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PubMed2000

The monosynaptic reflex: a tool to investigate motor control in humans. Interest and limits.

The principle of the monosynaptic reflex used as a tool to explore the excitability of the motoneurones (MNs) is explained and the general methodology of the H reflex is described. The different drawbacks inherent in the technique are then considered: mechanisms other than the monosynaptic la excitation of MNs contributing to the H reflex size (limitation of the H reflex size by disynaptic IPSPs, presynaptic inhibition of la terminals, post-activation depression); non-linearity and changes in the 'recruitment gain' in the MN pool; and poor time resolution of the method. Despite these drawbacks, it is emphasized that the H reflex is the only available technique enabling one to investigate changes in transmission in spinal pathways during motor tasks.

Animals↗
PubMed1987

Inhibition of monosynaptic reflexes in the human lower limb.

1. Presynaptic inhibition of muscle spindle Ia afferents by afferents from the same and other muscles has been studied in the human lower limb. The experiments have utilized conditioning of test monosynaptic reflexes by vibration of both the test and other muscles. 2. The pattern of inhibition invariably includes autogenetic actions. 3. There are powerful effects from flexor to extensor Ia afferents. Actions from flexor to flexor, and from extensor to extensor, are weaker. Actions from extensors to flexors are very weak. 4. The strength of presynaptic inhibition from one muscle type to another weakens as the muscles considered become more anatomically distant. 5. The inhibition studied both by vibration and by electrical conditioning stimulation of nerves becomes weaker during voluntary isometric contraction of the test muscle. It is strongest at rest and during antagonist contraction. 6. Evidence is provided suggesting that descending control is the primary cause of this modulation of inhibition during contraction. 7. Stimulation of afferents in cutaneous nerves reduces group I presynaptic inhibition of Ia afferents.

Adolescent↗
PubMed1989

Effect of magnesium on depression of the monosynaptic reflex induced by 2-chloroadenosine or hypoxia in the isolated spinal cord of neonatal rats.

Superfusion of the isolated spinal cord of neonatal rats (4-9 days postpartum) with physiological medium containing 2-chloroadenosine (2-CA) or anoxic medium (equilibrated with 95% N2-5% CO2) depressed the evoked monosynaptic reflex (MSR) recorded extracellularly from a ventral spinal root. The effectiveness of 2-CA or anoxic medium in depressing the MSR was significantly reduced when the concentration of Mg2+ in the physiological medium was lowered from 1.25 X 10(-3) M to zero. The absence of Mg2+ resulted in a 7-fold shift to the right of the concentration-response curve to 2-CA and a reduction in the maximal depression of the MSR from 100% to 65 +/- 4% (mean +/- S.E.M.) of control. A 10 min exposure to anoxic medium containing 1.25 X 10(-3) M Mg2+ decreased the amplitude of the MSR to 23 +/- 6% of control, whilst in zero Mg2+ a decrease to only 50 +/- 5% of control was observed. These data provide further evidence that the response to adenosine, at the A1-receptor, is sensitive to Mg2+ ion concentration and suggest that there is an absolute requirement for Mg2+ in order to obtain full expression of the adenosine effect. Furthermore, the data are consistent with the hypothesis that adenosine is an important mediator of hypoxia-induced depression of the evoked MSR in the spinal cord, and suggest a potential role for Mg2+ during or after exposure to hypoxia in altering the actions of adenosine on neuronal activity or synaptic events.

2-Chloroadenosine↗
PubMed1986

Presynaptic inhibition of monosynaptic reflexes in the lower limbs of subjects with upper motoneuron disease.

Presynaptic inhibition of muscle spindle Ia afferents by group I afferents from the same and other muscles has been studied in the lower limbs of subjects with upper motoneuron lesions. The experiments utilised conditioning of soleus test monosynaptic reflexes during controlled voluntary contraction. The protocol was designed to isolate presynaptic inhibition from postsynaptic components. The relation between estimate of inhibition and test reflex amplitude was examined. The subjects showed less inhibition than controls at all levels of voluntary torque investigated (less than or equal 15 Nm). Two thirds had weak inhibition which did not show the decrease during muscle contraction characteristic of controls. The degree of difference from the normal situation correlated with severity of the clinical sign (weakness of voluntary ankle flexion).

Adult↗
PubMed1975

Effects of increased ambient pressure and nitrogen on man's monosynaptic reflexes.

Neurological signs during dives may result from altered excitability of central neurons. The present study assesses the effect of an increase in pressure from 1 to 3 ATA on the excitability of muscle spindles and alpha motoneurons by comparing the EMG amplitudes of the mechanically and electrically elicited monosynaptic reflexes of the gastrocnemius-soleus muscle in 10 normal adults breathing a normoxic oxygen-nitrogen gas mixture. At the surface the amplitude of the electrically elicited H response was matched to that of the mechanically elicited Achilles tendon reflex (ATR), but at depth these amplitudes became significantly different. In every subject the amplitude of the ATR, which depends upon the excitability of both muscle spindles and the alpha motoneurons, was reduced on an average of 38% (with a range of 12-75%). The H response bypasses the muscle spindles and hence, depends primarily upon alpha motoneuron excitability. Its amplitude was unaltered in four, reduced in three, and increased in three subjects. Since the ATR was always depressed despite the direction of change in the H response, we have concluded that an increase in ambient pressure (i.e., pressure per se, or nitrogen, or both) must have decreased the responsiveness of muscle spindles to the tendon tap via a reduction in fusimotor activity.

Achilles Tendon↗
PubMed1988

[Furosemide depression of the dorsal root potentials and of the presynaptic inhibition of monosynaptic reflexes in the cat spinal cord].

In experiments on spinal narcotized cats perfusion of the lumbosacral cord through the central canal with artificial cerebrospinal fluid containing furosemide (15-48 mmol/l) led to the reversible selective depression of negative DRP and to the depression of prolonged "presynaptic" inhibition of extensor monosynaptic reflexes produced by volleys in flexor muscle afferents of group 1.

Animals↗
PubMed1989

Presynaptic inhibition of the monosynaptic reflex during local tetanus in the cat.

Tetanus toxin at doses of 2-2000 mouse MLD/kg was injected into the gastrocnemius muscle of the left hind limb of the cat. Acute experiments were performed at various times thereafter, when the intoxicated hind leg was strongly extended. Presynaptic inhibition of the monosynaptic reflex (MSR) of gastrocnemius motoneurones was tested by applying conditioning single electric stimuli to the antagonistic deep peroneal nerve. In most intoxicated animals the delayed inhibition of the MSR could still be observed at time intervals typical for presynaptic inhibition. However, the amplitude of the MSR often showed a strong toxin-induced facilitation at about 30 msec after the conditioning stimulus which could mask the presynaptic inhibition and sometimes made it difficult to observe it at all. After spinal transection at the Th1 level the inhibition could be better observed in such cases. Further evidence for the resistance of the presynaptic inhibitory system against the tetanus toxin in the given dose range was given by recordings of distinct dorsal root potentials which were abolished, together with the MSR inhibition by i.v. injection of picrotoxin. It is concluded that the mechanism of presynaptic inhibition remains intact or is even lengthened during local tetanus after i.m. injection of moderate, clinically relevant, toxin doses.

Animals↗
PubMed1970

Excitatory postsynaptic potential and monosynaptic reflex discharge of spinal motoneurons during anoxic insult.

Almost universally held is the concept that in transmission from one neuron to another the so-called postsynaptic potential is the essential step leading to discharge of the secondary neurons. According to the present experiments this is not so in the monosynaptic reflex system of the cat spinal cord. Its role in facilitation of response and certain other essential data are mentioned.

Animals↗
PubMed1991

2-phenylethylamine and methamphetamine enhance the spinal monosynaptic reflex by releasing noradrenaline from the terminals of descending fibers.

Experiments were performed on spinalized rats transected at C1. Intravenous administration of 2-phenylethylamine-HCl (PEA-HCl) (0.3 and 1 mg/kg, i.v.) and methamphetamine-HCl (MAP-HCl) (0.1 and 0.3 mg/kg, i.v.) increased the amplitude of the monosynaptic reflex (MSR). The increase of the MSR caused by PEA and MAP was antagonized by prazosin-HCl and abolished by the pretreatment with reserpine (i.p.) and 6-hydroxydopamine (intracisternally, 14 days previously). A dopamine D1 antagonist, SK&F 83566-HBr (0.01 mg/kg, i.v.), and a D2 antagonist. YM-09151-2 (0.3 mg/kg, i.v.), did not antagonize the increasing effects produced by PEA and MAP. An inhibitor of type-B monoamine oxidase, (-)deprenyl-HCl (1 mg/kg, i.v.), prolonged the effect of PEA but not that of MAP, suggesting that PEA alone, and not its metabolites, enhanced the MSR. These results suggest that PEA and MAP increase the amplitude of the MSR by releasing noradrenaline from the terminals of descending noradrenergic fibers, and that PEA, an endogenous trace amine, has a mechanism of action similar to that of MAP.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1993

Depression of the monosynaptic reflex by apomorphine or bromocriptine is not mediated by D1/D2 receptors.

The role of dopamine in spinal motor transmission was investigated using spinal reflexes in acutely spinalized rats. Intravenous administration of a relatively high dose of the dopamine receptor agonist apomorphine-HCl (3 mg/kg) or the D2 receptor agonist bromocriptine mesylate (1 mg/kg) reduced the amplitude of the monosynaptic reflex (MSR). Depression of the MSR by both drugs was antagonized by haloperidol (1 mg/kg), but not by the D2 receptor antagonists YM-09151-2 (0.2 mg/kg) and sulpiride (10 mg/kg), or by a combination of the D1 receptor antagonist SKF 83566 (0.01 mg/kg) and sulpiride (10 mg/kg). Intravenous administration of the selective D1 receptor agonist SKF 77434 (0.1 and 1 mg/kg) and the D2/D3 receptor agonist quinpirole-HCl (0.1 and 1 mg/kg) had no significant effect on the MSR. Simultaneous administration of SKF 77434 and quinpirole had no significant effect on the MSR. These results show that stimulation of D1/D2 receptors has little influence on the MSR, and suggest that descending dopaminergic systems mediating these receptors have little influence on MSR transmission. Apomorphine and bromocriptine may inhibit the MSR via other subtypes of D1/D2 or other, as yet undiscovered, dopamine receptors or via non-dopaminergic mechanisms.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed2003

Ptychodiscus brevis toxin enhances the frequency-dependent depression of the monosynaptic reflex in neonatal rat spinal cord in vitro.

The involvement of frequency-dependent depression (FDD) of synaptic transmission for the depressant action of the Ptychodiscus brevis toxin (PbTx) was investigated in neonatal rat spinal cord in vitro. The stimulation of a dorsal root by train of pulses (five stimuli) at different frequencies evoked potentials in the ventral root (monosynaptic reflex, MSR). Amplitude of the fifth response as percent of first response at 0.1, 0.2, 0.5, 1.0 and 2.0 Hz were 90, 80, 75, 70 and 50%, respectively. In Mg2+-free medium, PbTx depressed the MSR and also enhanced the FDD in a concentration-dependent manner. Further, the PbTx-induced depression can well be correlated with the enhancement of FDD (r=0.98). In the presence of Mg2+ (1.3 mM), the FDD was greater than that in the absence of Mg2+. But in the presence of Mg2+ PbTx did not alter FDD, even though there was 25% depression at 28 microM (significantly lesser than in Mg2+-free medium). The results indicate that the Mg2+-sensitive component of PbTx-induced depression of MSR is mediated via the neuronal systems involving FDD.

Action Potentials↗
PubMed1986

Facilitation of lumbar monosynaptic reflexes by locus coeruleus in the rat.

The present study was initiated to delineate whether species difference exists between cats and rats in the descending influence of locus coeruleus (LC) on spinal motoneuronal activity. In male Sprague-Dawley rats anesthetized with chloral hydrate (400 mg/kg, i.p.), localized activation of LC promoted an exclusive facilitation of lumbar spinal extensor and flexor monosynaptic reflexes (MSRs). Such LC-evoked potentiations may vary in degree (37.5-147.4%), duration (70.6-72.9 ms) and latency (3.0-5.5 ms) among different animals. While minimally affecting the control MSRs, the alpha 1-adrenoceptor blocker prazosin (20 micrograms/kg, i.v.) significantly antagonized the enhancing effect of the LC on MSRs, suggesting the participation of noradrenergic neurotransmission in the process. Since these results are in general agreement with previous observations from our laboratory on the cat, we conclude that the LC exerts similar facilitatory actions on both extensor and flexor motoneuron activity of the hindlimb in at least two animal species, rat and cat.

Animals↗
PubMed1980

[Depolarization of primary afferents and presynaptic inhibition of monosynaptic reflexes].

In experiments on anesthetized spinal cats, perfusion of the lumbosacral spinal cord through the central canal with artificial cerebrospinal fluid containing ammonium ions led to reversible suppression of slow negative dorsal root potentials (DRP). The suppression of DRP proceeded in parallel to suppression of postsynaptic inhibition of motoneurons but was not related to a marked weakening of prolonged "presynaptic" inhibition of extensor monosynaptic reflexes produced by repetitive impulse volleys in group I flexor muscle afferents. It is concluded that primary afferent depolarization alone does not lead to presynaptic inhibition of synaptic transmission. A decisive factor for the inhibition might be the GABA-induced increase in chloride conductance of the presynaptic membrane, which, however, does not result in the terminal depolarizing current flow after the blockade of chloride pump with ammonium ions.

Ammonium Chloride↗
PubMed1997

Low-frequency depression of the monosynaptic reflex is not altered by tetrodotoxin-induced nerve conduction blockade.

The present study is part of ongoing investigations into activity-related synaptic plasticity in the intact animal. In this investigation we sought to determine whether the previously reported increase in synaptic efficacy at the Ia-motoneuron connection following nerve conduction blockade could be attributed to changes in circuitry external to the monosynaptic pathway. Specifically, we used the phenomena of low-frequency depression of the extracellularly recorded group I monosynaptic reflex (MSR) as an indirect measure of presynaptic inhibition. Tibial nerve conduction blockade was achieved by superfusion of the sodium channel blocker tetrodotoxin (TTX). An osmotic pump delivered the TTX to the tibial branch of the sciatic nerve for a period of either 3 or 10 days. Control rats were either unoperated or received implants of pumps not containing TTX. Data collection consisted of tibial nerve stimulation (0.1-20 Hz) with bilateral recordings of the MSR from the L5 ventral roots. The extent of low-frequency depression was compared between treated and untreated sides of TTX-treated animals and between treated and untreated animals. Results showed that the extent of low-frequency depression was unchanged by either 3 or 10 days of complete blockade of tibial afferents. On the basis of this finding, it is concluded that the previously reported TTX-induced increase in Ia excitatory postsynaptic potential amplitude is unlikely to be due to changes in presynaptic inhibitory pathways.

Animals↗
PubMed1978

Muscle responses and monosynaptic reflexes in falling monkey. Role of the vestibular system.

The free fall has been used in our laboratory as a way to test vestibular function in baboons in order to quantify vestibular compensation in the hemilabyrinthectomized animal. This study presents only those results that concern the contribution of the vestibular system to muscle responses due to sudden fall. EMG activity was recorded from the fully conscious animal using chronic electrodes implanted in various muscles. Spinal monosynaptic reflexes (Hoffmann's and tendon reflexes) were studied in the soleus muscle. Baboons were seated in a special chair suspended from an electromagnet and unexpectedly dropped 90 cm. Experiments were performed in normal, unilateral and bilateral vestibular neurectomized baboons. 1. In normal baboons, results showed a first short-latency response in all tested muscles, followed by a second peak of EMG activity in these muscles. Comparison with data from bilateral vestibular neurectomized baboons demonstrates that normal vestibular function is essential for the appearance of the first peak; the second peak rapidly disappears in our experimental situation where the animal's fall is mechanically braked and interrupted, so the animal does not have to make the postural adjustments necessary for landing, It is suggested that the first peak is concerned with the automatic and reflex control of landing, the second with the voluntary breaking of landing. 2. The modulation of monosynaptic spinal reflexes is closely related to the EMG response in soleus muscle. Facilitation of the H-reflex begins just prior to the onset of the EMG activity and continues as long as the baboon is falling. The T-reflex modulation presents a similar time course except in its early phase where it is depressed. Decrease in T and increase in H-reflexes suggest that the EMG response is most likely due to direct activation of alpha-motoneurons and not by means of the gamma-loop. 3. In unilateral vestibular neurectomized baboons, EMG and reflexological data show the classical asymmetry characterized by a strong decrease of the responses on the side of the lesion, and by a pronounced increase on the contralateral side. It is concluded that this represents the imbalance between the resting discharge of the vestibular neurons, and discloses the influence of labyrinthine afferences at the spinal level. We suggest consequently the use of EMG responses and modulation of spinal reflexes to fall in order to quantify vestibular compensation.

Animals↗
PubMedDate not supplied

[Presynaptic inhibition in the rat spinal cord in ontogeny and its relationship to depression of monosynaptic reflexes].

Cheking the parameters of potentials from the dorsal surface of the spinal cord, studies have been made on the development of depolarization in the primary afferent terminations. It was shown that during the development of animals the amplitude of N- and P components increase indicating progressive development of afferent connections in the spinal cord and maturation of presynaptic inhibition mechanisms. Parallel studies were made on the depression of monosynaptic reflexes conditioned by stimulation of antagonists. It was shown that maximum inhibition develops 20-40 ms after the conditioning coinciding with the highest amplitude of P component. In new-born rats, the recovery of the reflex takes more time than depolarization of the primary afferent terminations, this difference indicating that the depression is only partially due to presynaptic inhibition. Homosynaptic depression plays an important role, its duration and intensity being more significant in new-born animals. The duration of homosynaptic depression decreases with age. Under these conditions, the main mechanism of limitation of afferent input involves the depolarization of the primary afferent terminations.

Afferent Pathways↗
PubMed1975

Neurochemical aspects of post-tetanic potentiation of monosynaptic reflexes in the cat spinal cord. I. Analysis of amino acids at maximum of potentiation.

In order to determine the chemical changes which might occur during post-tetanic potentiation, amino acids from the motor regions of the ventral horn of the spinal cord (potentiated and unpotentiated sides) of 10 different cats were analyzed. The intermittent tetanic stimulation of the Nn. gastroc. (only on the potentiated side) was carried out until a maximum of potentiation was reached (3--4 min). The monosynaptic reflexes were obtained from the ventral roots (L7 or S1) of both sides. The amino acids of the potentiated side were compared to those of the unpotentiated side (control) using a 14-C-dansyl chloride procedure. The two main amino acids considered to be excitatory neurotransmitters, glutamic acid and aspartic acid, showed a more than 20 per cent increase on the potentiated side as compared to the control side. Glycine, which plays an inhibitory role, especially in the spinal cord, reacted with 6 per cent decrease, whereas GABA which is also considered as an inhibitory neurotransmitter showed a change of + 11 per cent on the potentiated side as compared to the unpotentiated side. The importance of the potentiation time for those changes is pointed out.

Action Potentials↗