The identification and characteristics of sacral parasympathetic preganglionic neurones

1. Sacral parasympathetic preganglionic neurones were identified by intracellular and extracellular micro-electrode recording of antidromic potentials in response to stimulation of the pelvic nerve or the second or third sacral ventral roots.

2. The segmental distribution of autonomic neurones varied in different cats. In some cats they were mainly in S2 segment, in others in S3 and in the remainder, in both S2 and S3.

3. The antidromic potentials showed initial segment-somadendritic (IS-SD) inflexions and delayed depolarizations and were slightly less prolonged than those of sympathetic neurones but more prolonged than those of spinal motoneurones. After-hyperpolarization was observed after the antidromic spike potential.

4. The conduction velocities for sacral parasympathetic preganglionic fibres were less than 12·5 m/sec and thus were similar to those of sympathetic preganglionic fibres.

5. Parasympathetic neurones were not excited by micro-electro-phoretically applied 5-hydroxytryptamine, noradrenaline or acetylcholine.

     

A propriospinal-like contribution to electromyographic responses evoked in wrist extensor muscles by transcranial stimulation of the motor cortex in man

We tested the hypothesis that some of the electromyographic (EMG) responses elicited in preactivated forearm muscles by transcranial stimulation of the human motor cortex are produced by activity in a disynaptic corticospinal linkage involving propriospinal-like interneurones with cell bodies in the spinal C3–4 segments. The experimental design incorporated a previous observation that stimulation of afferents in the superficial radial nerve inhibits propriospinal-like neurones projecting to the extensor carpi radialis (ECR) muscle. Surface EMG responses were recorded from the active ECR muscle after transcranial electrical or magnetic stimulation over the motor cortex. In random trials, single conditioning stimuli at twice perceptual threshold were given to the superficial radial nerve at the wrist at different times before a cortical shock. When the cortex was stimulated electrically, the conditioning stimulus suppressed the EMG responses when the interval between the shocks was 11 ms or more. This was about 3.5 ms longer than the minimum time calculated for a possible direct cutaneous effect on spinal motoneurones. The time course of suppression began earlier and was more complex during magnetic stimulation of the cortex. It is argued that this difference is due to the repetitive I waves generated by the magnetic shock. Whether electrical or magnetic stimulation was used, the first 1–3 ms of the EMG response was relatively unaffected by superficial radial nerve stimulation at any interstimulus interval, whereas clear suppression was seen in the later portion of the response. In contrast, if the EMG response in ECR was suppressed by a conditioning stimulus to the median nerve at the elbow, then all portions of the EMG response were inhibited including the first 1–3 ms. The median nerve effect is thought to be due to direct reciprocal inhibition of the extensor motoneurones. Thus sparing of the initial part of the cortically evoked response with superficial radial stimulation suggests that the latter type of inhibition occurs at a premotoneuronal level. The timing of the effect is compatible with the explanation that corticospinal excitation is produced in ECR motoneurones through both monosynaptic and disynaptic (including propriospinal premotoneuronal) pathways, with superficial radial nerve inhibition being exerted at the propriospinal level.     

Monosynaptic excitatory connexions of reticulospinal neurones in the nucleus reticularis pontis caudalis with dorsal neck motoneurones in the cat

Summary 1. Projections of reticulospinal neurones (RSNs) in the nucleus reticularis pontis caudalis (N.r.p.c.) to dorsal neck motoneurones supplying splenius (SPL, lateral head flexor) and biventer cervicis and complexus (BCC, head elevator) muscles were studied in the cat anaesthetized with pentobarbiturate or -chloralose. 2. Threshold mapping for evoking antidromic spikes revealed that most of RSNs tested projecting down to brachial segments but not to lumbar segments (C-RSNs) gave off collaterals to the gray matter of the upper spinal cord in C2–C3 segments. 3. Spike triggered averaging showed that negative field potentials were evoked after firing of a single C-RSN (single fibre focal synaptic potentials, FSPs) in the region of C2–C3 where large antidromic field potentials from nerves supplying SPL or BCC muscles were evoked. The single fibre FSPs ranged between 1 and 10 V in amplitude and had latencies between 0.7 and 1.2 ms from the onset of the triggering spike. In most cases, a presynaptic spike preceded the negative potential by 0.3 ms. These results indicated that C-RSNs project to the SPL or BCC motor nucleus. 4. Spike triggered averaging of postsynaptic potentials revealed EPSPs (single fibre EPSPs) in 36 dorsal neck motoneurones, predominantly in SPL (25) and less in BCC (11) motoneurones, evoked from 15 C-RSNs. The amplitude of the single fibre EPSPs ranged from 5 to 310 V, and had latencies of 0.8–2.0 ms from the onset of the triggering spikes of C-RSNs, or 0.3–0.5 ms from the presynaptic spike when recorded. The results indicated monosynaptic excitatory connexions of C-RSNs to dorsal neck motoneurones. 5. Single fibre EPSPs from a C-RSN were usually recorded from either BCC or SPL motoneurones but not from both types of motoneurones, when tested in many motoneurones. This showed that connexions of C-RSNs with dorsal neck motoneurones were muscle specific. 6. RSNs projecting down to the lumbar segment (L-RSN) also showed branching in C2–C3 segments. Excitatory monosynaptic connexion of L-RSNs with neck motoneurones were demonstrated by recording single fibre postsynaptic population potentials (p.s.p.p.s.) from the C2 ventral root perfused with sucrose. The probability of evoking monosynaptic single fibre p.s.p.p.s. was less (19%) than for C-RSNs (59%).     

Electrical activity of rat ocular motoneurons recorded in vitro

The electrophysiological properties of rat oculomotor neurons were studied in an in vitro slice preparation. Motoneurons were identified by their antidromic response to third nerve rootlet stimulation, and by their orthodromic responses to medial longitudinal fasciculus and reticular stimulations. Passive membrane properties showed the existence of an inward rectification mechanism in all the recorded motoneurons. The action potential is comprised of several distinct components. The fast initial spike, composed of an initial segment spike and a somatodendritic spike, is followed by a delayed depolarization, an afterhyperpolarization and a late afterdepolarization. The afterhyperpolarization has a maximum duration of 55 ms. The late afterdepolarization is a voltage-dependent mechanism that produces an oscillatory behavior in depolarized cells. Two types of motoneurons were distinguished on the basis of their response to long-lasting depolarizing current pulses. The intensity-frequency curves show the existence of a primary and secondary range of discharge and the study of the interspike intervals points to specific properties of the conductance underlying the afterhyperpolarization. It is concluded that large, stellate motoneurons of the brainstem maintained in vitro retain specific electrophysiological properties, comparable to those described in vivo and which differentiate the ocular motoneurons from spinal motoneurons.     

Centrifugal dorsal root discharges induced by motoneurone activation

1. It has been confirmed that antidromic stimulation of motoneurones in the cat lumbar cord can induce, when properly conditioned, a centrifugal discharge in dorsal root afferent fibres.2. The effective conditioning can be (a) an orthodromic volley to the same or an adjacent dorsal root, (b) a volley to the dorsal column one or two segments above the tested level, or (c) a natural stimulus applied to the ipsi- or contralateral hind limb.3. The conditioning stimulus acts by increasing presynaptic excitability; the peak of its effect (maximum presynaptic depolarization) occurs 7-10 msec after the arrival of the conditioning volley to the cord and then quickly decays.4. A large antidromic field potential in the ventral horn is not necessary for the production of a centrifugal dorsal root discharge. Activation of a ventral root filament of approximately 100 mu in diameter can still induce such a discharge in a single dorsal root fibre. Furthermore, antidromic stimulation of the remaining fibres of the same ventral root cannot affect the terminals activated by the thin ventral root filament.5. The phenomenon of motoneurone-presynaptic interaction was obtained in different types of experimental preparations: acute and chronic spinal, anaemic and midcollicular decerebrate, animals with intact supraspinal centres, and one animal without acute laminectomy.     

The effect of temperature on electrical interactions between antidromically stimulated frog motoneurons and dorsal root afferent axons

The effect of temperature on electrical interactions between antidromically stimulated motoneurons and dorsal root afferents was studied in the isolated and hemisected spinal cord of the frog, superfused with Ringer in which Ca2+ was equimolarly replaced by Co2+ or Mn2+ to suppress chemical synaptic transmission. Suction electrodes were used for stimulating and/or recording from dorsal and ventral roots from segments IX or X. Intrafibre recordings from sensory fibres were made at their point of entry into the spinal cord. Supramaximal ventral root stimuli elicited two distinct responses in the segmental dorsal root. First a brief short-latency depolarizing potential. Second, at temperatures below 11 degrees C, a second depolarizing root potential appeared following the short-latency depolarizing potential-I. Amplitude and duration of short-latency depolarizing potential-II reversibly increased as the bath temperature was decreased, reaching a maximum at 3 degrees C. Between 8 and 3 degrees C, short-latency depolarizing potential-II increased in amplitude by 20%/degrees C. In contrast short-latency depolarizing potential-I did not show substantial changes with temperature. The short-latency depolarizing potential-II, unlike short-latency depolarizing potential-I showed stepped fluctuations in amplitude, and appeared to be composed of unitary events. Intrafibre records revealed that the unitary events corresponded to action potentials on individual dorsal root fibres. Double shocks applied to the ventral root, at constant bath temperatures (below 11 degrees C), revealed facilitation of the short-latency depolarizing potential-II, which was maximal between 50 and 80 ms and lasted about 200 ms. Neither the antidromic motoneurone field potential nor the short-latency depolarizing potential-I were facilitated.(ABSTRACT TRUNCATED AT 250 WORDS)     

Group II excitations from plantar foot muscles to human leg and thigh motoneurones

Projections of group II afferents from intrinsic foot muscles to lower limb motoneurones were investigated in humans after electrical stimuli were applied to the tibial nerve (TN) at ankle level, using modulation of the quadriceps H reflex, on-going EMG of the quadriceps and peroneus brevis, and PSTHs of single quadriceps, biceps, semitendinosus, tibialis anterior, and peroneus brevis motor units. TN stimulation evoked late and high-threshold excitation in all leg and thigh muscles investigated. The mean latency of the late excitation was 13.5+/-0.4 ms longer than that of the heteronymous monosynaptic Ia excitation, and the more caudal the motor nucleus the longer the central delay of the late effect, suggesting mediation through interneurones located rostral to motoneurones. The electrical threshold and conduction velocity of the largest diameter fibres evoking the late excitation were estimated to be approximately 2 and 0.67 times, respectively, those of the fastest Ia afferents, i.e. consistent with a mediation by group II afferents. Stimulation of the skin areas innervated by TN did not evoke late excitations. Further support for mediation through group II afferents was provided by the findings that: 1. the latency of the TN-induced late and high-threshold excitation in Per brev units was more delayed by cooling the nerve than that of the excitation evoked by group I afferents, and 2. tizanidine intake (known to depress selectively transmission of group II effects) suppressed the TN-induced late and high-threshold excitation whereas the group I facilitation was not modified.     

Electrophysiological properties of sympathetic preganglionic neurons in the cat spinal cord in vitro

Intracellular recordings were obtained from sympathetic preganglionic neurons of the intermedio-lateral nucleus of the adult cat in slices of upper thoracic spinal cord maintained in vitro. The neurons were identified by their antidromic responses to stimulation of various ipsilateral sites. Sites from which antidromic responses could be evoked were the white ramus, the ventral root, the ventral root exit zone, the white matter between the latter and the outer edge of the tip of the ventral horn, the lateral edge of the ventral horn. Resting membrane potential was –61.3±1.6 mV (mean±SEM), input resistance 67.5±3.7 M, time constant 11.5±1.2 ms. The amplitude of the action potential generated by antidromic or direct stimulation was 77.4±2.3 mV. Threshold for direct spikes was 18.2±1.8 mV. The action potential had an average duration of 3.03±0.16 ms. It showed a prominent hump on the falling phase. The action potential had a tetrodotoxin (TTX)-sensitive and a TTX-resistant component. The latter was abolished by cobalt.Tetraethylammonium, cesium and barium prolonged the action potential duration which acquired a plateau-shape. A prolonged after-hyperpolarization (AHP) followed the sympathetic preganglionic neuron spike. Following a single spike, AHP duration and peak amplitude were 2.8±0.3 s and 16.6±0.7 mV, respectively. The AHP was abolished by cesium or barium, but enhanced by tetraethylammonium. An AHP followed the TTX-resistant spike. EPSPs and IPSPs could be generated by focal stimulation. The EPSP triggered spikes when threshold (15.0±2.0 mV) was reached. The slice of the thoracic spinal cord provides a useful experimental preparation for analysis of cellular properties and synaptic mechanisms of the sympathetic preganglionic neuron.     

Electrophysiological properties of spinal motoneurones of normal and dystrophic mice.

1. The properties of spinal motoneurones of normal and dystrophic mice (129/ReJ) were examined with intracellular electrodes. 2. The following parameters of spinal motoneurones showed no significant differences between normal and dystrophic mice: resting and action potentials, the amplitude and duration of after-hyperpolarization, rheobasic current for excitation, threshold for excitation of the somadendritic membrane (IS-SD inflexion) and input resistance. 3. The changes in motoneurone properties observed 13-16 days after section of the sciatic nerve (axotomy) were similar in both normal and dystrophic mice. 4. The axonal conduction velocity of motoneurones in dystrophic mice was about ten times slower than that in normal mice. The conduction velocity of the sciatic nerve was only about 25% slower in dystrophic mice than in the normal animal. The estimated ventral root conduction velocity as well as the observed dorsal root conduction velocity in dystrophic mice was at least twenty times slower than that in normal mice. 5. In dystrophic mice, spinal motoneurones often showed multiple discharges in response to single, antidromic stimuli. The site of initiation of multiple discharge was located in the motor axon rather than in the motoneurone cell body. 6. In dystrophic mice, nerve impulses were transmitted from fibre to fibre ('cross-talk'). The site of impulse transmission among nerve fibres was near the distal portion of the spinal roots. 7. Synaptic potentials and peripheral reflex discharges evoked by stimulation of the dorsal roots showed a longer latency and were more prolonged in dystrophic mice than in the control mice. 8. The motoneurone properties of dystrophic mice showed no tendency of progressive changes with age ranging from 63 to 148 days. 9. It is concluded that the properties of motoneurone cell bodies examined in dystrophic mice are indistinguishable from those in normal mice and that the only abnormality in motoneurones of the former residues in the motor axon. 10. It is suggested that integrity of the discharge pattern of spinal motoneurones in dystrophic mice is interfered by anomalous impluse transmission in the motor axons and that the motoneurones in dystrophic mice are a homogeneous group rather than a mixture of "normal" and "abnormal" neurones.     

Enhancement of synaptic transmission by dendritic potentials in chromatolysed motoneurones of the cat

1. Monosynaptic transmission in cat lumbosacral motoneurones undergoing chromatolysis was studied by intracellular recording from 7 to 20 days after section of the appropriate ventral roots.2. The average input resistance measured by passing polarizing currents across the cell membrane showed no significant difference between normal and chromatolysed motoneurones. Average rheobasic current for chromatolysed motoneurones was significantly lower (by about 30%) than that for normal motoneurones.3. Spike-like partial responses were commonly superimposed on monosynaptic EPSPs in chromatolysed motoneurones. These responses could be eliminated by stimulation of the bulbar inhibitory reticular formation, but could not be blocked by hyperpolarization applied to the motoneurone soma.4. The spike-like partial response in chromatolysed motoneurones showed a refractory period following (i) the antidromic invasion of the neurone generated by ventral root stimulation, and (ii) in response to two successive afferent stimuli. The refractory period ranged from 5 to 13 msec.5. Initiation of the partial response had no direct relation with the amplitude of the underlying EPSP. The partial response could be evoked by small EPSPs of about 0.5 mV.6. The action potential of a chromatolysed motoneurone arose from the partial response at different levels of depolarization, showing multiple trigger zones for spike initiation. Occasionally, chromatolysed motoneurones discharged in response to stimulation of a single afferent fibre.7. In neurones where more than one spike-like response was obtained, interaction between dendritic responses showed no refractoriness.8. It is concluded that the partial response is an all-or-none event originating at some discrete site on dendrites, and that its presence increases the efficacy of synaptic excitation in chromatolysed motoneurones.     

Synaptic organization in teleost spinal motoneurons.

Glass microelectrodes were inserted into motoneurons innervating pectoral fin muscles to record action and synaptic potentials, evoked by electrical stimulation of ventral and dorsal roots, and the medulla oblongata. Ventral root stimulation evoked a small depolarizing response which had properties compatible with those of the EPSP; its amplitude changes were graded, being increased by membrane hyperpolarization and decreased by high frequency repetitive stimulation. The latency of the response was sufficiently longer than that of the antidromic spike to allow for a monosynaptic delay. Stimulation of the dorsal root produced EPSPs with relatively long latencies, suggesting mediation by a polysynaptic pathway. EPSPs with short latencies were evoked by stimulation of the medulla oblongata, indicating the presence of a monosynaptic excitatory connection. Action potentials, recorded from peripheral nerve after stimulation of the medulla oblongata, were facilitated by conditioning volleys via ventral roots. This facilitation was blocked by dihydro-beta-erythroidine hydrobromide and atropine sulphate, indicating the cholinergic nature of the EPSP of ventral root origin. The conduction velocities of motor axons and of the ventral roots fibers responsible for production of EPSPs were about the same. The EPSP of ventral root origin had a slower rising time course and lesser sensitivity to shifts of membrane potential than the EPSP of medulla oblongata origin, suggesting that the sites of generation of the former EPSP were on the peripheral dendrites. From the above results, it was concluded that the EPSP of ventral root origin was mediated by recurrent axon collaterals of motoneurons.     

Hemilingual spasm: Pathophysiology

In the present offering, the authors provide evidence for the role of the hypoglossal motonucleus in causing a cranial nerve hyperactivity syndrome, namely hemilingual spasm. During a microvascular decompression operation to treat hemilingual spasm, transcranial stimulation elicited a delayed electromyographic (EMG) response from the tongue. This late volley of EMG activity occurred with a latency of approximately 40 ms, lasted approximately 50 ms, and disappeared when the offending vessel was displaced away from the exit zone of the hypoglossal nerve root along medulla oblongata. This late tongue EMG response resembles those found in facial muscles of the patients with hemifacial spasm (HFS). In HFS, electrical stimulation of a branch of facial nerve may elicit an EMG response with a latency of approximately 10 ms in muscles innervated by another branch of the nerve, followed by a variable volley of EMG activity that may last 100 ms or longer. This abnormal response, known as the lateral spread response, is a characteristic sign for hemifacial spasm that disappears after the offending vessel is moved off the facial nerve root. The results of the present study indicate that the EMG signs of hemilingual spasm are similar to those of HFS and that the tongue spasms are most likely caused by hyperactivity of the hypoglossal motonucleus. Based on the authors’ knowledge, the above detailed electrophysiological findings related to hemilingual spasm have not been previously reported in the literature.     

Relationships between the spike components and the delayed depolarization in cat spinal neurones.

1. Changes in the delayed depolarization (DD) following composite (IS-SD) intracellular spikes in motoneurones and neurones of the ventral spinocerebellar tract were recorded in a variety of experimental conditions. Cell activation was either antidromic or by direct intracellular stimulation. 2. It was observed that under all conditions in which IS-SD coupling changes took place (as a consequence of spontaneous fluctuations, membrane conductance variations, variations of direct-stimulation parameters, changes in steady membrane polarization), SD spike delays were always accompanied by a progressive concomitant reduction of the DD depolarizing hump amplitude. 3. Under the same conditions the latency of the DD peak from the stimulus artifact remained constant. Accordingly, any increase of the SD delay was accompanied by a reciprocal reduction of the time interval between the SD spike and the DD peak. This variability of temporal relationships between SD spike and DD would appear to contradict the hypothesis that the DD might represent the image of the excitation spreading from the soma to the dendrites (Kernell, 1964; Nelson & Burke, 1967). 4. as the gradual reduction of the DD hump progressed, the time course of the decay phase of the afterhyperpotential more and more closely approximated the decay phase of the IS spike. As an alternative hypothesis it is suggested that the DD might originate from the current which generates the IS spike.     

Double stimulation modulates afterhyperpolarization phase following action potentials evoked in rat motoneurones

The influence of a pair of stimuli running in time sequence between 5-10 ms (a doublet) on the basic parameters of antidromic action potentials was studied in rat motoneurones. Electrophysiological experiments were based on stimulation of axons in the sciatic nerve and intracellular recording of antidromic action potentials from individual motoneurones located in L4-L5 segments of the spinal cord. The following parameters were analyzed after application of a single stimulus and a doublet: amplitude and duration of the antidromic spike, amplitude, total duration, time to minimum, half-decay time of the afterhyperpolarization (AHP). It was demonstrated that application of a pair of stimuli resulted in: (1) a prolongation of action potentials, (2) a prolongation of the total duration and half-decay time of the AHP, (3) a decline of the time to minimum of the AHP, (4) an increase of the AHP amplitude of the spike evoked by the second stimulus. Significant differences in AHP parameters were found either in fast or slow motoneurones. We suppose that doublet-evoked changes in the AHP amplitude and duration are linked to intrinsic properties of individual motoneurones and may lead to the prolongation of the time interval to subsequent motoneuronal discharges during voluntary activity.     

Distribution of histamine in the developing peripheral nervous system

The presence and ontogenetic distribution of histamine was studied in the developing peripheral nervous system of the rat by using an indirect immunofluorescence technique and a specific rabbit anti-histamine antiserum. Histamine immunoreactivity (IR) first appeared in peripheral nerves on embryonic day 14. The number and intensity of histamine-immunoreactive nerves was highest on embryonic days 16–18. During development starting from embryonic day 14, motoneurones in ventral horns of the spinal cord at cervical, thoracic and lumbar levels contained histamine IR. A subpopulation of sensory neurones in dorsal root ganglia exhibited histamine IR. Histamine IR was also present in nerve fibres of ventral and dorsal roots of spinal cord, as well as in spinal nerves. Population of neurones and nerve fibres in sympathetic and pelvic ganglia as well as in myenteric ganglia of the intestine were also labelled with the histamine antiserum. In peripheral target organs, histamine IR was observed in nerve fibres around bronchi of the lungs, in the atria of the heart, in the adrenal gland, in the intestinal wall, in muscular tissues and in subepithelial tissue of the skin.The results of this study indicate that histamine is widely distributed in different types of neurones and nerve fibres of the developing peripheral nervous system.     

Current-to-frequency transduction in CA1 hippocampal pyramidal cells: Slow prepotentials dominate the primary range firing

Summary (1)In order to study how hippocampal pyramidal cells transform a steady depolarization into discharges, CA1 pyramids (n = 32) were injected with 1.5 s long pulses of constant depolarizing current. (2) The firing in response to weak currents was in most cells, characterized by low frequency (0.2–5 Hz), slowly increasing depolarizations preceding each action potential (slow prepotentials, SPPs), a long latency (0.2–5 s) to the initial spike and lack of adaptation. (3) The SPPs, which lasted 30–2,000 ms, showed an increasing steepness with increasing current, and seemed to be a major regulating factor for the slow firing. (4) In response to stronger currents the discharge had a high initial frequency (100–350 Hz), followed by adaptation to steady state firing (5–50 Hz). Thirty of 32 cells showed a dip in the frequency (n = 5), or a pause (n = 25) lasting 250–1,000 ms between the initial burst of firing and the steady state. The pause occurred only at intermediate current strengths. (5) Additional spikes to the initial burst seemed to be recruited through the development of depolarizing waves. The initial slope of these waves resembled those of the SPPs. Similar waves occurred at the expected tune of occasionally missing spikes during steady state firing. (6) The variability (SD/mean) of the interspike intervals decreased with increasing frequency of firing. (7) The frequency-current (f/I) relation for the steady state firing showed a simple linear or convex shape, and lacked a secondary range. In contrast, the f/I plots for the initial few interspike intervals had both primary, secondary and tertiary ranges, like motoneurones.Supported by the Norwegian Research Council for Science and the Humanities and The National Institute of Health, USA     

A study of the interaction between motoneurones in the frog spinal cord

1. A short-latency interaction between motoneurones has been studied with intracellular and root potential recordings from the isolated spinal cord of the frog. Antidromic stimulation of one ventral root causes brief depolarization (VR-EPSP) of the motoneurones of adjacent, non-excited motoneurones. The summed activity of many such VR-EPSPs can be seen as a brief depolarization (VR-VRP) passing out an adjacent ventral root.

2. Both intracellular and root-recorded signs of this interaction are graded in amplitude.

3. It was found that this interaction decreased with increasing temperature. This is in contrast to the behaviour of the ventral root potential resulting from dorsal root stimulation (DR-VRP) or the dorsal root potentials resulting from either dorsal root (DR-DRP) or ventral root (VR-DRP) stimulation, all of which increased in amplitude from below 10 to about 17° C.

4. Pharmacological evidence suggests that the interaction between motoneurones is not chemically mediated. The VR-VRP was not affected by a large variety of transmitter blocking agents, including curare, dihydro-β-erythroidine, atropine, succinylcholine, hexamethonium and DOPA, while the VR-DRP, which probably originates with the release of ACh from an axon collateral, was consistently blocked.

5. Mg²⁺ suppressed the VR-VRP more slowly than the other potentials, and this suppression was increased by adding Ca²⁺, rather than reversed, as in the case of the other root potentials, which are presumably mediated by chemical transmission.

6. The interaction between motoneurones is strongly facilitated by orthodromic depolarization of the motoneurones being antidromically stimulated. Extracellular recordings within the cord support the conclusion that this facilitation is a result of the enhancement of antidromic invasion, perhaps especially of the dendrites, by slight depolarization.

7. One VR-VRP (or VR-EPSP) first suppresses response to another (for about 10 msec), then facilitates response to the second, with maximum effect around 20-40 msec. This is the case whether both stimuli go to the same or to different ventral roots, although occlusion is less and facilitation greater in the latter case. Occlusion of the VR-EPSP also results from full excitation of the cell in which recording is being done.

8. The mechanism of this interaction remains uncertain, but it would seem likely that overlapping dendrites of adjacent motoneurones interact with each other electrically through close apposition or specialized contacts. Occlusion would result from the refractoriness of strongly depolarized dendrites, facilitation from the enhancement of invasion of antidromically stimulated motoneurones by the weaker (or residual) depolarization occurring after earlier activity of motoneurones or their dendrites.

     

Long-loop reflex from arm afferents to remote muscles in normal man

The present study was designed to examine the effects of median nerve stimulation on motoneurones of remote muscles in healthy subjects using H-reflex, averaged EMG and PSTH methods. Stimulation of the median nerve induced facilitation of soleus H-reflex from about 50 ms and it reached a peak at about 100 ms of conditioning-test interval. Afferents that induced the facilitation consisted of at least two types of fibres, the high-threshold cutaneous fibres and the low-threshold fibres. When the effects were examined by the averaged surface EMG and PSTH, no facilitation but rather inhibition or inhibition-facilitation was induced in all tested muscles except for the upper limb muscles on the stimulated side. The inhibition latency was shortest in masseter muscle and longest in leg muscles, while values for the contralateral upper limb muscles were in the middle, indicating that the onset of inhibition was delayed from rostral to caudal muscles. Inputs from the median nerve converged to inhibitory interneurones, which mediate the masseter inhibitory reflex. Our findings suggested that inputs from the median nerve initially ascend to the brain, at least to the brainstem, and then descend to the spinal cord. Therefore, inhibition induced by median nerve stimulation was not considered as an interlimb reflex mediated by a propriospinal pathway, but long-loop reflex, at least via the pons. The discrepancy between the results of reflex and motor units suggests that facilitation of soleus H-reflex following median nerve stimulation was mainly due to reduced presynaptic inhibition.     

Integration in trigeminal premotor interneurones in the cat

A population of last-order interneurones within the rostrodorsal part of the oral nucleus of the spinal trigeminal tract (NVspo-) has been investigated in 21 chloralose anaesthetised cats. The neurones were identified by their antidromic (AD) response to microstimulation (median current 9 A, range 3–39 A) of the ipsior the contralateral masseteric subnucleus of the trigeminal motor nucleus. Fifty-one of 113 interneurones tested were discharged from the ipsilateral and eight from the contralateral motor nucleus. The average conduction time was 0.50 ms from the ipsilateral and 0.74 ms from the contralateral motoneurone pool. Conduction velocities of the axons ranged from 2.0 to 14.0 ms. The pattern of primary afferent input onto the selected neurones was analysed by graded electrical stimulation of dissected trigeminal nerves. Low-threshold afferents innervating the intraoral mucosa including the tongue and the perioral skin of the lower lip were the most effective inputs, as judged from both the frequency of occurrence and from the latencies of the evoked spike discharges. Ninety-six percent of the neurones responded to stimulation of the inferior alveolar nerve (Alv inf) and 83% responded to stimulation of the lingual nerve (Ling). The median threshold strength required to evoke the Alv inf and the Ling responses was 1.7 T (range 1.0–3.6 T) and 1.3 T (range 1.0–5.0 T), respectively. The median latency to spike discharges evoked by the Alv inf was 2.0 ms (range 1.3–4.8 ms) and to the Ling it was 2.5 ms (range 1.4–7.0 ms). Action potentials elicited by stimulation of the masseteric and digastric nerves were observed in 40% and 10% of the neurones, respectively. These responses, which had median latencies of more than 8 ms (range 4.7–16.0 ms), were only seen at stimulation intensities above 2 T (range 2.5–25 T). An input from the maxillary whisker nerve was seen in only one case. Postspike averages of the extracellular field potentials within the trigeminal motoneurone subnuclei evoked by interneuronal spikes were made in a subsample of 51 NVspo- neurones activated by iontophoresis of L-glutamic acid. Excitatory synaptic effects within the masseteric subnucleus were observed in eight cases. An inhibitory effect was seen in one case. One specific neurone gave an excitatory extracellular field potential within the digastric motoneurone subnucleus. This interneurone was AD activated from the digastric, but not from the masseteric subnucleus. The physiological properties of the NVspo--mass interneurones are discussed in relation to their suggested roles in the phase-dependent control of the trigeminal motoneurones during oro-facial masticatory behaviours.     

The synaptic excitation of Renshaw cells

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