Monosynaptic Transmission Research Articles

Percutaneous stimulation of human corticospinal tract: a single-fibre EMG study of individual motor unit responses

The technique of electrical stimulation of the brain through intact scalp was applied to activate the corticospinal tract (CST) of healthy human volunteers. Single motoneurone responses were picked up by a special (single fibre EMG) needle electrode. Our finding of relatively small latency variation of consecutive single motor unit responses seems to support the concept of predominantly monosynaptic transmission at the spinal level. The alternation between several discrete latencies seems to reflect a complexly shaped spinal motoneurone excitatory postsynaptic potential (EPSP), which could be due to either alternating direct/indirect (via other cerebral neurones) activation of the corticospinal tract (CST) neurones, or alternating mono- or oligosynaptic transmission at the spinal level, or multiple CST impulses in response to a single stimulus.

Recurrent inhibitory connexions among neck motoneurones in the cat.

1. Intracellular recordings were made from motoneurones innervating neck muscles in the cat. Dorsal roots were cut and muscle nerves electrically stimulated to activate alpha motor axons. 2. Recurrent inhibitory post-synaptic potentials (i.p.s.p.s) evoked by antidromic volleys in homonymous or heteronymous nerves were found in the majority of motoneurones studied, including those to dorsal neck muscles (biventer cervicis, splenius and complexus) as well as to occipitoscapularis and levator scapulae ventralis. 3. Central latencies of the recurrent i.p.s.p.s indicate disynaptic transmission. Amplitudes ranged from 100 microV (criterion level) to 2.2 mV. Average amplitudes were less than 0.6 mV. 4. The recurrent i.p.s.p.s were distributed to non-synergistic as well as to synergistic motoneurones. Analysis of relative strength of recurrent inhibition indicates influence of proximity of motoneurone pools, functional relatedness of muscles, as well as other factors. Variation in intrinsic motoneuronal properties probably underlies positive correlations (independent of variation in resting potential) between recurrent i.p.s.p.s evoked from different sources in motoneurones of a single pool. 5. Recordings (mainly extracellular) were also made from interneurones (Renshaw cells), located in the C3 and C4 segments of the spinal cord, that were excited by antidromic volleys in muscle nerves. The response varied from a single action potential to a burst of up to nineteen action potentials. Central latencies to the first response indicate monosynaptic transmission. Many Renshaw cells were excited by antidromic volleys in several muscle nerves, though this was restricted to nerves of the same segmental level as the Renshaw cell. All the muscle nerves studied were effective in activating Renshaw cells. 6. The results indicate that in many ways the recurrent i.p.s.p.s and the responses of Renshaw cells recorded in the neck segments resemble those in the hind-limb segments. Thus, the basic organization of recurrent inhibition in the neck segments resembles that occurring elsewhere in the spinal cord. A difference is the tendency for recurrent i.p.s.p.s in neck motoneurones to be relatively small in amplitude and Renshaw cell responses to be less strong than those recorded in the hind-limb segments. It is suggested that this is related to the segmentation of neck muscles and their motoneurone pools. 7. It is concluded that recurrent inhibition is a prominent feature of spinal organization governing neck muscles. It can therefore be expected to participate in control of head movements.

Presynaptic Depolarization Mediates Presynaptic Inhibition at a Synapse Between an Identified Mechanosensory Neurone and Giant Interneurone 3 in the First Instar Cockroach, Periplaneta Americana

ABSTRACT Intracellular microelectrodes were used to study presynaptic inhibition at a cholinergic synapse between identified neurones: the lateral filiform hair sensory neurone (LFHSN) and giant interneurone 3 (GI 3) in the terminal ganglion of the first instar cockroach Periplaneta americana. The LFHSN-GI3 synapse was shown to fulfil physiological criteria for monosynaptic transmission : the latency of the EPSPs was 1·4ms and was constant during high-frequency firing of LFHSN; transmission was progressively and reversibly abolished by replacement of Ca2+ with Mg2+. Movement of the lateral filiform hair towards the cereal tip produced a burst of spikes in LFHSN and a burst of EPSPs in GI 3. Movement of the medial filiform hair towards the base of the cercus produced a burst of spikes in the medial filiform hair sensory neurone (MFHSN) and a burst of EPSPs in GI2. EPSPs evoked in GI 3 by LFHSN spikes were inhibited during bursts of EPSPs in GI 2 which were evoked by MFHSN spikes. LFHSN was depolarized and its spikes were reduced in amplitude during spike bursts in MFHSN. Reduction in LFHSN spike amplitude reduced GI 3 EPSPs. This phenomenon was attributed, therefore, to presynaptic inhibition. The occurrence of presynaptic inhibition was dependent upon the degree of delayed rectification exhibited by the LFHSN axon. Hyperpolarization of LFHSN increased spike height, but did not increase the amplitude of GI 3 EPSPs. The delay between the onset of MFHSN-evoked EPSPs in GI2 and MFHSN-evoked depolarizations in LFHSN suggested that MFHSN does not synapse directly onto LFHSN. Neither depolarization nor hyperpolarization of GI 2 had any effect on MFHSN-mediated presynaptic inhibition of LFHSN-GI 3 transmission, therefore it was considered unlikely that GI2 synapses onto LFHSN. Prolonged hyperpolarization lowered the LFHSN spike threshold and temporarily abolished presynaptic inhibition. Bursts of spikes in LFHSN mediated presynaptic inhibition of MFHSN-GI2 EPSPs. Mutual presynaptic inhibition by the FHSNs may have a functional significance in sharpening the boundaries of the GIs’ directional sensitivities.

Monosynaptic Transmission in the Spinal Cord

The synaptic action of afferent fibers on motoneurons in the spinal cord is among the longest studied problems in the central nervous system but is still far from being fully understood. This article reports on the remarkable feat of recording from a single motoneuron activated by a single fiber, followed by labeling of both to identify unequivocally the relevant synapses.

The magnitude of long-term potentiation of field potentials induced monosynaptically in region CA3 of guinea pig hippocampus

The magnitude of long-term potentiation (LTP) was re-examined for monosynaptic transmission between mossy fibers and CA3 neurons in thin sections of the hippocampus of the guinea pig. Although an initial negative deflection in the field potential showed apparent short-term potentiation, this deflection was concluded to reflect non-synaptic activation of CA3 neurons. Accordingly, the magnitude of LTP of monosynaptic transmission was re-calculated at 3.4 ± 0.9.

Development of the monosynaptic stretch reflex in the rat: an in vitro study.

The properties and development of the stretch reflex pathway were investigated in new-born and fetal rats using the isolated spinal cord-hind limb preparation. Muscle afferent discharge was elicited by small stretch of the triceps surae muscle in the new-born rat and in the fetus. It appeared as early as embryonic day 18.5. Ramp-and-hold stretch elicited only phasic discharges in most afferent fibres. A phasic reflex response was evoked in the triceps surae muscle by brief or ramp-and-hold stretch of the muscle in the new-born rat. The threshold stretch required for evoking the reflex response was close to that for eliciting the afferent discharge. A reflex response in the triceps surae muscle was also evoked by electrical stimulation of the triceps surae muscle nerve or the sciatic nerve in the new-born rat. Excitatory post-synaptic potentials (e.p.s.p.s) in the triceps surae motoneurones were evoked by stimulation of the muscle nerve in the new-born rat. The amplitude of the e.p.s.p.s was large enough to generate spike potentials. Homonymous e.p.s.p.s were significantly larger than heteronymous e.p.s.p.s. The amplitudes of the e.p.s.p.s were very susceptible to the rate of stimulus repetition. At a stimulus frequency of 10 Hz they were depressed to less than 10% of the control value. Presynaptic impulses evoked by stimulation of afferents in the muscle nerve appear in the motor nucleus less than 1.0 ms before the onset of synaptically evoked field potentials. The interval between the arrival of impulses evoked by dorsal root stimulation and the onset of e.p.s.p.s in motoneurones was 0.56 +/- 0.16 ms, indicating monosynaptic transmission from the primary afferents to the motoneurones. In the fetus, a reflex response in the triceps surae muscle was observed following a small stretch of the muscle (or electrical stimulation of the sciatic nerve) in all preparations at embryonic day 20.5 and in about half of those examined at embryonic day 19.5. Neither stimulation evoked a reflex response at embryonic day 18.5. Latencies of the reflex responses evoked by muscle stretch or by nerve stimulation were similar to those in the new-born rat. It is concluded that the monosynaptically evoked stretch reflex response in the triceps surae muscle first appear at embryonic day 19.5. Natural and electrical stimulation of the plantar skin evoked a reflex response with long latencies in flexor muscles. Such a cutaneous reflex was first present at embryonic day 17.5, two days earlier than the onset of the stretch reflex.

Synapses Between an Identified Giant Interneurone and A Filiform Hair Sensory Neurone in the Terminal Ganglion of First Instar Cockroaches (Periplaneta Americana L.)

ABSTRACT The ultrastructure of input and output synapses of various identified insect neurones has recently been studied (for example Titmus & Hoyle, 1977; Altman, Shaw & Tyrer, 1980; Phillips, 1980; Watson & Burrows, 1981, 1982, 1983; Tolbert & Hildebrand, 1981) and connections between anatomically and physiologically defined axons have been described (King & Wyman, 1980). To date though, synapses have not been visualized in an insect central pathway in which aspects of the anatomy, physiology, pharmacology and associated behaviour have been investigated. The cereal afferent, giant interneurone synapses in the sixth abdominal (A6) ganglion of the cockroach Periplaneta americana are well suited for such studies. Using cobalt staining (Pitman, Tweedle & Cohen, 1972) of single neurones, seven giant interneurones (GIs 1–7) can be identified on the basis of their morphology (Harrow, Hue, Pelhate & Sattelle, 1980; Daley, Vardi, Appignani & Camhi, 1981). In adult cockroaches these interneurones receive sensory input from numerous cereal mechanoreceptor afferents (Callec, Guillet, Pichon & Boistel, 1971 ; Daley et al. 1981). There is considerable evidence for cholinergic monosynaptic transmission at these synapses (Callec, 1974; Sattelle, 1980) and postsynaptic acetylcholine receptors sensitive to the nicotinic cholinergic antagonist a-bungarotoxin are present on GI2 and GI 3 (Harrow, Hue, Pelhate & Sattelle, 1979; Sattelle, David, Harrow & Hue, 1980; Harrow & Sattelle, 1983 ; Sattelle et al. 1983). It has been shown that the cereal afferent, giant interneurone pathways play a part in mediating the escape response of the cockroach following stimulation of the cereal mechanoreceptors (Ritzmann & Camhi, 1978; Camhi, Tom & Volman, 1978).

Are baclofen-sensitive GABAB receptors present on primary afferent terminals of the spinal cord?

The site of action of the antispastic drug baclofen has long been considered to reside in the spinal cord although supraspinal effects have also been reported. This beta-chlorophenyl derivative of the neurotransmitter gamma-aminobutyric acid (GABA) depresses both monosynaptic and polysynaptic transmission in the cord possibly through a decrease in transmitter release rather than by any antagonism at postsynaptic receptors. Recently, baclofen has been shown to be a selective ligand for a bicuculline-insensitive GABA receptor (GABAB) site that occurs widely in the mammalian central nervous system including the spinal cord. The apparent importance of the cord in the therapeutic effects of this drug prompted us to ask whether they involve GABAB site activation. As an initial step we have located these receptors by autoradiography, comparing them with classical GABAA sites. We report here that GABAB sites, unlike GABAA sites, are present in high concentrations in laminae I, II, III and IV of the dorsal horn and that after the neonatal administration of capsaicin this binding is reduced by 40-50%.

Actions of guanidine hydrochloride on cat spinal monosynaptic reflex transmission

The effects of a single intravenous dose of guanidine hydrochloride were examined on the function of the lumbar dorsal-ventral root and triceps surae nerve-ventral root monosynaptic reflex (MSR) in unanesthetized acute spinal (C-1 sectioned) cats. Guanidine, in a dose of 25 mg/kg, consistently depressed the amplitude of the monosynaptic reflex response while a dose of 200 mg/kg always exerted a facilitatory action. Intermediate doses of 50 or 100 mg/kg produced variable actions on the amplitude of the monosynaptic reflex from one preparation to another. The differential effects of guanidine on the evoked monosynaptic reflex are postulated to represent the ability of the drug to enhance both excitatory and inhibitory transmission, the latter predominating at smaller doses and the former becoming apparent with an increasing dose of guanidine. The facilitatory and the depressant effects of guanidine on the function of spinal reflexes were slow to develop, suggesting an intracellular site of action. These results may have significance for an understanding of the possible efficacy of guanidine in motor neuron disease in man.

Dopamine receptor-mediated depression of spinal monosynaptic transmission

The effects of the dopamine agonists apomorphine, lisuride and lergotrile were evaluated on cat spinal cord monosynaptic transmission by stimulating the dorsal root and recording the ventral root compound action potential. All 3 agonist decreased the area of the monosynaptic response. This effect was prevented by pretreatment with the dopamine antagonist haloperidol and metoclopramide, but not with the alpha-adrenergic antagonist phentolamine. These results suggest the existence of spinal cord dopamine receptors which can modulate motor output.

Baclofen-induced decrease of excitability of primary afferents and depression of monosynaptic transmission in cat spinal cord

The relationship of the depressant effect of baclofen on spinal monosynaptic transmission and its effect on the excitability of primary afferents was examined in spinal unanesthetized cats. Baclofen (1.0 mg/kg, i.v.) produced a deep and long-lasting depression of spinal reflex responses with a concomitant decrease of terminal excitability. Primary afferent depolarization, as indicated by an increase of terminal excitability, evoked by conditioning of an antagonistic muscle nerve, was greatly reduced by this drug. Depression of monosynaptic transmission induced by baclofen was temporarily reversed by posttetanic potentiation. However, the same high frequency orthodromic stimulation further reduced excitability of terminals. It is therefore unlikely that block of terminal invasion is responsible for baclofen-induced depression of spinal monosynaptic transmission. These results are compatible with the suggestion that baclofen causes a reduction of transmitter release. In the spinal cord, this action is probably limited to the excitatory transmitter of primary afferents.

Microvascular perfusion and metabolism in injured spinal cord after methylprednisolone treatment.

The purpose of this study was to determine the effect of treatment with the synthetic glucocorticoid, methylprednisolone, on the microvasulature and metabolism of the traumatized spinal cord. Spinal cords of cats were compressed with a 170-gm weight for 5 minutes and were treated with either high-dose methylprednisolone (HDMP, 15 mg/kg/24 hrs) or megadose methylprednisolone (MDMP,60 mg/kg/24 hrs). Animals were sacrificed at 2, 8, or 24 hours following injury. Treatment with HDMP resulted in substantial preservation of injured spinal cord microvascular perfusion at 8 hours as compared with injured untreated cats. Compression trauma caused a partial derangement of energy metabolism and a shift toward anaerobic glycolysis in both treated and untreated groups for the entire 24-hour postinjury period. Tissue levels of adenosine triphosphate, phosphocreatine, and total adenylates in the HDMP-treated cats sacrificed at 8 hours after trauma were significantly elevated over untreated controls, but those in the 2- and 24-hour groups were not. Concentration of energy intermediates in MDMP-treated cat were either equal to or below those of injured untreated animals al all three postinjury time period. The postinjury metabolite pattern and concentrations seen in this study possibly result from differing levels of blood flow and neuronal activity in the injured untreated, HDMP-, and MDMP-treated spinal cords. Better tissue perfusion in the HDMP-treated cats might be expected to result in an improved tissue energy state in these animals. However, intensive high-dose glucocorticoid treatment has been demonstrated to augment spinal cord monosynaptic and polysynaptic reflex transmission and primary afferent excitability. Furthermore, acute single intravenous dose studies have shown this direct neuronal action to be dose-related. Thus, additional high-energy phosphate molecules that may be reformed as a result of HDMP treatment were perhaps used as the energy source for any increased neuronal activity caused by steroid administration. The beneficial effects of glucocorticoid treatment in experimental spinal cord trauma might derive from preserved cellular structural integrity. This could result in increased levels of neuronal activity, energy utilization, and production in treated as compared with untreated tissue.

Monosynaptic transmission during epileptiform activity induced by penicillin in hippocampal slices in vitro.

Synaptic transmission was studied in the CA1 region of transverse hippocampal slices in vitro before and after the addition of the epileptogenic agent sodium benzyl penicillin. The presynaptic fibre volley and the field potential associated with the intracellular EPSP, 'field EPSP', were recorded from the layer of the activated synapses. Addition of penicillin did not change either response. The rising phase of the intracellularly recorded EPSP did not change. However, the peak amplitude and, particularly, the duration of the EPSP both increased. The prolongation of the EPSP may be of importance for the triggering of epileptiform bursts.

Prolonged time course for vibratory suppression of stretch reflex in the decerebrate cat.

We studied the effects of longitudinal tendon vibration on the stretch reflex of the soleus and gastrocnemius muscles in 11 decerebrate cats. Vibration was applied at amplitudes (40-80 micrometer) and frequencies (120-250 HZ) sufficient to provide a strong tonic vibration reflex. In keeping with previous reports, we found that during an established tonic vibration reflex, the force and emg response to superimposed ramp and hold stretch are largely suppressed. This suppression is most obvious during the dynamic phase of stretch where it gives rise to a complex force response resembling that of active areflexic muscle. If stretch initiation is delayed until after vibration is terminated, the suppressed effects of vibration persist for 5 s or more. These suppressive effects are marked in the first 200 ms, and then decay gradually over the ensuing time period, paralleling the decline in emg and force which follows vibration offset. Simultaneous recordings from homonymous Ia afferents showed that this suppression persists even though the stretch responsiveness of primary spindle endings has returned to normal immediately following the end of vibration. When stretch is initiated shortly after vibration commences, the suppressive effects are first evident at 50-100 ms latency, but are not well established until 1 s or more after vibration onset. Tests of monosynaptic transmission using small amplitude tendon taps or electrical stimulation of synergist nerves to activate Ia fibers revealed that reductions in the magnitude of the response following vibration are usually modest (12% mean reduction at 50 ms, n = 5), and they are quite sensitive to the initial level of excitation of the motoneuron pool. These reductions were also rather shortlived, being largely completed within 500 ms of vibration offset. Although the relative contributions of presynaptic and postsynaptic inhibition are not readily dissociated in this type of experiment, it is likely that the magnitude of presynaptic inhibition is quite small. We argue that the effects of vibration on the stretch reflex are best explained by invoking an excitatory autogenetic projection from Ia interneurons to extensor motor neurons, which lies in parallel with the Ia monosynaptic projection. In order to account for the vibratory suppression, we propose that these interneurons are driven to saturation by vibration. When vibration ceases, the discharge rate of these interneurons declines with a prolonged time-course that coincides with the recovery of stretch responsiveness. This recovery would contribute to the return of stretch reflex force.

Non-serotonergic depression of spinal monosynaptic reflex transmission by 5-hydroxytryptophan

Administration of a 50 mg/kg (i.v.) dose of either 1−, or the racemic D,L-mixture of 5-hydroxytryptophan (5-HTP) in acute unanesthetized spinal (C-1) cats produced a depression of the lumbar monosynaptic response (MSR) amplitude when the reflex was evoked by supramaximal triceps surae (TS) nerve stimulation. Neither pretreatment with the serotonin receptor antagonists cincanserin or cyproheptadine, nor the L-aromatic amino acid decarboxylase inhibitor methyldopa antagonized the depressant effect of 5-HTP on the MSR in TS-stimulated animals. Administration of amitriptyline, a selective serotonin reuptake inhibitor, reversed the depression in the MSR amplitude produced by 5-HTP and produced an increase in the MSR above the original pre-5-HTP control level. These data suggest that 5-HTP has a depressant action upon spinal monosynaptic reflex transmission that is unrelated to an increase in spinal serotonergic activity. The site of the depressant effect of 5-HTP within the MSR pathway is postulated to be the la afferent terminal. This non-serotonergic 5-HTP action should be considered when interpreting the results of neuropharmacologic studies employing 5-HTP as a serotonin precursor.

A simple in vivo method for evaluating drug action at central and peripheral synapses

A simple in vivo method for studying spinal reflexes and neuromuscular transmission in anaesthetized mice is described. The technique utilizes electromyographic recording from muscles of both hind limbs following stimulation of the sciatic nerve in one limb. Drug effects on the neuromuscular junction, on monosynaptic reflex transmission and on crossed polysynaptic reflexes can be assessed. In addition a method for distinguishing between drugs which affect neuromuscular transmission and those which affect nerve conduction is described using their different effects on reexcitation of motoneurons. Details of data collection and analysis using a laboratory microcomputer are presented. The effects of a variety of representative compounds which have been shown to affect central and peripheral neurotransmission in other systems have been evaluated. The actions of these drugs in this system are compared with those obtained using spinal animals and more sophisticated recording techniques. The results compare favourably with those obtained using more complex methods and the technique offers a simple and inexpensive way of evaluating drug action at these synapses.

Glucocorticoid effects on serotonergic and noradrenergic facilitation of spinal monosynaptic transmission

The ability of an intensive glucocorticoid regimen (i.e., triamcinolone diacetate, 8 mg/kg i.m./7 days) to modify the lumbar spinal monosynaptic reflex response to serotonergic and noradrenergic agents has been examined in unanesthetized acute spinal (C-1 sectioned) cats. Triamcinolone pretreatment enhances the 2N facilitatory actions of amitriptyline (AMIT), 5 mg/kg i.v., when given after D, L -5-hydroxytryptophan (5-HTP), 50 mg/kg i.v., as compared to untreated control preparations. Subsequent administration of methysergide, a serotonin receptor blocking drug, in a dose of 1 mg/kg i.v. promptly and completely reverses the monosynaptic response increase by AMIT in untreated animals, but not in the glucocorticoid treated ones. In contrast, the monosynaptic facilitation normally produced in untreated preparations by methoxamine (MX), 1 mg/kg i.v., a centrally active noradrenergic agonist, is prevented as a result of triamcinolone dosing. These results demonstrate a glucocorticoid effect on spinal biogenic amine function such that serotonergic monosynaptic reflex activation is enhanced while noradrenergic reflex stimulation is depressed. Furthermore, they suggest that the elevations in plasma cortisol in certain cases of psychiatric depression may contribute to alterations in central biogenic amine synaptic activity.

Glucocorticoid enhancement of serotonergic facilitation of cat spinal monosynaptic motor neuron excitation

Intensive pretreatment with triamcinoline diacetate (8 mg/kg, i.m. once daily for 7 days) was found in the acute spinal (decerebrate) cat to potentiate the increase in monosynaptic spinal reflex transmission caused by coadministration of the serotonin precursor, d, l-5-hydroxytryptophan, and amitriptyline, a selective serotonin reuptake inhibitor. In addition, the ability of methysergide, a selective serotonin receptor antagonist, to reverse the monosynaptic excitatory actions of d, l-5-hydroxytryptophan plus amitriptyline was significantly reduced. This apparent glucocorticoid enhancement of the actions of a serotonergic spinal system that is facilitatory to motor neuron excitation may have relevance to the therapy of degenerative motor neuron disorders.

Acute effects of methylprednisolone sodium succinate on spinal reflexes

The acute effects of single intravenous doses of methylprednisolone sodium succinate (30, 60, or 90 mg/kg) on segmental spinal cord function were examined by stimulating the triceps surae nerves and recording the monosynaptic (2N) and polysynaptic discharges at ventral root L7. Five to ten seconds after injection, an intense but short-lived, spontaneous discharge concomitant with a dose-related reduction in the stimulus-evoked 2N response occurred. This was rapidly followed by enhancement in the 2N discharge amplitude which peaked by 45 s after administration. The duration of the 2N increase was 10 to 60 min. Polysynaptic discharge was augmented to a lesser extent and for a shorter time. The reflex enhancement was reproducible in preparations in which the distally transected dorsal roots were stimulated. All drug-induced responses were prevented by preadministration of 2.5 to 10.0 mg/kg Na pentobarbital i.v. These results indicate that i.v. glucocorticoid enhances mainly monosynaptic transmission perhaps by an action on the primary afferent terminals which augments their spontaneous and evoked transmitter release. Furthermore, they provide additional support for the view that the beneficial effects of glucocorticoids in central nervous system trauma and stroke may in part reflect an improved synaptic function.

Observations on stretch reflexes in lumbar back muscles of the cat.

Reflex responses to brief muscle stretch and to electrical stimulation of dorsal roots were studied in cat longissimus and iliocostalis muscles by myographic and electromyographic recordings in spinal and anesthetized preparations. Brief stretch applied simultaneously to both muscles, by pulling at an isolated segment of the iliac bone, elicited contractions only in the central region of longissimus, composed of slowly contracting fibers, the time to peak tension varying between 70 and 100 ms. No reflex responses were observed in the faster contracting parts of this muscle or in the iliocostalis under the stimulation conditions used. The total reflex time usually varied from 4.5 to 7 ms which is shown to correspond to intra-spinal conduction times, approximately between 2 and 5 ms. Only exceptionally was a central reflex delay corresponding to a monosynaptic transmission observed. Reflexes evoked by dorsal root simulation (L4, L5) have a central conduction time similar to those elicited by adequate stimulation. The possibility that the central pathway for stretch reflexes in longissimus may involve more than two neurons is considered. In decerebrate preparations the central region of longissimus displays a prominent tonic stretch reflex. With the longissimus in situ the magnitude of the reflex is highly dependent on the position of the lumbar spine relative to the pelvic girdle.