Group Ia Afferent Fibres Research Articles

Effect of Breathing 7% Carbon Dioxide on the Human Soleus Hoffmann Reflex Recruitment Curve

The Hoffmann reflex (H wave) is a measure of afferent synaptic transmission via electrical stimulation. The motor response (M wave) denotes a direct muscle response via electrical stimulation. An H wave without a motor response can be recorded because electrical stimulation first activates group Ia afferent fibers, which are larger in diameter than motor axons. By gradually increasing stimulation intensity, first H waves, then M waves, and finally Hmax and Mmax can be obtained (the H reflex recruitment curve). Notable parts of the curve include H wave threshold, motor (M wave) threshold, slope of the ascending curve of the H reflex, Hmax/Mmax ratio, and the latency of the H wave. PURPOSE: To examine the effect of inhaling 7% carbon dioxide on the recruitment curve of the soleus H-reflex. METHODS: 5 males and 5 females (apparently healthy; 21-40 yr) sat with hip at 90 degree flexion, knee at 120 degree flexion, and ankle at 90 degree flexion with surface EMG electrodes over the soleus muscle and a percutaneous electrical stimulator over the tibial nerve. Subjects then randomly breathed room air or a 7% CO2, 21% O2, balance N2 mix through a respiratory mask for 10 minutes. Then, electrical stimuli (1 per 10 sec) of random intensity were given until a complete H reflex recruitment curve was elicited while simultaneously collected EMG data at a recording rate of 2000 Hz. H wave threshold, motor threshold, slope of ascending H reflex curve, Hmax/Mmax ratio, and latency of Hmax were compared by a paired t-test, with statistical significance set at p< 0.05. RESULTS: H wave threshold (as a percent of motor threshold) significantly increased from 0.92 (SD 0.09) to 0.97 (SD 0.12; p< 0.05) while on CO2. Hmax/Mmax ratio decreased significantly from 0.504 (SD 0.290) to 0.403 (SD 0.253; p< 0.05) while on CO2. H wave latency (in msec) significantly increased from 32.8 (SD 1.6) to 34.6 (SD 2.6; p< 0.05) while on CO2. Slope of ascending H reflex curve (room air: 1.19 (SD 1.09); CO2: 1.39 (SD 1.38); p> 0.05), Mmax (room air: 3.70 mV (SD 1.57); CO2: 3.69 mV (SD 1.53); p> 0.05), and motor threshold (p> 0.05) remained unchanged. CONCLUSIONS: Breathing 7% carbon dioxide reduces afferent synaptic transmission in the soleus muscle by slowing transmission, increasing threshold stimulus, and reducing H wave size.

Changes in the recruitment curve of the soleus H-reflex associated with chronic low back pain

Objective We investigated whether patients with chronic low back pain (CLBP) manifest changes in the excitability of the soleus H-reflex. Methods H-reflex stimulus–response curve was studied in 14 CLBP patients and 14 age-matched healthy subjects. H-threshold, H-maximum size, H-steepness and H-latency were determined for both legs. Homosynaptic depression (HD), following a train of H-reflexes, and presynaptic inhibition (PI) from flexor afferents onto soleus Ia afferents were also evaluated. Results H-threshold was significantly increased, H-size as a function of stimulus intensity was significantly different, and H-recruitment curve steepness was significantly lower in CLBP patients compared to healthy subjects. No significant difference in the amount of HD and PI of the H-reflex was found between the two groups. H-latency and H max/ M max ratio was comparable between the subjects groups. Conclusions In CLBP there is a reduced excitability of group Ia afferent fibres from the soleus muscle to which presynaptic factors do not seem to contribute and that presumably depend on changes in the peripheral sensory input. Significance Changes in H-reflex excitability may underlie a decrease in the gain of a peripheral sensor in CLBP. Estimation of soleus H-threshold and H-recruitment curve may contribute to the diagnostic evaluation of CLBP and may be used to monitor the efficacy of treatment.

Vibration-induced activation of muscle afferents modulates bioassayable growth hormone release.

The effects of tendon vibration on bioassayable growth hormone (BGH) secretion from the pituitary gland were investigated in anesthetized adult male rats. The tendons from predominantly fast-twitch ankle extensor muscles (gastrocnemius and plantaris) or a predominantly slow-twitch ankle extensor (soleus) were vibrated by using a paradigm that selectively activates group Ia afferent fibers from muscle spindles. The lower hindlimb was secured with the muscles near physiological length, and the tendons were vibrated for 15 min at 150 Hz and a displacement of 1 mm. Control rats were prepared similarly, but the tendons were not vibrated. Compared with control, vibration of the tendons of the fast ankle extensors markedly increased (160%), whereas vibration of the slow soleus decreased (68%), BGH secretion. Complete denervation of the hindlimb had no independent effects on the normal resting levels of BGH, but it prevented the effects of tendon vibration on BGH secretion. The results are consistent with previous findings showing modulation of BGH release in response to in vivo activation or in situ electrical stimulation of muscle afferents (Bigbee AJ, Gosselink KL, Grindeland RE, Roy RR, Zhong H, and Edgerton VR. J Appl Physiol 89: 2174-2178, 2000; Gosselink KL, Grindeland RE, Roy RR, Zhong H, Bigbee AJ, and Edgerton VR. J Appl Physiol 88: 142-148, 2000; Gosselink KL, Grindeland RE, Roy RR, Zhong H, Bigbee AJ, Grossman EJ, and Edgerton VR. J Appl Physiol 84: 1425-1430, 1998). These data provide evidence that this previously described muscle afferent-pituitary axis is neurally mediated via group Ia afferents from peripheral skeletal muscle. Furthermore, these data show that activation of this group Ia afferent pathway from fast muscles enhances, whereas the same sensory afferent input from a slow muscle depresses, BGH release.

Prolonged GABA(B) receptor-mediated synaptic inhibition in the cat spinal cord: an in vivo study.

In pentobarbitone-anaesthetised spinal cats, a comparison was made of the effects of intravenous bicuculline hydrochloride, a GABA(A)-receptor antagonist, and several (-)-baclofen (GABA(B)-receptor) antagonists (CGP 35348, 4638 , 56999A) on the prolonged inhibition of extensor-muscle monosynaptic reflexes, recorded from lumbar ventral roots, by brief or continuous tetanic stimulation of low-threshold afferent fibres of hindlimb flexor muscles. Two components of brief tetanus inhibition were detected. Whilst possibly of similar central latency, the inhibition associated with GABA(B) receptors had a longer time course than that reduced by bicuculline. Furthermore, whereas bicuculline reduced primary afferent depolarization, generated by the inhibitory volleys, and detected as dorsal-root potentials, such potentials were generally enhanced by intravenous baclofen antagonists. The inhibition of reflexes during and after continuous (333 Hz) tetanic flexor-nerve stimulation appeared to be predominantly associated with the activation of GABA(B) receptors. In the period following continuous tetanic flexor-nerve stimulation, during which monosynaptic extensor reflexes were reduced in amplitude, the action potentials of the intraspinal terminations of extensor-muscle group-Ia afferent fibres were reduced in duration, as detected by the time course of the recovery of the threshold to extracellular microstimulation following the arrival of an orthodromic impulse. A reduction in termination action-potential duration also accompanied the reduction by microelectrophoretic (-)-baclofen of the release of excitatory transmitter from group-Ia terminations, both presynaptic effects being blocked by microelectrophoretic baclofen antagonists. However, the reduction of the duration of the action potential of individual group-Ia terminations, which followed continuous flexor-nerve stimulation, was not sensitive to the baclofen antagonist CGP 55845A, but was diminished by bicuculline methochloride. Intravenously administered bicuculline hydrochloride, however, had little or no effect on the inhibition of reflexes following continuous flexor-nerve stimulation. These observations are discussed in the context of possible intraspinal pathways and pre- and postsynaptic mechanisms for GABA(A) and GABA(B) receptor-mediated inhibition of the monosynaptic excitation of spinal motoneurones and of the functional significance of central GABA(B) receptor-associated inhibitory processes, given the relatively minimal effects on motor activity and behaviour produced by baclofen antagonists that penetrate the mammalian blood-brain barrier.

The lack of effect of baclofen on action potentials of spinal motor axon collateral terminations in vivo

In the lumbar ventral horn of pentobarbitone-anaesthetised cats, (-)-baclofen reduces both the synaptic release of excitatory transmitter from muscle group Ia afferent terminations and the duration of the presynaptic action potentials of these terminations, presumably by interfering with the influx of calcium ions through voltage-activated channels. Baclofen, however, has little or no effect on cholinergic excitation at motor axon collateral synapses on spinal Renshaw cells and, in the present study, was found not to reduce the duration of the action potential of axon collateral terminations located in the vicinity of Renshaw cells in pentobarbitone-anaesthetised cats. Furthermore, in contrast to group Ia terminations, a 4-aminopyridine-sensitive potassium conductance could not be detected as contributing to axon collateral termination action potentials. These results suggest that there may be differences in presynaptic ion fluxes associated with transmitter release at the intraspinal terminations of group Ia afferent fibres and motor axon collaterals in the cat spinal cord.

The neurophysiological basis of reciprocal inhibition in man

The current paper reviews the current evidence on the neurophysiological basis of reciprocal inhibition, and in particular the role of Ia inhibitory interneurones, both as a basis for normal motor development and in providing a better understanding of the clinical presentation of a number of neurological conditions (e.g. stroke and cerebral palsy). The Ia inhibitory interneurones which mediate reciprocal inhibition have been studied extensively in animals and in man. Stimulation of low threshold Group Ia afferent fibres leads to excitation of the homonymous muscle and inhibition of its antagonist via this disynaptic pathway. It has been demonstrated that α-motoneurones are inhibited not only by strict antagonists but also from other muscles connected to them in Ia synergism. On the basis of convergence from supraspinal and spinal pathways it has been proposed that they act as integrative centres. Moreover, their extensive distribution to α-motoneurones within upper and lower limbs supports their role as pattern registers. Reciprocal inhibition thus contributes to the patterning of movement required for different motor synergies. However, in normal development in man, it is not clear whether this pathway plays a role in the fundamental shaping of spinal cord circuitry, as it does in animals by suppressing inappropriate heteronymous excitatory projections in the spinal cord.

An in vivo electrophysiological investigation of group Ia afferent fibres and ventral horn terminations in the cat spinal cord.

An extracellular microstimulation technique has been used to investigate and compare the properties of group I primary afferent myelinated fibres in the dorsal column and group Ia unmyelinated terminations in the lumbar spinal cord of cats anaesthetised with pentobarbitone sodium. Fibres were distinguished from terminations on the basis of location, anodic blocking factor and sensitivity to GABAA mimetics. The recovery curves of threshold following an orthodromic impulse provided an estimate of both action potential duration and rate of repolarization. The action potentials of group Ia terminations were of briefer duration (by a factor of approximately 2) with more rapid rates of repolarization (factor of approximately 3) than those of the myelinated fibres. The prolongation of termination but not fibre action potentials by microelectrophoretic tetraethylammonium and 4-aminopyridine indicated the presence of voltage-activated potassium channels in the termination membrane. Differences in the effects on Ia termination action potentials of depolarizations (reductions in threshold) associated with a preceding action potential, synaptically released GABA, microelectrophoretic piperidine-4-sulphonic acid or DL-homocysteic acid suggest that an increase in termination membrane conductance is the major factor in the reduction of transmitter release during the activation of presynaptic GABAA receptors.

Reciprocal Ia inhibition between elbow flexors and extensors in the human.

1. Reciprocal inhibition between elbow flexor and extensor muscles (biceps and triceps brachii) has been investigated in nine healthy subjects. Two techniques were used to assess changes in motoneurone excitability after stimulation of antagonist muscle afferents: (1) monosynaptic reflexes elicited by a mechanical stimulation of the distal muscle tendon (tendon tap); (2) post-stimulus time histograms (PSTH) of voluntarily activated motor units. 2. Electrical stimulation of the antagonist muscle nerve produced a short-latency and short-lasting inhibition of the flexor and extensor motoneurones. The amount of this inhibition was found to be similar in both motor nuclei. 3. The inhibition could be evoked with conditioning electrical stimuli as low as 0.7 x motor threshold (MT) or by very weak tendon taps applied to the antagonist tendon. In the former case the threshold of this inhibition was found to be consistently increased after raising the threshold of Ia afferent fibres by a long-lasting muscle vibration. Since a contribution from cutaneous afferent fibres was ruled out, it is concluded that this inhibition was Ia in origin. 4. Post-stimulus time histograms of voluntarily activated triceps and biceps motor units were made following electrical stimulation of homonymous and antagonist muscle afferents. This enabled an estimate of the central synaptic delay of the inhibitory process. An average central delay of 0.94 ms in excess of that of monosynaptic facilitation was found, thus suggesting that the inhibitory process could be mediated by only one interneurone. 5. A conditioning reflex discharge elicited in the antagonist muscle by a tendon tap depressed or suppressed this inhibition. This depression was maximal when the reflex discharge was elicited 10-20 ms before the conditioning stimulus for the inhibition and never lasted more than 30 ms. It is argued that the only mechanism compatible with such a depression is the inhibitory activity of Renshaw cells acting on the pathway mediating reciprocal inhibition. 6. We conclude that group Ia afferent fibres from elbow extensor and flexor muscles project monosynaptically onto Ia inhibitory interneurones to mediate disynaptic reciprocal inhibition of antagonist motoneurones.

Cortical projection of putative group Ib afferent fibres from the human forearm

The possibility was investigated that impulses in group Ib afferents from fore-arm flexors have access to cerebral cortex in man. A long-lasting increase in the threshold (Th) of group Ia afferent fibres from flexor carpi radialis muscle (Fcr) was obtained after prolonged (100 Hz for 20 min) tendon vibration at the wrist. It was assumed that under this condition a weak electrical stimulation of the median nerve at the elbow, insufficient to reactive Ia fibres because of the rise in their threshold (as verified by the method of homonymous Ia facilitation of Fcr H reflex), engaged Ib fibres only. Peripheral volleys at Erb's point and cerebral cortical potentials to median nerve stimulation at the elbow were evoked before and after prolonged vibration of Fcr. During 10–30 min after the end of vibration, in which homonymous facilitation of Fcr H reflex was abolished, both the ongoing peripheral volley and the cortical responses were markedly reduced with respect to their control values. Recovery to pre-vibration control amplitudes coincided with recovery of Fcr H reflex homonymous facilitation. In order to verify if activity in afferents other than group Ib fibres might contribute to the cortical response after vibration, specially designed experiments were also performed. It is concluded that the cortical wave recorded after 20 min vibration represents the arrival of Ib impulses from flexor carpi radialis to the human cerebral cortex.

Vibration insensitivity of a short latency reflex linking the lower leg and the active knee extensor muscles in humans

The study indirectly investigated the afferent source of a human lower limb reflex that spans two joints and may link limb muscular activity during movement. Low threshold (motor nerve threshold (MT) to 1.6 MT) single, 1 msec, pulses were delivered to the common peroneal nerve at caput fibula. Heteronymous excitatory responses were observed in the electromyogram of the knee extensor muscle vastus medialis (VM), when the latter was prior contracted. The briefest latency for the VM reflex was 24.2 msec. The distal belly and tendon of the tibialis anterior muscle were vibrated for 20 min at a frequency of 105 Hz, amplitude 1–2 mm, to inhibit the reflex potential evoked by group Ia afferent fibres from that muscle. This significantly reduced the amplitude of the group Ia mediated Hoffmann (H) reflex in TA. Such vibration did not depress the amplitude of the heteronymous reflex to VM, when initially the latter was at peak amplitude or at its mid-range for amplitude. Reflex latency, threshold, and stimulation current for peak expression suggested that group II fibres were unlikely to be the major initiators of the reflex. The results support the view that this human reflex is primarily Ib mediated.

Post-tetanic influences on primary afferent depolarization in the cat spinal cord.

In the spinal cord of pentobarbitone anaesthetised cats, increases in the electrical threshold of the terminations of extensor muscle group Ia afferent fibres, produced by tetanic stimulation of either the appropriate peripheral nerve or the central termination, were associated with parallel changes in the bicuculline-sensitive reduction in electrical threshold of the termination produced synaptically by impulses in flexor muscle low threshold afferent fibres (primary afferent depolarization, PAD) or by microelectrophoretic piperidine-4-sulphonic acid (P4S), an analogue of GABA. Since this post-tetanic hyperpolarization (PTH) could be produced by tetanic stimulation of a single termination centrally, and not by peripheral stimulation of heteronymous nerves, it presumably resulted from changes intrinsic to the tetanized termination. Increases in PAD and the effectiveness of P4S were probably associated with post-tetanic activation of an electrogenic Na+/K+ pump as the predominant cause of PTH, whereas decreases may have been largely the consequence of post-tetanic increases in intracellular Ca2+ levels. These results provide further evidence that GABA is the depolarizing transmitter at axo-axonic synapses upon primary afferent terminals, and that the underlying membrane conductance increase has a reversal potential at a more depolarized level than the resting potential.

A pharmacological study of group I muscle afferent terminals and synaptic excitation in the intermediate nucleus and Clarke's column of the cat spinal cord.

When administered microelectrophoretically GABA and piperidine-4-sulphonic acid depolarized the central terminations of muscle group Ia and Ib afferent fibres in the lumbar intermediate nucleus and Clarke's column of cats anaesthetised with pentobarbitone sodium. Both this depolarization, and primary afferent depolarization, generated by impulses in other primary afferent fibres which produce prolonged bicuculline-sensitive inhibition of the firing of group I afferent fibre-excited interneurones in the intermediate nucleus and cells in Clarke's column, are reduced by microelectrophoretic bicuculline methochloride. Systemically administered (+/-)-baclofen hydrochloride (maximum dose 8 mg kg-1) depressed the monosynaptic excitation of Clarke's column neurones by impulses in muscle and cutaneous afferent fibres. Microelectrophoretically administered (-)-baclofen reduced the bicuculline-sensitive primary afferent depolarization of group I terminations without, however, reducing the depolarizing action of GABA or piperidine-4-sulphonic acid. The depression by (-)-baclofen of the group I monosynaptic excitation of intermediate nucleus neurones is not reduced by concentrations of bicuculline methochloride adequate to suppress prolonged inhibition of these neurones.

A neurophysiological analysis of the effect of kainic acid on nerve fibres and terminals in the cat spinal cord.

Kainic acid was administered micro-electrophoretically in relatively small amounts (approx. 0.15 nmol) near gastrocnemius motoneurones in the spinal cord of cats anaesthetized with sodium pentobarbitone. After initial excitation, extracellularly recorded orthodromic and antidromic field potentials were reduced. Such neurophysiological evidence for motoneuronal damage or death persisted for 5 h, the longest period of observation. At the site of administration, the terminations of gastrocnemius group Ia afferent fibres were electrically inexcitable for approximately 1 h. Subsequently, the number and excitability of these terminations appeared to be normal, as were the depolarizing actions at bicuculline-sensitive receptors of micro-electrophoretic piperidine-4-sulphonic acid and of gamma-aminobutyric acid (GABA) released at axoaxonic synapses on these terminations. Central myelinated and non-myelinated fibres and terminals of muscle group Ia afferent fibres, and the synaptic release of GABA on these terminals at axo-axonic synapses formed by certain spinal interneurones, thus appear to be relatively insensitive to kainic acid administered in amounts which damage or destroy motoneurones.

Aging of motoneurons and synaptic processes in the cat

The aging of spinal cord alpha motoneurons was explored in old cats with intracellular recording techniques to determine the basic membrane properties of these neurons and their monosynaptic response following activation of group Ia afferent fibers. The conduction velocity of the motoneurons' axons decreased in old animals (14 to 15 years of age) compared with adult controls (1 to 3 years of age). The input resistance of the motoneurons increased in the old cats; no change occurred in the resting membrane potential or spike amplitude. There was a reduction in the delay between the initial segment and the somadendritic components of the antidromic spike. The half-width duration of the monosynaptic EPSP in the old cats increased, but its amplitude did not change. These data indicate that a host of different membrane properties of spinal cord motoneurons and their Ia-monosynaptic input are affected by the aging process. Analysis of the results suggests that the degradation of neuronal processes occurs in all motoneurons rather than preferentially affecting a specific population of motoneurons.

The ultrastructural basis for synaptic transmission between primary muscle afferents and neurons in Clarke's column of the cat

The synaptic connection between primary muscle afferents and dorsal spinocerebellar tract (DSCT) neurons has been studied in an attempt to reveal some of the mechanisms underlying excitatory transmission in the mammalian central nervous system. Previous electrophysiological experiments have shown that the excitatory postsynaptic potentials (EPSPs) evoked DSCT neurons by impulses in a single muscle afferent fluctuate in amplitude. These fluctuations occur between discrete amplitudes which are separated by quantal increments. Two alternative hypotheses relate such a quantal increment to all-or-nothing transmitter release from either (1) an entire synaptic bouton or (2) an individual transmitter release site, given that a bouton may contain multiple release sites. The present study was undertaken primarily to gain ultrastructural evidence on these proposals. Electrodes filled with horseradish peroxidase (HRP) were used to label single identified group Ia afferent fibers and DSCT neurons in the lumbar spinal cord of anesthetized cats. HRP-labeled Ia synaptic boutons, and the contacts formed between HRP-labeled Ia boutons and the dendrites of a DSCT neuron labeled intracellularly with HRP, were examined in serial sections under the electron microscope. Group Ia boutons were found to contain multiple synaptic specializations, as evidenced by pre- and postsynaptic thickenings and presynaptic clusters of vesicles. Careful examination of a bouton in serial sections revealed each specialization as a separate structure. These observations support the proposal that synaptic transmission between group I muscle afferents and DSCT neurons occurs with discrete all-or-nothing EPSPs associated with transmitter release sites, rather than boutons per se.

The effects of naloxone, morphine and methionine enkephalinamide on Ia afferent terminations in the cat spinal cord

Naloxone, morphine, Met 5-enkephalinamide (MENKA) and procaine were administered microelectrophoretically near extracellularly stimulated extensor muscle group Ia afferent fibres and terminations in the lumbar spinal cord of cats anaesthetized with pentobarbitone sodium. Observations were made of effects on the electrical threshold, on the depolarizing action of GABA or piperidine-4-sulphonate (P4S), and on bicuculline-sensitive primary afferent depolarization (PAD) generated by tetanic stimulation of flexor muscle low threshold afferents. All 4 agents reversibly elevated the threshold of Ia fibres in the dorsal column and Ia terminations in the ventral horn. The depolarizations of terminations by GABA or P4S were also reduced, an effect, which for all except MENKA, probably accounted for a concomitant reduction in PAD. In the absence of a consistent effect on either threshold or depolarization by GABAmimetics, MENKA reversibly diminished PAD, an action blocked by naloxone. Intravenously administered naloxone, in doses known to enhance spinal monosynaptic excitation in the cat, had no effect on GABAergic PAD and little or no effect on Ia termination threshold. The results are discussed in relation to a naloxone-sensitive effect of MENKA which reduces transmitter release from GABAergic axo-axonic synapses on Ia terminals, but which does not account for the enhancement of spinal reflexes by naloxone.

Synaptic input from identified muscle afferents to neurones of the dorsal spinocerebellar tract in the cat.

Single identified group I a and I b muscle afferent fibres were injected with horseradish peroxidase in the lumbar dorsal columns of anaesthetized cats. The morphological details of the axon collaterals and terminal boutons of these muscle afferents within Clarke's column were subsequently reconstructed. The rostro-caudal extent of synaptic terminals from a single afferent fibre within Clarke's column was found to be restricted to less than 1 mm. In the same experiments, dorsal spinocerebellar tract (d.s.c.t.) neurones were retrogradely labelled by injection of horseradish peroxidase into the cerebellum. Synaptic contacts between labelled group Ia and Ib afferent fibres and the soma and proximal dendrites of d.s.c.t. neurones were found. The synaptic contacts from both Ia and Ib fibres varied greatly in size, from 1 X 1 micron up to 'giant' synapses of 20 X 3 micron. Excitatory post-synaptic potentials (e.p.s.p.s) were evoked in d.s.c.t. neurones by impulses in single group I muscle afferent fibres. The fluctuations in peak amplitude of each e.p.s.p. were determined from e.p.s.p. and noise recordings, using a numerical deconvolution procedure. In general, these single-fibre e.p.s.p.s fluctuated between discrete amplitudes separated by an incremental amplitude which was approximately constant. This incremental amplitude did not depend on the average peak amplitude of the particular e.p.s.p. examined. Our anatomical observations of 'giant' boutons arising from Ia and Ib afferent fibres contacting d.s.c.t. neurones raises the possibility of multiple transmitter release sites within an individual synaptic bouton. It is proposed that synaptic transmission between group I muscle afferents and d.s.c.t. neurones occurs with discrete all-or-nothing e.p.s.p.s associated with transmitter release sites.

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.

Direct observations on the contacts made between Ia afferent fibres and alpha-motoneurones in the cat's lumbosacral spinal cord.

1. The enzyme horseradish peroxidase was injected into identified lumbosacral alpha-motoneurones and Group Ia afferent fibres in cats anaesthetized with chloralose and paralysed with gallamine triethiodide. Subsequent histological examination allowed the determination of (a) the extent of the motoneuronal dendritic trees, (b) the number and location of Ia synapses upon the motoneurones. 2. alpha-motoneurones had seven to eighteen primary dendrites and each produced daughter branches up to the fourth to the sixth order. At dendritic bifurcations Rall's 3/2 Power Law was obeyed. There was little or no dendritic tapering up to about 800 micrometers from the soma. Beyond this distance, however, there was considerable tapering. 3. Horseradish peroxidase injections revealed that motoneuronal dendrites are much longer than previously thought. Individual dendrites could be traced for up to 1600 micrometers from the soma and dendritic trees were usually 2-3 mm from tip to tip. Nearly all the motoneurones had dendrites that entered the white matter of the cord. Dendrites could also reach as far dorsally as laminae V and VI. 4. Ia synapses upon motoneuronal somata were examined in cords counterstained with cresyl violet or methylene green. About 10% of Ia boutons in lamina IX were on somata and each Ia collateral terminated on 3.66 motoneuronal somata or the most proximal (30 micrometer) dendrites, with on average about two contacts per motoneurone. 5. Ten Ia afferent fibre-motoneurone pairs were injected with horseradish peroxidase. The following conclusions were drawn: (i) only one collateral of any given Ia axon makes contact with a motoneurone even though other collaterals from the same axon might pass through the dendritic tree, (ii) usually all contacts made between a Ia fibre and a motoneurone are at about the same geometrical distance from the soma, even when on different dendrites, (iii) between two and five contacts are made upon the dendritic tree (average 3.4) at distances of between 20 and 820 micrometers from the soma. 6. The results are discussed in relation to previous anatomical and electrophysiological work.

Trajectory of group Ia afferent fibers stained with horseradish peroxidase in the lumbosacral spinal cord of the cat: three dimensional reconstructions from serial sections.

A reconstruction was made of the intramedullary trajectory of 23 physiologically identified Ia afferents from cat hind limb muscles (medial gastrocnemius, soleus, plantaris, flexor digitorum-hallucis longus, and hamstring). The afferents were stained by intra-axonally injected HRP. The axons of these afferents were traced over distances of 5.8 mm to 15.7 mm rostrocaudally. In the dorsal funiculus fibers from all the muscles showed a similar course and similarly bifurcated into an ascending and a descending branch. The mean diameters of stem axons, ascending branches, and descending branches were 6.6 micrometer, 5.8 micrometer, and 3.0 micrometer, respectively. Within the analyzed lengths of the spinal cord five to eleven collaterals were given off from the two branches. The distances between adjacent collaterals of the ascending and descending branches averaged 1200 micrometer and 790 micrometer, respectively. The collaterals as a rule passed through the medial half of the dorsal horn before they entered the deeper parts of the gray matter. The terminal distribution areas common to all Ia collaterals were: (1) the medial half of the base of the dorsal horn, mainly lamina VI: (2) lamina VII; and (3) lamina IX. The numbers of terminals were largest in lamina IX and smallest in lamina VII. The density of terminals in lamina IX was highest in the homonymous motor cell column. The terminal distribution areas of adjacent collaterals showed no overlap in the sagittal plane. Terminal branches carried one bouton terminal and up to six boutons en passage with an average of 1.8 terminals per terminal branch. Apparent axosomatic and axodendritic contacts were seen on small-sized and medium-sized neurons in laminae V-VI, medium-sized neurons in lamina VII, and large neurons in lamina IX. One motoneurons was contacted by an average of 3.3 terminals. In addition to the common features, Ia collaterals of various muscles of origin showed some differences in their trajectories in the ventral horn, and in their terminations in the gray matter.