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Results for “Reflex, Monosynaptic”

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PubMed1993

Effects of excitatory amino acid receptor antagonists on a capsaicin-evoked nociceptive reflex: a comparison with morphine, clonidine and baclofen.

The rat isolated spinal cord-tail preparation has been employed to examine the effects of several antinociceptive drugs and excitatory amino acid (EAA) receptor antagonists on nociceptive reflexes (recorded in ventral roots) stimulated by peripheral application of capsaicin (CAP). Non-nociceptive monosynaptic and polysynaptic dorsal root-evoked ventral root potentials (DR-VRPs) were also examined. Morphine (0.01-3 microM) and clonidine (0.03-1 microM) inhibited CAP-stimulated activity, but not the non-nociceptive dorsal root-evoked monosynaptic reflex (MSR) or polysynaptic (PSR) activity. These effects were antagonized by naloxone and efaroxan, respectively. The AMPA/KA receptor antagonists CNQX (0.1-100 microM) and DNQX (0.1-30 microM) blocked nociceptive activity and were 4-fold selective for CAP-evoked potentials compared to the monosynaptic reflex. Kynurenate (1-300 microM), DL-AP-4 (3-300 microM), L-AP-4 (3-300 microM), and the GABAB receptor agonist baclofen (0.1-10 microM), inhibited all evoked potentials with relatively little selectivity between nociceptive and non-nociceptive responses. NMDA receptor antagonism by AP-5 (100 microM) reduced nociceptive and non-nociceptive potentials by a maximum of 30-33%. These data indicate that AMPA/KA receptor-mediated synapses are involved in acute spinal nociceptive transmission and suggest that AMPA/KA receptor subtypes could provide novel analgesic targets.

Animals↗

PubMedDate not supplied

[The effect of DOPA on segmental reflexes in rat pups].

In acute experiments on spinal 5-30-day rat puppies, studies have been made of the effect of DOPA (100 mg/kg intraperitoneally) on monosynaptic reflex in extensors (evaluated by parameters of H-reflex) as well as on polysynaptic segmentary reflexes. In 5-7-day animals, mainly the inhibitory effect was observed with a short phase of facilitation of monosynaptic reflex. From the 10th day, facilitatory effect of DOPA becomes a predominant one reaching maximum to the 16th day. Within first 16 days of postnatal life, DOPA exhibits facilitatory effect on short-latent polysynaptic reflexes and inhibits long-latent ones. To the 30th day, reactions which are typical of adult animals are observed: inhibition of short-latent and facilitation of long-latent polysynaptic discharges. The data obtained indicate that in early postnatal development the effect of DOPA on mono- and polysynaptic reflexes qualitatively differs from that in adult animals.

Aging↗

PubMed2003

Different susceptibility of facilitatory and inhibitory spinal pathways to ischemia in the cat.

The sensitivity of different excitatory and inhibitory segmental reflex pathways to ischemia was investigated by monosynaptic reflex testing in the spinal cat. Spinal cord ischemia was established by aortal snare occlusion of 1-10 min duration. Excitatory and inhibitory spinal pathways showed statistically significant different susceptibility to ischemic impact. In the period of decreasing responses after the onset of ischemia the transmission through oligo- or polysynaptic, facilitatory or inhibitory pathways was found to be depressed earlier than that of monosynaptic pathways. The period from the end of ischemia until the beginning of recovery of reflex effects was significantly longer for inhibitory effects, compared to the monosynaptic reflexes alone.The results indicated that interneurones of excitatory segmental pathways may be less sensitive to ischemia than motoneurones, and motoneurones seem to be less sensitive to ischemia than interneurones of inhibitory pathways. In high spinal animals, with a relatively high level of extensor inhibition, the enhanced excitability of inhibitory interneurones to GS motoneurones may be responsible for their sensitivity to ischemia, due to an increased rate of O(2) consumption and exhaustion of high-energy phosphate resources.

Animals↗

PubMed1996

Effect of (+/-)-8-hydroxy-2-(di-n-propylamino)tetralin hydrobromide on spinal motor systems in anesthetized intact and spinalized rats.

In the present study, we examined the effect of the 5-HT1A receptor agonist (+/-)-8-hydroxy-2-(di-n-propylamino)tetralin hydrobromide (8-OH-DPAT), on the mono- and polysynaptic reflexes in intact and spinalized rats. 8-OH-DPAT (10 micrograms/kg i.v.) significantly potentiated the amplitude of the monosynaptic reflex in intact rats. In contrast, 8-OH-DPAT (30 and 100 micrograms/kg i.v.) produced a significant dose-related inhibition of the amplitude of the monosynaptic reflex in spinalized rats. These results suggest that 8-OH-DPAT predominantly excites spinal motor systems at the supraspinal site, and inhibits such systems at a spinal cord site.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed1984

Orofacial fine motor control impairments in congenital spasticity: evidence against hypertonus-related performance deficits.

Motor impairments in the fine force control of lips, tongue, and jaw were measured in subjects with congenital spasticity. Because these orofacial motor systems are not uniformly endowed with muscle spindles and monosynaptic reflexes, quantification of these motor impairments addresses the question of whether stretch reflex hypertonus is a positive or negative sign. The results indicated that hyperactive muscle spindle-based monosynaptic reflexes are not a causal factor in these voluntary orofacial motor impairments. These data also indicated that motor impairments were disproportionately greater at finer levels of isometric force control. These fine control measures appear useful as a quantitative index of general voluntary motor deficit.

Adult↗

PubMed2000

Do synaptic rearrangements underlie compensatory reflex enhancement in spinal motoneurons after partial cell loss?

In adult cats, avulsion of a spinal ventral root induces retrograde cell death among the corresponding motoneurons and, also, enhanced monosynaptic reflexes ipsilaterally in the adjacent uninjured spinal cord segments. The present study investigates possible mechanisms behind this reflex potentiation. At 1-12 weeks after unilateral L7 ventral root avulsion, the L7 dorsal root ganglia were bilaterally injected with choleragenoid-HRP to light microscopically quantify the amount of HRP-labeled terminals in the motor nuclei of the lesioned L7 segment and adjacent intact L6+S1 segments. In addition, motoneuron synaptology and individual HRP-labeled boutons were analyzed electron microscopically. In the L7 segment, the loss of motoneurons at 12 weeks after ventral root avulsion was accompanied by a marked loss of HRP-labeled boutons in the corresponding ventral horn. In the L6/S1 segments, the monosynaptic reflex enhancement found ipsilaterally at 12 weeks postoperatively (mean 212%) was not accompanied by an increased HRP-labeling in the ventral horn (mean 109%), indicating that no sprouting or enlargement of the monosynaptic boutons had occurred. Ultrastructurally, the values for apposition length, total active site length, cross-sectional area, and mitochondrial density of the labeled boutons were also similar between the two sides. However, ipsilaterally the L6/S1 motoneurons exhibited an increased membrane covering by presumably excitatory boutons. The present results indicate that after partial cell death in a motoneuron pool the remaining motoneurons may undergo compensatory synaptic rearrangements leading to increased excitability and enhanced reflexes.

Adaptation, Physiological↗

PubMed1996

Physiological adjustments in a reflex pathway following partial loss of target neurons.

This investigation was undertaken to study plasticity in a reflex pathway following partial elimination of target neurons. Adult cats were subjected to unilateral avulsion of the L7 spinal ventral root, which induces retrograde cell death among the motoneurons of the L7 segment. At 1, 3, 6 and 12 weeks after the lesion, the monosynaptic reflexes were recorded in the L6 and S1 ventral roots during stimulation of the L6, L7 and S1 dorsal roots. Since the group Ia muscle spindle afferents passing through these dorsal roots were deprived of their target motoneurons in the L7 segment, compensatory reflex changes were searched for in the remaining monosynaptic contacts with the intact target motoneurons of the L6 and S1 segments. The results indicate that a partial loss of target motoneurons triggers changes leading to increased monosynaptic reflexes of the remaining intact target motoneurons. On average, the reflexes had more than doubled their size at 12 weeks postoperatively. Possible mechanisms for this reflex potentiation are discussed.

Animals↗

PubMed1997

Functional analysis of the sensory motor pathway of resistance reflex in crayfish. II. Integration Of sensory inputs in motor neurons.

The in vitro preparation of the fifth thoracic ganglion of the crayfish was used to analyze the connections supporting the monosynaptic reflex responses recorded from the depressor motor neurons (Dep MNs). Dep MNs are directly connected by the release-sensitive afferents from a proprioceptor, the coxo-basipodite chordotonal organ (CBCO), which is released by upward movements of the leg. Sine-wave movements, applied to the CBCO strand from the most released position, allowed us to stimulate the greatest part of release-sensitive CBCO fibers. Systematic intracellular recordings from all Dep MNs performed in high divalent cation saline allowed us to determine the connections between CBCO afferents and their postsynaptic Dep MNs: it highlighted the sequential activation of the different Dep MNs involved in the monosynaptic reflex. The convergence of different sensory afferents onto a given Dep MN, and the divergence of a given sensory afferent onto several Dep MNs illustrates the complexity of the sensory-motor reflex loops involved in the control of locomotion and posture. Electrophysiological experiments and simulations were performed to analyze the mechanisms by which Dep MNs integrate the large amount of sensory input that they receive. Paired intracellular recording experiments demonstrated that postsynaptic response shapes characteristic of both phasic and phaso-tonic afferents could be induced by varying the presynaptic firing frequency, whatever the postsynaptic Dep MN. Compartment model simulations were used to analyze the role of the sensory-motor synapse characteristics in the summation properties of postsynaptic MN. They demonstrated the importance of the postsynaptic compartment geometry, because large postsynaptic compartments allowed to generate greater excitatory postsynaptic potential (EPSP) summations than small ones. The results presented show that velocity information is the most effective to elicit large compound EPSPs in MNs. We therefore suggest that the negative feedback reflex is mainly based on the detection of leg movements.

Animals↗

PubMed1992

Mechanisms of spinal reflex depressant effects of CS-722, a newly synthesized centrally acting muscle relaxant, in spinal rats.

The mechanisms of the depressant action of (R)-4-chloro-2-(2-hydroxy-3-morpholinopropyl)-5-phenyl-4-isoxaz olin-3-one hydrochloride (CS-722), a newly synthesized centrally acting muscle relaxant, on spinal reflexes were investigated in spinal rats. The drug CS-722 (50 mg/kg, i.v.) depressed the polysynaptic reflex but was less effective on the monosynaptic reflex. Eperisone-HCl (10 mg/kg, i.v.) and baclofen (2 mg/kg, i.v.) markedly decreased the monosynaptic and polysynaptic reflexes, with longer durations than CS-722; CS-722, eperisone and baclofen depressed the dorsal root reflex. The excitability of the motoneurone was reduced by CS-722 and eperisone. Excitability of the primary afferent fibres was reduced by CS-722, while eperisone and baclofen had no effect. Both CS-722 and eperisone did not have a depressant influence on the focal synaptic potential. These results suggest that CS-722 and eperisone but not baclofen, have a common motoneurone-membrane-stabilizing action and that this action may contribute, in part, to the spinal reflex depressant effects of CS-722 and eperisone.

Animals↗

PubMed1987

Gender-specific action of thyrotropin-releasing hormone in the mammalian spinal cord.

Thyrotropin-releasing hormone (TRH) potentiated the monosynaptic reflex in isolated spinal cords obtained from 7- to 9-day-old rats. A concentration-dependent increase in the monosynaptic reflex was observed in spinal cords obtained from male but not from female or castrated male rats. In contrast, the magnitude of potentiation in cords from ovariectomized control female rats and in ovariectomized female rats treated with testosterone approached that seen in intact males. The results provide evidence that gender plays a prominent role in the variability of response both of humans with amyotrophic lateral sclerosis and of animal tissues to TRH. Furthermore, exposure to androgen during the neonatal period may determine the responsiveness of motoneurons to TRH. Thus the use of TRH in the treatment of amyotrophic lateral sclerosis may be more effective in males than in females.

Animals↗

PubMed1976

Neurophysiologic changes in hemiplegia. Possible explanation for the initial disparity between muscle tone and tendon reflexes.

In an attempt to clarify the neurophysiologic changes that may follow a cerebral lesion in man, we have studied patients with recent and with long-standing hemiplegia from cerebral infarction. In patients with recent cerebral lesions, inhibition of the monosynaptic reflex by vibration is enhanced. In patients with long-standing cerebral lesions, this inhibitory mechanism is less effective and a comparison of the electrically and mechanically induced monosynaptic reflexes suggests that fusimotor drive may be increased. Related clinical findings are reduced muscle "tone" immediately after the lesion and increased muscle "tone" and exaggerated tendon jerks in patients with long-standing hemiplegia.

Adult↗

PubMed1984

Viscero-somatic reflexes following distension of urinary bladder in cats: role of supraspinal neuraxis.

Viscero-somatic reflexes have been studied by recording monosynaptic reflexes following distension of the urinary bladder in intact, decerebrate and spinal animals. It was observed that the viscero-somatic responses following bladder distension are inhibitory in nature and this inhibition was highest in decerebrates and least in spinal animals. The site of viscero-somatic interaction probably lies in the bulbar area (supraspinal) and spinal cord.

Animals↗

PubMed1993

Descending inhibition in the neonate rat spinal cord is mediated by 5-hydroxytryptamine.

The inhibitory effects of a stimulus to the thoracic cord on lumbar segmental reflexes were investigated in the superfused cord of the neonate rat. A single stimulus to the latero-ventral cord surface at T11-T12 evoked fast and slow responses in both L4 ventral roots and inhibited rapid segmental reflexes, both ipsi- and contralaterally. The monosynaptic reflex (MSR) was strongly inhibited and the polysynaptic reflex (PSR) and contralateral fast reflex (CON FAST) were inhibited by 30-40%. The inhibition rose to a maximum 2 sec after the conditioning stimulus, plateaued between 2-20 sec and gradually waned to low levels by 100 sec. The slow segmental responses were not inhibited. Inhibition of the MSR was only elicited ipsilaterally and that of PSR was reduced by about 50% on stimulation of the contralateral thoracic cord; inhibition of CON FAST could be evoked from either side of the cord. Inhibition of the MSR from 2-50 sec was greatly reduced by 5-HT2 receptor antagonists. Ketanserin (1 microM) and ritanserin (1 microM) were equally effective but LY 53857 (1 microM) had a weaker blocking action. Only ketanserin reduced inhibition of the PSR. Prazosin (0.1 microM) did not affect inhibition of the MSR but yohimbine (1 microM) blocked it as effectively as ketanserin. This was probably due to 5-HT2 receptor blockade, since 0.1 microM yohimbine had little blocking action and 1 microM idazoxan none, nor did 0.1 microM clonidine mimic inhibition of the MSR. Inhibition of the MSR and PSR was not reduced by 1 microM naloxone, 1 microM strychnine, 1 microM bicuculline nor 10-30 microM APV. Consistent with the release of 5-HT by descending pathways, the 5-HT uptake blocker, citalopram 0.1 microM and the 5-HT releaser, p-chloroamphetamine 1 microM, depressed segmental reflexes, especially the MSR. 5-Hydroxytryptamine did not have the same depressant action on segmental reflexes as stimulation of the thoracic cord; the slow responses were most affected. Both 8-OH-DPAT (1-3 microM) and dipropyl-5-CT (1 microM) preferentially depressed the MSR. Neither spiroxatrine (0.1 microM) nor methysergide (5-10 nM) altered inhibition of the MSR. The concentration of ketanserin required to reduce sub-maximal inhibition by 50% was estimated using 2 concentrations of antagonist. The pIC50, estimated for the blockade by ketanserin of inhibition 20-50 sec after a conditioning stimulus, was 7.3-7.5. It is concluded that inhibition of the MSR and PSR does not involve mediation by glycine, GABAA nor NMDA receptors, nor release of enkephalins nor noradrenaline.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1973

Actions of morphine on the segmental reflex of the decerebrate-spinal cat.

1. The actions of morphine were studied on the segmental reflex of the decerebrate-spinal cat. Morphine decreased arterial blood pressure.2. Morphine inhibited mono- and polysynaptic reflexes. The influence of morphine on monosynaptic reflexes was more obvious at stimulation of the dorsal root at a frequency of 12.5 Hz than at 0.5 or 2.5 Hz.3. The total amount of activity recorded from the ventral root after morphine depended on whether or not the evoked reflex was maximal or submaximal.4. These actions of morphine were antagonized by naloxone.

Animals↗

PubMed1983

Comparative study on the effects of haloxazolam and estazolam, new sleep inducing drugs, on the alpha- and gamma-motor systems.

The pharmacological actions, in vivo, of estazolam and haloxazolam were comparatively studied. Spontaneous discharges of spinal motoneurons in cats were markedly suppressed by estazolam (3 mg/kg, i.d.), but unaffected by similarly administered haloxazolam. The facilitatory effect of stimulation of the posterior hypothalamus on the gamma-activity was suppressed by both haloxazolam and estazolam (3 mg/kg, p.o., for each). The stimulus threshold was raised 1.7 times by haloxazolam and 1.6 times by estazolam. The facilitation of the gamma-activity induced by stimulation of the mesencephalic reticular formation was also depressed by both drugs. The stimulus threshold was raised 6 times by estazolam, but unchanged by haloxazolam. The spinal monosynaptic reflex was unaffected by haloxazolam, while its amplitude was depressed to a half by estazolam (3 mg/kg, p.o., for each). The facilitation of the monosynaptic reflex induced by conditioning stimulation was depressed by both drugs (3 mg/kg, p.o.), but estazolam showed a stronger suppressive action. The seizure-like responses of spinal motoneurons, which were induced by stimulation of the gastrocnemius nerve following strychnine administration, were unaffected by 30 mg/kg of haloxazolam, while they were suppressed by estazolam of the same dose. Thus, the results of all experiments in the present study indicate that estazolam blocks the descending activating functions of both alpha- and gamma-motor systems, whereas the blockade by haloxazolam is limited only to the gamma-system, and also that the suppressive actions of estazolam on both alpha- and gamma-motor systems are stronger than that of haloxazolam.

Animals↗

PubMed1985

Functional change in the rat spinal cord by chronic spinal transection and possible roles of monoamine neurons.

Two types of spinal reflex responses, extensor reflex and ventral root potential, were compared physiologically and pharmacologically in acute and chronic spinal cord transected rats. The recovery curve of the extensor reflex, recorded as evoked electromyogram, in chronic spinal rats was strikingly different from that in acute spinal rats. Namely, shortening of the reflex amplitude suppression period (stimulus interval: 20 msec) and appearance of the supernormal period (30-60 msec) were observed in chronic spinal rats. The recovery curves of ventral root potential (monosynaptic reflex) and M wave were almost the same in both preparations. In the frequency depression curve, the amplitude of the extensor reflex in chronic spinal rats was higher at high frequency stimulation than that in acute spinal rats. 5-Hydroxytryptophan, 5-methoxy-N,N-dimethyltryptamine and quipazine enhanced the extensor reflex in chronic spinal rats with a potency of 200-400, 8 and 4 times stronger than that in acute spinal rats, respectively. These drugs did not show consistent effects on the monosynaptic reflex of ventral root potential in chronic spinal rats. These results strongly suggest that the spinal interneurons where descending serotonergic fibers terminate become supersensitive and functionally modified in chronic spinal rats. It is speculated that the supersensitivity of these interneurons may play an important role in spasticity.

5-Hydroxytryptophan↗

PubMed1971

Primary afferent depolarization and flexion reflexes produced by radiant heat stimulation of the skin.

1. The reflex effects of pulses of intense radiant heat applied to the skin of the central plantar pad have been studied in unanaesthetized (decerebrate) spinal cats.2. Pad heat pulses produced flexion of the ipsilateral hind limb and increased ipsilateral flexor monosynaptic reflexes, due to post-synaptic excitation of flexor alpha motoneurones. These effects were accompanied by reduction of extensor monosynaptic reflexes and post-synaptic inhibition of extensor motoneurones.3. Ipsilateral (and contralateral) pad heat pulses consistently evoked negative dorsal root potentials (DRPs) as well as increased excitability of both cutaneous and group Ib muscle afferent terminals. The excitability of group Ia afferents was sometimes also increased during pad heat pulses, but to a lesser extent.4. Pad heat pulses produced negative DRPs in preparations in which positive DRP components could be demonstrated following electrical stimulation of both skin and muscle nerves.5. The motor and primary afferent effects of heat pulses always accompanied one another, beginning after the pad surface temperature had reached rather high levels (usually 48-55 degrees C).6. Negative DRPs increased excitability of cutaneous and group Ib afferents, and motoneurone activation produced by pad heat pulses was essentially unmodified when conduction in large myelinated afferents from the central plantar pad was blocked by cooling the posterior tibial nerve trunk.7. It is concluded that adequate noxious activation of cutaneous afferents of small diameter produces primary afferent depolarization in a variety of large diameter afferent fibres, as well as post-synaptic effects in alpha motoneurones.

Animals↗

PubMed1989

Motoneurone recurrent inhibition is enhanced by L-acetylcarnitine in humans.

Renshaw cells, which mediate the recurrent inhibition of spinal a-motoneurones, are activated by acetylcholine, both through motoneurone collaterals and the reticulo-spinal system. Since it is known that L-acetylcarnitine (L-AC) has central cholinergic effects, we tested in ten normal subjects and three spastic patients the ability of L-AC to induce changes in excitability of the Renshaw cells. These were activated by a conditioning monosynaptic reflex of the soleus muscle, evoked by electrical stimulation of the tibial nerve, and the resulting recurrent inhibition of the motoneurones was assessed by a subsequent monosynaptic reflex (H'). Recurrent inhibition was tested prior to, during and after an intravenous administration of a solution containing 2000 mg of L-AC. L-AC administration proved to be able to induce in all subjects a decrease in the H'-reflex. This effect ensued approximately 30 min after onset of L-AC administration, reached the peak after 40 min and vanished in about one hour. The extent of the decrease in H' varied among subjects, being on the average 22% of the control values. A relationship was found between duration of L-AC administration and time for reaching the maximal effect. These results show that L-AC is able to decrease a-motoneurone excitability by increasing Renshaw cell activity, both in normal and spastic subjects.

Acetylcarnitine↗