produced by a steady synaptic input is approximately equal to the product of the effective synaptic current measured at the resting potential (I(N)) and the slope of the linear relation between somatically injected current and motoneuron discharge rate (f-I slope). However, previous studies in the unanesthetized decerebrate cat indicate that firing rate modulation may be strongly influenced by voltage-dependent dendritic conductances. To quantify the effects of these conductances on motoneuron firing behavior, we injected suprathreshold current steps into medial gastrocnemius motoneurons of decerebrate cats and measured the changes in firing rate produced by superimposed excitatory synaptic input. In the same cells, we measured I(N) and the f-I slope to determine the predicted change in firing rate (Delta F = I(N) * f-I slope). In contrast to previous results in anesthetized cats, synaptically induced changes in motoneuron firing rate were greater-than-predicted. This enhanced effect indicates that additional inward current was present during repetitive firing. This additional inward current amplified the effective synaptic currents produced by two different excitatory sources, group Ia muscle spindle afferents and caudal cutaneous sural nerve afferents. There was a trend toward more prevalent amplification of the Ia input (14/16 cells) than the sural input (11/16 cells). However, in those cells where both inputs were amplified (10/16 cells), amplification was similar in magnitude for each source. When these two synaptic inputs were simultaneously activated, their combined effect was generally very close to the linear sum of their amplified individual effects. Linear summation is also observed in medial gastrocnemius motoneurons of anesthetized cats, where amplification is not present. This similarity suggests that amplification does not disturb the processes of synaptic integration. Linear summation of amplified input was evident for the two segmental inputs studied here. If these phenomena also hold for other synaptic sources, then the presence of active dendritic conductances underlying amplification might enable motoneurons to integrate multiple synaptic inputs and drive motoneuron firing rates throughout the entire physiological range in a relatively simple fashion.

Group I disynaptic excitation of cat hindlimb flexor and bifunctional motoneurones during fictive locomotion.

The incidence of short latency excitation of motoneurones innervating flexor and bifunctional muscles evoked by group I intensity (<= 2 x threshold) electrical stimulation of hindlimb muscle nerves was investigated during fictive locomotion in decerebrate cats. Intracellular recordings were made from hindlimb motoneurones in which action potentials were blocked by intracellular diffusion of a lidocaine (lignocaine) derivative (QX-314) and fictive locomotion was evoked by electrical stimulation of the midbrain. Few motoneurones (16%) received group I-evoked oligosynaptic excitation in the absence of fictive locomotion. During fictive locomotion 39/44 (89%) motoneurones innervating ankle, knee or hip flexor muscles and 18/28 (64%) motoneurones innervating bifunctional muscles received group I-evoked oligosynaptic EPSPs. In flexor motoneurones, locomotor-dependent excitation was present in both step cycle phases but largest during flexion. In bifunctional motoneurones, EPSPs were often largest at the transition between flexion and extension phases. Activation of homonymous afferents most consistently evoked the largest locomotor-dependent excitation (amplitude up to 4.6 mV), but in some cases stimulation of heteronymous flexor or bifunctional muscle nerves evoked large EPSPs. EPSP amplitude became maximal as stimulation intensity was increased to about twice threshold. This suggests that tendon organ afferents can evoke group I EPSPs during locomotion. The EPSPs resulting from brief, small stretches of extensor digitorum longus tendons indicate that group Ia muscle spindle afferents can also evoke the group I excitation of flexors. Stimulation of extensor group I afferents did not result in excitation of flexor motoneurones. The mean latency of locomotor-dependent group I excitation in flexor and bifunctional motoneurones was 1.64 +/- 0.16 ms, indicating a path consisting of a single interneurone interposed between group I afferents and motoneurones innervating flexor and bifunctional muscles. This disynaptic excitation is analogous to that recorded in extensor motoneurones and evoked from extensor group I afferents during locomotion. Differences in the phase dependence and sources of group I excitation to flexor and extensor motoneurones during locomotion suggest the existence of separate groups of excitatory interneurones exciting flexor and extensor motoneurones. The wide distribution of group I disynaptic excitation in motoneurones innervating extensor, flexor and bifunctional muscles acting on hip, knee and ankle joints suggests that these pathways can play an important role in the reinforcement of ongoing locomotor activity throughout the limb.

Neuronal basis of afferent-evoked enhancement of locomotor activity.

Activation of ankle extensor group Ia muscle spindle or Ib tendon organ afferents during locomotion can prolong and enhance hindlimb extensor motoneuron activity. A growing body of evidence suggests that these group I evoked reflexes not only compensate for a changing environment but also help shape extensor activity during normal, unperturbed locomotion. In this paper we review four mechanisms that underlie the group I evoked enhancement of ipsilateral extensor activity during locomotion. The first three are pre-motoneuronal mechanisms that are part of group I reflex pathway reorganization during locomotion. They are (1) a suppression of group I evoked nonreciprocal inhibition, (2) a release from inhibition of excitatory interneurons in disynaptic pathways from group I afferents to extensor motoneurons, and (3) longer latency excitation evoked through extensor portions of the locomotor circuitry. The fourth factor contributing to group I evoked increases in motoneuron activity during locomotion is the increase in motoneuron excitability produced by postsynaptic changes in motoneuron membrane conductances. Most results to be discussed were obtained during locomotion in decerebrate cats in which fictive locomotion was evoked by stimulation of the midbrain following neuromuscular blockade.

Group I extensor afferents evoke disynaptic EPSPs in cat hindlimb extensor motorneurones during fictive locomotion.

1. Intracellular recording from extensor motoneurones in paralysed decerebrate cats was used to examine the distribution of short-latency non-monosynaptic excitation by group I afferents during fictive locomotion produced by stimulation of the mesencephalic locomotor region (MLR). 2. During the extension but not the flexion phase of fictive locomotion, stimulation of ankle extensor nerves at 1.2-2.0 times threshold evoked excitatory postsynaptic potentials (EPSPs) in motoneurones innervating hip, knee and ankle extensors. Disynaptic EPSPs were also evoked by selective activation of group Ia muscle spindle afferents by muscle stretch. 3. The central latencies of these group I-evoked EPSPs (mean, 1.55 ms) suggest their mediation by a disynaptic pathway with a single interneurone interposed between extensor group I afferents and extensor motoneurones. Disynaptic EPSPs were also evoked during periods of spontaneous locomotion following the cessation of MLR stimulation. 4. Hip extensor motoneurones received disynaptic EPSPs during extension following stimulation of both homonymous and ankle extensor nerves. Stimulation of hip extensor nerves did not evoke disynaptic EPSPs in ankle extensor motoneurones. 5. The appearance of disynaptic EPSPs during extension appears to result from cyclic disinhibition of an unidentified population of excitatory spinal interneurones and not postsynaptic voltage-dependent conductances in motoneurones or phasic presynaptic inhibition of group I afferents during flexion. 6. The reorganization of group I reflexes during fictive locomotion includes the appearance of disynaptic excitation of hip, knee and ankle extensor motoneurones. This excitatory reflex is one of the mechanisms by which group I afferents can enhance extensor activity and increase force production during stance.

Physiological adjustments in a reflex pathway following partial loss of target neurons

This investigation was undertaken to study plasticity in a reflex pathway follofwing partial elimination of target neurons. Adult cats were subjected to unilateral avulsion of the L7 spinal ventral root, which induces retrograde cell death among the motoneurons of the L7 segment. At 1, 3, 6 and 12 weeks after the lesion, the monosynaptic reflexes were recorded in the L6 and S1 ventral roots during stimulation of the L6, L7 and S1 dorsal roots. Since the group Ia muscle spindle afferents passing through these dorsal roots were deprived of their target motoneurons in the L7 segment, compensatory reflex changes were searched for in the remaining monosynaptic contacts with the intact target motoneurons of the L6 and S1 segments. The results indicate that a partial loss of target motoneurons triggers changes leading to increased monosynaptic reflexes of the remaining intact target motoneurons. On average, the reflexes had more than doubled their size at 12 weeks postoperatively. Possible mechanisms for this reflex potentiation are discussed.

Signal transmission from motor axons to group Ia muscle spindle afferents: Frequency responses and second-order non-linearities

Spinal recurrent inhibition via Renshaw cells and proprioceptive feedback via skeletal muscle and muscle spindle afferents have been hypothesized to constitute a compound feedback system [ Windhorst (1989) Afferent Control of Posture and Locomotion; Windhorst (1993) Robots and Biological Systems—Towards a New Bionics]. To assess their detailed functions, it is necessary to know their dynamic characteristics. Previously we have extensively described the properties of signal transmission from motor axons to Renshaw cells using random motor axon stimulation and data analysis methods based thereupon. Using the same methods, we here compare these properties, in the cat, with those between motor axons and group Ia muscle spindle afferents in terms of frequency responses and nonlinear features. The frequency responses depend on the mean rate (carrier rate) of activation of motor axons and on the strength of coupling between motor units and spindles. In general, they are those of a second-order low-pass system with a cut-off at fairly low frequencies. This contrasts with the dynamics of motor axon-Renshaw cell couplings which are those of a much broader band-pass with its peak in the range of c. 2–15 Hz [ Christakos (1987) Neuroscience 23, 613–623]. The second-order non-linearities in motor unit-muscle spindle signal lines are much more diverse than those in motor axon-Renshaw cell couplings. Although the average strength of response declines with mean stimulus rate in both subsystems, there is no systematic relationship between the amount of non-linearity and the average response in the former, whilst there is in the latter. The qualitative appearance of motor unit-muscle spindle non-linearities was complicated as was the average response to motor unit twitches. Thus, whilst Renshaw cells appear to dynamically reflect motor output rather faithfully, muscle spindles seem to signal local muscle fibre length changes and their dynamics. This would be consistent with the hypothesis that the two feedback pathways monitor different state variables determining the production of muscle force: neural input and length and its changes. Specifically, the dynamic properties of both subsystems may combine favourably to decrease the risk of instability (tremor) in the motoneuron-muscle spindle loop.

Further evidence for synaptic actions of muscle spindle secondaries in the middle lumbar segments of the cat spinal cord.

1. The aim of this study has been to investigate the receptor origin of postsynaptic actions evoked by group II muscle afferents in mid-lumbar segments of the cat spinal cord. The experiments tested the hypothesis that the afferents involved were the secondary endings of muscle spindles. 2. Spindle afferents were activated by contractions of intrafusal muscle fibres which were induced by electrical stimulation of fusimotor axons in the distal parts of transected ventral roots by one to three stimuli at 150-500 stimuli/s. A separate series of experiments has shown that such stimuli are effective in activating a considerable proportion of muscle spindle secondaries when contractions of extrafusal muscle fibres are eliminated by differential fatigue of these fibres, provided that several fusimotor axons are stimulated simultaneously. 3. Extracellular field potentials were recorded in the dorsal horn, at such locations where synaptic actions were evoked by electrical stimulation of group II but not group Ia muscle spindle or group Ib tendon organ afferents of pretibial flexors. Effects of activation of spindle afferents following stimulation of fusimotor axons were then compared with effects evoked by electrical stimulation of group II afferents of anterior tibial or extensor digitorum longus nerves and by small stretches of these muscles. 4. Distinct field potentials were evoked by stimulation of ventral root fibres at all locations at which field potentials were obtained from group II afferents stimulated electrically. The latencies of these field potentials were in both cases shorter in the dorsal horn than in the ventral horn. 5. The appearance of these field potentials was not related to contractions of extrafusal muscle fibres and was also observed when these contractions were practically eliminated. Furthermore, their threshold and similar dependence on a potentiating effect of two to three stimuli, as found for single secondaries, allow them to be attributed to secondary endings of muscle spindles.

Sensory input to cells of origin of uncrossed spinocerebellar tract located below Clarke's column in the cat.

1. Sensory inputs to and locations of uncrossed spinocerebellar tract neurones in the lower lumbar cord were studied in chloralose-anaesthetized cats. 2. Neurones with axons ascending in the ipsilateral thoracic funiculi and projecting to the cerebellum were found mainly dorsal to the central canal (laminae V and VI) in the L5-L6 segments, i.e. at levels caudal to Clarke's column. Axons considered to originate from these cells were located in the dorsal half of the lateral funiculus at the level of L2, intermingled with axons of the dorsal spinocerebellar tract originating at the levels of Clarke's column. 3. Synaptic actions of primary afferents on neurones with antidromic invasion following stimuli applied to ipsilateral thoracic funiculi or to the cerebellum were investigated using intracellular or extracellular recording in the caudal lumbar segments. 4. Monosynaptic excitatory effects were evoked by electrical stimulation of group I muscle afferents of the hindlimb ipsilateral to the cell body. The majority of neurones received monosynaptic excitation from two or more muscles, predominantly extensors. They were frequently co-excited by group Ia muscle spindle and group Ib tendon organ afferents. 5. Volleys in cutaneous afferents produced excitation with short central latencies. In addition to the monosynaptic and disynaptic excitation from low-threshold cutaneous afferents, there were indications of monosynaptic effects from slightly slower conducting fibres. The majority of these neurones also received monosynaptic excitation from group I muscle afferents. Neurones with cutaneous input tended to be located more dorsally compared with those responding only to muscle afferents. 6. Volleys in joint afferents produced monosynaptic excitatory postsynaptic potentials (EPSPs) in the neurones with EPSPs from group I or group I and cutaneous afferents. 7. Some neurones were disynaptically inhibited from group I muscle afferents. Convergence of monosynaptic group I excitation and disynaptic group I inhibition occurred in varieties of patterns. 8. Polysynaptic excitation, inhibition or mixed effects of both were evoked from ipsilateral cutaneous afferents and high-threshold muscle and joint afferents, whereas effects from the controlateral afferents were feeble.(ABSTRACT TRUNCATED AT 400 WORDS)

Projection of Ia and Ib afferents from forelimb muscles to the C3-C4 segments of the cat spinal cord.

Group Ia muscle spindle afferents were activated separately by small stretches applied to the tendons of antibrachial muscles in the forelimb in the cat. Group Ib tendon organ afferents were stimulated electrically after a selective increase of the threshold of the Ia afferents. Recordings of focal synaptic potentials were made in the C3-C4 segments in the medial part of the base of the dorsal horn. It has been found that both Ia and Ib afferents have monosynaptic connections with neurones in this medial region. Quantitatively, these two groups of afferents produced focal synaptic potentials of approximately the same size. The connections may be to inhibitory interneurones projecting to the C3-C4 propriospinal neurones, which are known to receive disynaptic IPSPs from group I muscle afferents.

Light and electron microscopy of contacts between primary afferent fibres and neurones with axons ascending the dorsal columns of the feline spinal cord

In addition to primary afferent fibres, the dorsal columns of the cat spinal cord contain ascending second-order axons which project to the dorsal column nuclei. The aim of the present study was to obtain morphological evidence that certain primary afferent axons form monosynaptic contacts with cells of origin of this postsynaptic dorsal column pathway. In ten adult cats, neurones with axons ascending the dorsal columns were retrogradely labelled with horseradish peroxidase using a pellet implantation method in the thoracic dorsal columns. In the lumbosacral regions of the same animals, primary afferent fibres were labelled intra-axonally with ionophoretic application of horseradish peroxidase. Tissue containing labelled axons was prepared for light and combined light and electron microscopy. Ultrastructural examination demonstrated that slowly adapting (Type I), hair follicle, Pacinian corpuscle and group Ia muscle spindle afferents formed monosynaptic contacts with labelled cells and light microscopical analysis suggested that they also received monosynaptic input from rapidly adapting (Krause) afferents. This evidence suggests that sensory information from large-diameter cutaneous and muscle spindle afferent fibres is conveyed disynaptically via the postsynaptic dorsal column pathway to the dorsal column nuclei. Some of the input to this pathway is probably modified in the spinal cord as the majority of primary afferent boutons forming monosynaptic contacts were postsynaptic to other axon terminals. The postsynaptic dorsal column system appears to constitute a major somatosensory pathway in the cat.

Convergence onto interneurons subserving primary afferent depolarization of group I afferents.

The aim of the study was to investigate whether common or independent neuronal pathways are used to evoke primary afferent depolarization (PAD) from selectively activated group Ia and Ib afferents of different muscles. To this end, the spatial facilitation of effects of various afferents, indicating convergence on the same interneurons, was used as a test. Its occurrence was assessed on dorsal root potentials (DRPs) evoked in unspecified fibers or using intra-axonal recording from identified group Ia muscle spindle afferents or group Ib tendon organ afferents. Spatial facilitation has been found in PAD pathways a) from various Ia-afferents, whether of flexors or extensors; b) from various Ib-afferents, whether of flexors or extensors; and c) from flexor Ib-afferents and flexor or extensor Ia-afferents. In contrast, no indications have been found for common pathways from extensor Ib- and any Ia-afferents under conditions that proved effective in other combinations. Latencies of those components of PAD that appeared as a result of the spatial facilitation ranged from 2 to more than 7 ms, indicating that the convergence occurred in the shortest (trisynaptic) as well as longer pathways. The same patterns of convergence have been found in PAD pathways to extensor and flexor Ia-afferents (in experiments with intraaxonal recording from these afferents). The possibility might thus be considered that some neuronal pathways are used to modulate transmission via Ia-afferents independently of their muscle origin. The same might hold true for extensor and flexor Ib-afferents. Generally, it is concluded that the minimal number of distinct neuronal populations subserving PAD of group I afferents may be two to six. Additionally, actions of cutaneous, joint, and interosseous afferents on DRPs from Ia-afferents were reexamined to further the comparison between neurons mediating PAD and those mediating postsynaptic excitation or inhibition of motoneurons. Only depression of Ia DRPs followed stimulation of these afferents at intensities of 1.5-2.0 times threshold and higher; lower threshold afferents were apparently ineffective. On the basis of lack of convergence of extensor Ib and Ia muscle afferents and of low-threshold cutaneous afferents, interneurons mediating PAD may thus be distinguished from the interneurons subserving Ib and Ia-like-Ib postsynaptic actions in motoneurons. The latter are coexcited by these three groups of afferents.

Ultrastructure of muscle spindle afferent terminations in lamina VI of the cat spinal cord

Two group Ia muscle spindle afferents were impaled in the lumbosacral enlargement of the cat's spinal cord and intra-axonally labeled with horseradish peroxidase. Terminations in lamina VI were examined with the electron microscope. Boutons formed synaptic associations with somata and large dendritic shafts in the lamina VI neuropile and received axo-axonic contacts. It is concluded that group Ia terminals synapse with the proximal regions of lamina VI neurons and are under strong presynaptic control.

Inhibitory interactions between interneurones in reflex pathways from group Ia and group Ib afferents in the cat.

A hypothesis has been verified that laminae V-VI interneurones which mediate non-reciprocal inhibition of motoneurones from group I muscle afferents have collateral actions on other laminae V-VI interneurones. Stimulation within the areas of projection of these inhibitory interneurones in motor nuclei and in Clarke's column would be expected to give rise to monosynaptic i.p.s.p.s in interneurones with disynaptic i.p.s.p.s from group I afferents if the hypothesis were correct. Intracellular records were made from eighty-five laminae V-VI interneurones with input from group Ia muscle spindle and/or group Ib tendon organ afferents. Weak intraspinal stimuli applied in motor nuclei in L7 and S1 segments, or in the lateral funiculus just caudal to Clarke's column in L4, were found to evoke monosynaptic i.p.s.p.s in seventy-two interneurones. These i.p.s.p.s were systematically correlated with disynaptic inhibition from group Ia or Ib afferents but not from other fibres. Such monosynaptic i.p.s.p.s evoked by intraspinal stimuli were seen in forty-two interneurones which themselves projected to the level of Clarke's column and therefore (on the basis of previous evidence) should mediate inhibition of motoneurones. For seven of these interneurones it was also shown directly that they projected to motor nuclei. The inhibition of such interneurones demonstrates mutual interactions between those interneurones which are interposed in inhibitory pathways from group I afferents. Only indirect indications have been obtained for inhibition of interneurones in the excitatory pathways.

Shared reflex pathways from Ib tendon organ afferents and Ia muscle spindle afferents in the cat.

The possibility was investigated that group Ia muscle spindle afferents and group Ib tendon organ afferents influence spinal motoneurones via shared neuronal pathways. Mutual facilitation of actions of these afferents at a premotoneuronal level has been taken as evidence that they use the same interneurones to evoke post-synaptic potentials (p.s.p.s) in motoneurones. Inhibitory p.s.p.s (i.p.s.p.s) or excitatory p.s.p.s (e.p.s.p.s) were evoked in motoneurones by selective activation of group Ia afferents or group Ib afferents. P.s.p.s following stimulation of both Ia and Ib afferents were then compared with the arithmetic sum of p.s.p.s evoked by each of them separately. When the former were larger the difference was used as a measure of synaptic actions mediated by interneurones co-excited by Ia and Ib afferents. Both excitatory and inhibitory pathways to motoneurones have been found to be shared by Ia and Ib afferents, although the proportion of interneurones actually used in common by these afferents could not be established. The latencies of post-synaptic actions mediated by such interneurones indicated that they were evoked disynaptically or trisynaptically. The study leads to two main conclusions: that group Ia muscle spindle afferents, and in consequence also fusimotor systems, may modulate the reflex action of tendon organs, and that the two groups of afferents are a source of information in a common feed-back system.

Electron microscopic observations on the synaptic contacts of group Ia muscle spindle afferents in the cat lumbosacral spinal cord

After intra-axonal injection of horseradish peroxidase (HRP) into afferent fibers originating from muscle spindle primary endings of the cat gastrocnemius, group Ia boutons located in the ventral horn of the spinal cord were identified and studied electron microscopically. The Ia boutons were invariably found to contain spherical synaptic vesicles (S-type boutons), and a number of them were also postsynaptic to smaller P-type boutons (large S-type boutons with axo-axonic contacts). None of the present Ia- boutons belonged to the previously described M-type 8. The vast majority of the studied boutons were considered to be located at less than 500 μm distance from the α-motoneuron soma. The results are discussed in relation to previous light and electron microscopic data.

Oligosynaptic excitation of motoneurones by impulses in group Ia muscle spindle afferents in the cat.

1. Intracellular recording from hind-limb motoneurones was used to investigate whether di- and trisynaptic (oligosynaptic) excitatory post-synaptic potentials (e.p.s.p.s) are evoked from group Ia muscle spindle afferents in those motoneurones in which such potentials are evoked from Ib tendon organ afferents or entire group I afferents. Ia afferents of triceps surae and plantaris were activated either selectively by single brief stretches of these muscles, or together with Ib afferents by electrical stimuli applied to the nerves.2. Muscle stretches below threshold for Ib afferents (10-35 mum) evoked e.p.s.p.s which appeared with latencies compatible with disynaptic and trisynaptic coupling between the afferents and the motoneurones. The latencies of a majority of these e.p.s.p.s were too short to allow their mediation by group II afferents, if any were activated by the applied stretches. They were also too short to be compatible with effects attributable to dorsal root reflexes. These e.p.s.p.s are thus attributed to oligosynaptic actions of Ia afferents.3. Stretch-evoked di- and trisynaptic Ia e.p.s.p.s were found in 83% of motoneurones in which e.p.s.p.s were evoked by stimuli which activated both Ia and Ib afferents; in five motoneurone species they were found in more than 90%. These observations lead to the conclusion that group Ia muscle spindle afferents evoke not only inhibitory but also excitatory actions in parallel with group Ib tendon organ afferents.4. The distribution of Ia oligosynaptic stretch-evoked excitation from ankle and toe extensor muscles was compared with the distribution of Ia non-reciprocal inhibition as described by Jankowska, McCrea & Mackel (1981b). Excitation pre-dominated in posterior biceps-semitendinosus motoneurones and inhibition in other species of motoneurones investigated, except those of intrinsic foot muscles (tibial motoneurones); similar proportions of the latter showed excitation and inhibition.5. Occurrence of oligosynaptic e.p.s.p.s as well as inhibitory post-synaptic potentials (i.p.s.p.s) of Ia origin in some motoneurone species, and in particular in individual motoneurones, is indicative of a number of reflex pathways between group I afferents and these motoneurones. Furthermore, the disappearance of some of the e.p.s.p.s evoked by near-threshold electrical stimulation following stronger stimuli indicates interactions between various functional groups of interneurones mediating group I actions.

Pattern of 'non-reciprocal' inhibition of motoneurones by impulses in group Ia muscle spindle afferents in the cat.

1. Inhibitory post-synaptic potentials (i.p.s.p.s) evoked by adequate stimulation of group Ia muscle spindle afferents of triceps surae and plantaris and by near-threshold electrical stimulation of quadriceps and hamstring nerves were recorded in a number of motoneurone species. The aim of the study was to compare the pattern of non-reciprocal Ia inhibitory actions on hind-limb motoneurones with the pattern of inhibition evoked from group Ib tendon organ afferents.2. In all the motoneurone species analysed in which i.p.s.p.s were evoked by electrical stimulation maximal for both group Ia and Ib afferents of triceps surae and plantaris, they were also evoked when these muscles were stretched and the amplitude of the stretch (10-35 mum) was below threshold for Ib afferents; 70-100% of motoneurones with Ib i.p.s.p.s showed stretch-evoked i.p.s.p.s. The stretch-evoked i.p.s.p.s appeared with latencies compatible with disynaptic and trisynaptic linkage. Since these latencies were too short to allow their mediation by group II afferents the i.p.s.p.s are attributed to a selective action of Ia afferents. The i.p.s.p.s did not appear after the nerves to triceps surae and plantaris had been cut.3. Electrical stimulation of quadriceps and hamstring nerves which was near threshold for Ia afferents and well below threshold for either the Ib component of the incoming volley or group II afferents, similarly evoked non-reciprocal i.p.s.p.s. They were found in those motoneurones in which inhibition was evoked by stimulation maximal for group I afferents. Such Ia i.p.s.p.s were evoked both in homonymous motoneurones and in motoneurones of four other hind-limb muscles. Their latencies corresponded to di- and trisynaptic coupling.4. In some motoneurones of the pretibial flexors (anterior tibial, extensor digitorum longus and peroneus longus), disynaptic i.p.s.p.s evoked from triceps surae and/or plantaris which were depressed by a conditioning ventral root stimulation (i.e. Ia reciprocal i.p.s.p.s) were followed by trisynaptic i.p.s.p.s which were not depressed in this way (Ia ;non-reciprocal' i.p.s.p.s). It thus appears that the same motoneurones may be inhibited by impulses in group Ia afferents via different spinal pathways.5. The study leads to the conclusion that the non-reciprocal inhibition from group Ia muscle spindle afferents operates in parallel with the inhibition from group Ib tendon organ afferents in all motoneurone species tested.

Common interneurones in reflex pathways from group 1a and 1b afferents of ankle extensors in the cat.

1. Input from group I afferents of ankle and toe extensors, other muscles, skin nerves and descending tracts to interneurones of Rexed's laminae V-VI in the cat spinal cord was analysed using intracellular recording from these interneurones. Adequate stimuli (muscle stretches) were used to activate selectively group Ia muscle spindle afferents of triceps surae and plantaris while other fibre systems were excited electrically. 2. Ia and Ib afferents of ankle and toe extensors were found to co-excite, co-inhibit or exert opposite synaptic actions in 41, 33, and 50% of the analysed interneurones, respectively. Taking into account both excitatory and inhibitory input from these two groups of afferents, 64% of the interneurones appeared to be used in common in reflex pathways from muscle spindles and tendon organs of ankle and toe extensors. 3. Selective input from Ib afferents of triceps surae and plantaris (excitation and/or inhibition) was found in 36% of the interneurones; there was evidence for a similarly selective input from Ia afferents. 4. A great majority (over 90%) of the interneurones excited by group I afferents were also inhibited by group I afferents, from either the same or other muscles. 5. Both monosynaptic and disynaptic e.p.s.p.s from Ia and/or Ib afferents from other muscles and from fibres in the ipsilateral funiculi were found in a great proportion of the same interneurones, together with disynaptic e.p.s.p.s from low threshold cutaneous afferents. 6. Intracellular staining with horseradish peroxidase revealed four different patterns of axonal projections of the analysed interneurones: (i) projections to motor nuclei and the intermediate region, (ii and III) projections only to the intermediate region, locally or combined with projections to different rostro-caudal levels, and (iv) projections to the opposite side of the spinal cord. 7. A large proportion of interneurones projecting to motor nuclei displayed input from both Ia and Ib afferents although such an input was a feature of interneurones with other projections as well. No systematic differences in the input from group I afferents were found for interneurones with different axonal projections. In contrast disynaptic e.p.s.p.s of cutaneous origin and monosynaptic e.p.s.p.s upon stimulation of ipsilateral spinal tracts appeared predominantly in interneurones projecting to motor nuclei.