Group Ia Afferents Research Articles

Primary afferent depolarization of central terminals of group II muscle afferents in the cat spinal cord.

1. The origin of primary afferent depolarization (PAD) of the central terminals of group II afferent fibres of tibialis anterior and extensor digitorum longus muscles has been investigated in the cat. Changes in the excitability of the terminals to intraspinal stimuli, upon application of conditioning stimuli to muscle nerves (quadriceps, sartorius, gracilis, posterior biceps-semitendinosus, anterior biceps-semimembranosus, gastrocnemius-soleus, deep peroneal), cutaneous nerves (sural, superficial peroneal) and the posterior nerve to the knee joint, were used as a measure of PAD. 2. PAD was most readily evoked by conditioning stimuli which were maximal for group II muscle afferents. However, some PAD was also evoked from group I afferents and evidence is presented that group Ia afferents contributed. Afferents of posterior biceps-semitendinosus and sartorius muscles appeared to be most effective. PAD was also evoked by stimulation of cutaneous and joint nerves, often in the same fibres which were affected by group Ia afferents. 3. It is concluded that there are several common sources of PAD of group II and group Ia afferent terminals on the one hand, and group Ib afferent terminals on the other. 4. The properties of PAD of group II afferents are discussed in relation to the problem of how PAD affects transmission from fibres with long terminal branches of small diameter.

Muscle afferent contribution to control of paw shakes in normal cats.

1. The discharge of various hindlimb muscle afferents was recorded during paw shakes in normal cats with the use of floating dorsal root electrodes. 2. Muscle spindle group Ia-afferents and tendon organ group Ib-afferents fired during muscle lengthening, reaching very high peak discharge rates and then silencing at or shortly after the onset of shortening. The timing of Ia firing was consistent with the predictions of a linear model as well as the responses of Ia endings subjected to identical length variations in separate anesthetized cats. 3. In the latter "reconstruction" experiments, waxing and waning dynamic fusimotor action straddling whole paw-shake sequences gave the most consistent matches with the data from the normal cats. The reproducibility of the inferred fusimotor action justifies the inclusion of paw shakes as a class of movement in which fusimotor set is high. 4. The peak ensemble Ia activity from single hindlimb muscles was estimated to be approximately 20 kiloimpulses/s (Kips). Ankle extensor and hamstrings length variations were nearly in phase in the first cycles of a paw-shake sequence. From published data on spindle populations in these muscles, this indicated that peak Ia input to the spinal cord exceeded 0.2 megaimpulses/s (Mips). 5. The phase relationship between origin-to-insertion muscle length and Ia firing during paw shakes was little affected by doubling or tripling the moment of inertia of the foot. We argue that this refutes the notion that in paw shakes phase reversals occur between muscle fibers and tendons in the muscles studied. 6. Inertial loading of the foot led to small but significant reductions in mean paw-shake frequency. This is consistent with an afferent contribution to the generation of these movements. 7. We conclude that in paw shakes in normal cats, the CNS "chooses" to sensitize Ia-afferents to muscle length variations by increasing dynamic fusimotor action. The resulting ensemble Ia input is very large and is likely to play a significant role in reflexly shaping the alpha-motoneuronal activity responsible for the paw shakes.

Demonstration of initial axon collaterals of cells of origin of the ventral spinocerebellar tract in the cat

Neurones of origin of the ventral spinocerebellar tract were stained with intracellularly applied horseradish peroxidase to investigate whether they give off any initial axon collaterals. The neurones were located in the fourth and fifth lumbar segments and were identified by their antidromic activation following stimulation in the contralateral superior cerebellar peduncle. Nine of the 23 neurones with well-stained axons were found to give off axon collaterals soon after the axons crossed the midline. The collaterals entered the contralateral ventral horn and branched within lamina VII and the dorsal part of lamina VIII. Collaterals were found arising only from neurones located in the middle of lamina VII and from axons which took a mediorostral direction. In all of these neurones excitatory postsynaptic potentials were evoked from group Ia afferents of at least some nerves, in addition to such potentials from Ib or unidentified group I afferents, and inhibitory postsynaptic potentials were evoked from group I and II afferents. The area of terminal branching of the collaterals suggests that they may supply contralateral ventral spinocerebellar neurones with information from muscles and/or mediate crossed reflexes from group I afferents.

Morphology of single mesencephalic trigeminal neurons innervating masseter muscle of the cat

The morphology of functionally identified single axons of mesencephalic trigeminal neurons was studied in the cat by the method of intra-axonal injection of horseradish peroxidase (HRP). Each axon can be divided into united (U), peripheral (P) and central branches (C). The united axon (U) descends from its soma within the tract of the trigeminal mesencephalic nucleus to the dorsal aspect of the trigeminal motor nucleus (Vmo), where it splits into peripheral and descending central branches with a Y-shaped bifurcation. The peripheral axon (P) joins the motor root of the trigeminal nerve to exit the brainstem. The central axon (C) travels caudally within the juxtatrigeminal regions (or lateral reticular formation). All 3 branches issue axon collaterals that distribute terminal boutons within the dorsolateral subdivision of Vmo, supra- and intertrigeminal regions. Collaterals emanating from the central axon (C) except for its proximal segment travel ventrolaterally within the juxtatrigeminal regions, and send their terminal branches into the lateral boundaries adjacent to the spinal trigeminal nucleus. The trajectory of terminal branches distinguishes group Ia afferents from the possible group II afferents. The majority of terminal boutons are found to distribute in the supra- and intertrigeminal regions for group II afferent fibers and in the dorsolateral subdivision of Vmo for group Ia afferents.

Excitability changes of ankle extensor group Ia and Ib fibers during fictive locomotion in the cat.

The present study examines the modulation of gastrocnemius-soleus (GS) monosynaptic reflexes as well as the intraspinal threshold changes of GS group I primary afferent terminals ending in the intermediate and motor nuclei during fictive locomotion in high decerebrate cats. The amplitude of the monosynaptic reflexes (MSR's) evoked in the medial gastrocnemius by stimulation of the lateral gastrocnemius nerve was increased during the extensor (E) phase, decreased during the flexion (F) phase of the step cycle and remained transiently increased after spontaneous episodes of fictive stepping. The intraspinal threshold of populations and of single group Ia GS afferent fibers ending in the motor pool, as well as of single Ia and Ib fibers ending in the intermediate nucleus, showed a sustained reduction during the episodes of fictive locomotion with superimposed cyclic changes in phase with the step cycle. During fictive walking and trotting the reduction of the intraspinal threshold of both Ia and Ib fiber terminals was maximal during the middle or late portion of the F-phase. During fictive gallop elicited by stimulation of the superficial peroneus nerve, the decrease in the intraspinal threshold of the Ia afferent fibers occurred however in phase with the activity of the GS motoneurons. During episodes of fictive locomotion slow, sustained negative DC potential shifts lasting tents of seconds, reflecting an increase in the extracellular potassium concentration were recorded at the base of the dorsal horn and in the intermediate nucleus. The present findings support the existence of tonic and phasic depolarization of the intraspinal terminals of GS group Ia and Ib primary afferents during spontaneous fictive locomotion. It is suggested that accumulation of potassium ions in the extracellular space contributes mainly to the sustained depolarization of group I fibers. The phasic depolarization would be mostly due to the activation of specific sets of interneurons and may, in the case of Ia fibers, contribute to the cyclic modulation of the MRS elicited during fictive locomotion.

Modification of primary afferent depolarization in cat group Ia afferents following high frequency intra-axonal tetanization of individual afferents

Intra-axonal tetanization of a single, functionally-identified group Ia afferent from the triceps surae muscle in the anesthetized cat produces marked enhancement and slowing of the primary afferent depolarization (PAD) generated in the Ia afferent by volleys in flexor muscle group Ia afferents, plus a pronounced transmembrane hyperpolarizing undershoot (HPU) which disappears more rapidly than the enhanced PAD. These alterations are qualitatively and quantitatively similar to those found after conditioning tetani are applied to the whole muscle nerve 9. The occurence of these PAD changes after intra-axonal tetanization of a single group Ia afferent appears to rule out the participation of non-specific alterations in extracellular ionic concentrations or activation of polysynaptic pathways in their genesis.

Effects of ischaemia upon reflex electromyographic responses evoked by stretch and vibration in human wrist flexor muscles.

1. The reflex electromyographic responses evoked in a wrist flexor muscle, flexor carpi radialis (f.c.r.), by forcible extension of the wrist ('stretch') and by vibration of the flexor tendon have been studied in normal subjects. Reflexes were elicited during the maintenance of a low level of voluntary flexor contraction (5% maximum). Stretch regularly produced a relatively prolonged (ca. 100 ms duration) increase in e.m.g. activity which was usually divisible into short-latency (ca. 25 ms, M1) and long-latency (ca. 50 ms, M2) peaks. Vibration produced a single, phasic peak, at short latency, with no sign of an accompanying long-latency wave comparable to the M2 stretch response. 2. Ischaemia was induced by inflation of a blood-pressure cuff around the upper arm and its effects upon the reflex patterns were studied. During ischaemia M1 stretch responses showed a more rapid and pronounced decline than did M2 responses and were abolished before voluntary power was appreciably affected. Vibration-evoked short-latency peaks changed in an essentially parallel manner to M1 stretch reflexes. During recovery from ischaemia M2 reflexes were restored before short-latency responses. 3. The patterns of reflex reductions in e.m.g. upon withdrawal of stimulation were also studied. Such troughs in activity, under non-ischaemic conditions, regularly commenced at short latency and were of relatively small amplitude. The records of several of the subjects, and particularly ones obtained during ischaemia, suggested that release of stretch (with concomitant stretch of antagonists) could elicit an additive, long-latency decline in e.m.g. The existence of any such separate, delayed component was never observed upon termination of vibration. 4. Measurements of changes in the latencies and durations of reflex components, accompanying the progression of ischaemia, indicated that depression of early reflex activity resulted in part from increases in the latencies of these initial peaks but predominantly reflected simultaneous and separate reductions in their amplitudes. 5. The generation of short-latency reflexes by stretch and vibration, both of which stimuli powerfully excite muscle spindle primary endings, and the marked susceptibility of these responses to ischaemia supports their being mediated by group Ia afferents. The contrasting behaviour of M2 stretch responses, both regarding their absence with vibration and their resistance to ischaemia, suggests that they depend crucially upon a separate group of reflex afferents.(ABSTRACT TRUNCATED AT 400 WORDS)

Lamina VIII interneurones interposed in crossed reflex pathways in the cat.

The location of a group of interneurones projecting to contralateral motor nuclei has been established using retrograde transneuronal transport of horseradish peroxidase conjugated with wheat germ agglutinin (WGA-HRP). After labelling the motoneurones of semitendinosus, medial gastrocnemius or quadriceps muscles, interneurones which were secondarily labelled were found in lamina VIII and in the neighbouring narrow strip of lamina VII. They were found to be distributed from the 4th lumbar to the 1st sacral segments, with the highest concentration in the 6th and 7th lumbar segments and at the border between the 4th and 5th lumbar segments. The electrophysiological properties of lamina VIII interneurones of the 6th lumbar segment have been investigated using both extracellular and intracellular recording. Many of these interneurones could be antidromically activated following weak stimuli applied in contralateral motor nuclei. Post-synaptic potentials were evoked from a variety of primary afferents including group I muscle afferents. However, when present, the post-synaptic potentials (p.s.p.s) of group I origin were of considerably smaller amplitudes than p.s.p.s. evoked from higher threshold muscle or cutaneous afferents and smaller than p.s.p.s. which followed stimulation of the spinal cord at the thoracic level. P.s.p.s. from the latter two sources appear to constitute the main input to lamina VIII interneurones. Group I input has been found in forty lamina VIII interneurones. These were usually affected by either ipsilateral or contralateral group I afferents and only exceptionally by both. Excitatory post-synaptic potentials (e.p.s.p.s) from ipsilateral afferents were evoked in about twice as many neurones as e.p.s.p.s from the contralateral afferents. E.p.s.p.s were often accompanied by inhibitory post-synaptic potentials (i.p.s.p.s). Group Ia afferents appeared to contribute to both e.p.s.p.s and i.p.s.p.s, whether these were evoked from ipsilateral or from contralateral afferents. In several cases Ia afferents were as effective as all group I afferents while in other cases Ib afferents appeared to be an important or even the exclusive source of the p.s.p.s. The latencies of e.p.s.p.s indicated that they were evoked mono-, di- or trisynaptically from ipsilateral group I afferents and di- or trisynaptically from contralateral afferents, I.p.s.p.s appeared to be evoked via pathways with only one additional interneurone. About one-third of all the intracellularly investigated lamina VIII interneurones were both affected by group I afferents and antidromically activated from the contralateral motor nuclei.(ABSTRACT TRUNCATED AT 400 WORDS)

Ia afferent excitation of motoneurones in the in vitro new-born rat spinal cord is selectively antagonized by kynurenate.

Intracellular recordings from motoneurones in in vitro preparations of new-born rat spinal cord were used to study the sensitivity of the Ia excitatory post-synaptic potential (e.p.s.p.) to antagonists of excitatory amino acids, in order to test whether group Ia primary afferents release L-glutamate, or a similar compound, as a neurotransmitter. The Ia e.p.s.p. was isolated for study by using low intensity stimulation of individual muscle nerves and by the addition to the superfusate of high concentrations of divalent cations which suppressed polysynaptic inputs to the motoneurones. The pattern of convergence of group Ia afferents from homonymous, heteronymous and antagonist muscle nerves onto motoneurones in the new-born rat was similar to that reported in the adult cat spinal cord. Homonymous muscle nerve stimulation evoked the largest amplitude Ia e.p.s.p.s while heteronymous muscle nerve stimulation elicited smaller e.p.s.p.s or had no effect. Stimulation of antagonist muscle nerves resulted in inhibitory post-synaptic potentials (i.p.s.p.). Superfusion of the specific N-methyl-D-aspartate (NMDA) receptor antagonist, 2-amino-5-phosphonovalerate, did not inhibit the Ia e.p.s.p. but did suppress later, polysynaptic components of the response evoked from dorsal roots. Kynurenate was a potent inhibitor of the Ia e.p.s.p. The site of action of kynurenate was examined by observing its effect on synaptic depression and was found to be consistent with a post-synaptic mechanism. Kynurenate selectively blocked the depolarization of motoneurones elicited by L-glutamate and had no effect on the depolarization evoked by carbachol. The selectivity of action of kynurenate was further examined by comparing its effect on the recurrent i.p.s.p. evoked by ventral root stimulation with its effect on the Ia e.p.s.p. The recurrent i.p.s.p. was antagonized by strychnine and dihydro-beta-erythroidine while kynurenate, at a concentration which greatly reduced the Ia e.p.s.p., had no effect. These results suggest that stimulation of group Ia primary afferents evokes the release of L-glutamate, or a similar compound, which activates non-NMDA excitatory amino acid receptors on motoneurones which, in turn, mediate the Ia e.p.s.p.

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

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

On the origin of presynaptic depolarization of group I muscle afferents in Clarke's column in the cat

The origin of presynaptic depolarization of group I afferents in Clarke's column has been re-investigated, using changes in excitability of single fibers as a measure of their depolarization. In contrast to the previously reported lack of effects following conditioning stimulation of group Ia afferents, these afferents have been found to increase the excitability of other group Ia afferent terminals in Clarke's column. Flexor Ia and Ib afferents were found to be more effective than extensor afferents. The group I origin of the presynaptic depolarization of group I afferents in Clarke's column thus appears to be as of other terminals of these afferents. In order to define the location of interneurones mediating primary afferent depolarization in Clarke's column, changes in the excitability of afferents in Clarke's column were measured after isolating L4 and more rostral segments form the sacral and caudal lumbar segments, except for the dorsal columns, or after transection of ipsilateral lateral and ventral funiculi. Primary afferent depolarization of group Ia, or unspecified group I origin, was also found after such lesions and its effectiveness appeared to be as in intact preparations. It may thus be evoked primarily by interneurones located in the same segments as Clarke's column.

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.

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.

Patterns of fusimotor innervation by gamma-efferents in cat peroneus tertius.

The pattern of gamma-efferent innervation of the muscle spindle was investigated in the peroneus tertius muscle of the cat. A number of spindle group Ia afferents were isolated and monitored during tetanic stimulation of isolated gamma-axons. The sample was dominated by efferents producing a static fusimotor effect on the afferent. An individual static axon normally projected to less than five but at times as many as seven muscle spindles. Each spindle normally received innervation from three to five static gamma-efferents but occasionally up to eight. The number of spindles innervated by a static gamma-axon was directly related to the efferent axonal conduction velocity. For each experiment, a probability distribution of the number of fusimotor effects was constructed from all available connections between the muscle spindles and static gamma-efferents considered in matrices of four afferents and four efferents. This distribution was then compared to a random binomial distribution. In each of the ten experiments, statistically significant differences (p less than 0.01) were noted between the experimental and random distributions. In order to interpret such deviations from the random distributions, similar analyses were performed on various combinations of afferents and efferents in simulated sets displaying grouping of effects. It was concluded that the observed differences between experimental and random distributions may be produced by a grouping of fusimotor innervation limited to a small set of spindles.

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.

Interactions between motor units in modulating discharge patterns of primary muscle spindle endings.

Discharge patterns of group Ia afferents of muscle spindles in the (isometric) cat semitendinosus muscle were recorded when subjected to the influence of contractions of three motor units elicited by stimulation of three alpha-efferents with different regular or stochastic stimulus patterns. In order to study conditioning interactions between motor unit contractions, defined time constellations of stimuli to different motor units were isolated from the stimulus trains by electronic means. This technique was also applied to discharge patterns of two Ia fibres to isolate "correlated discharges." The effects of defined time constellations of stimuli upon discharge patterns of single Ia afferents or "correlated discharges" of pairs of Ia afferents were assessed by poststimulus time histograms (PSTHs). It turned out that the influence exerted by one motor unit on spindle discharges was more or less strongly modulated by actions of the other motor units, dependent on the relative timing of their contractions. These effects could in part be explained by the relative locations of motor units and spindles within the muscle. These results are discussed with respect to possible mechanisms of low-amplitude physiological tremor.

Motoneuron properties during electromyogram pauses in sleep

Electrophysiological antecedents to electromyogram pauses of NREM sleep were studied intracellularly in hindlimb motoneurons. Phasic-event-related hyperpolarizing potentials (PRHP) were 0.2–7.1 mV in amplitude and 9–90 ms in duration, and coincided with dorsal neck EMG pauses and PGO waves. Motoneurons, if spontaneously discharging, were silenced during PRHPs. The discharge rate of spike trains elicited by depolarizing current reduced during PRHPs. Membrane conductance measurements indicated that PRHPs did not arise simply from soma inhibition but from either presynaptic inhibition or conductance changes in electrically-remote dendrites. EMP pauses, which normally occur spontaneously, could be evoked by stimulation of low threshold fibers in peripheral nerves. PRHPs were most prevalent in REM sleep. We concluded that EMG pauses are generated by the same cholinergic brainstem mechanism that generates spino-bulbo-spinal presynaptic inhibition of group Ia afferents. The pauses resemble the inhibitory phase of startle responses, providing evidence for the hypothesis that startle responses are spontaneously elicited in NREM and REM sleep.

The components of synaptic potentials evoked in cat spinal motoneurones by impulses in single group Ia afferents.

1. Excitatory post-synaptic potentials (e.p.s.p.s) were evoked in cat spinal motoneurones by impulses in single group Ia afferent fibres. The probability density of the fluctuations in peak amplitude of each e.p.s.p. was calculated from the recorded peak amplitude and the probability density of the recording noise. 2. Most e.p.s.p.s fluctuated between different components (i.e. individual e.p.s.p.s of a particular discrete amplitude) with peak amplitudes which were integer multiples of the increment between successive components. The average peak amplitude of this incremental e.p.s.p. was about 90 microV for e.p.s.p.s generated at or near the soma. 3. In general, the probability density of the peak amplitude could not be described using Poisson or binomial distributions. 4. For many e.p.s.p.s the complete time course of each component could be calculated. There was no variability in the amplitude of these components nor in their latency of onset. For some e.p.s.p.s there were differences in the latency and time course of the components. 5. The increments between successive components of e.p.s.p. generated proximally were no larger (at the soma) than the corresponding increments for e.p.s.p.s generated at more distal dendritic sites. 6. These results and those from subsequent papers (Jack, Redman & Wong, 1981; Hirst, Redman & Wong, 1981) reinforce earlier suggestions that each bouton behaves in an all-or-nothing manner with respect to post-synaptic effect, and the probability of failure varies at different boutons arising from the same afferent.

Modifications to synaptic transmission at group Ia synapses on cat spinal motoneurones by 4-aminopyridine.

1. The average amplitude of e.p.s.p.s evoked in cat spinal motoneurones by impulses in single group Ia afferents usually increased following the intravenous injection of 4-aminopyridine (4-AP). Most of this increase occurred over the first 30 min following injection of 4-AP. 2. The increase in the average amplitude following 4-AP occurred by a reduction in the probability of occurrence of component e.p.s.p.s with smaller peak amplitudes, and an increase in the probability of occurrence of component e.p.s.p.s with larger peak amplitudes. There was no evidence that the discrete amplitudes of components after 4-AP were a result of graded increases of the discrete amplitudes before 4-AP. 3. The interpretation suggested for these results is that each component e.p.s.p. is generated by transmission at a different combination of boutons. At each of these boutons sufficient transmitter is released to saturate all available receptors. The effect of 4-AP is to decrease the probability of failure to release transmitter at each bouton, including some boutons which, before 4-AP, did not release transmitter.

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.