PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Reflex, Monosynaptic”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 433 records · Page 24Linked to original sources
PubMed1976

[Electrophysiologic study of trace changes in the excitability of the rat spinal cord].

In white rats, retention of the amplitude asymmetry of the monosynaptic reflex responses (MSRR) in the ventral roots of the spinal lumbosacral segments due to removal of half of the cerebellum, was studied. The MSRR asymmetry remained after the consequent spinal cord section at the thoracic level if it had existed over 20 min (fixation period) before this section. When tested with electric stimuli applied to the nerves of muscles-antagonists, the stable MSRR asymmetry could be unidirectional or reciprocal. Prolonged unilateral stimulation of the muscle nerve central end in the spinal rat with stimuli of different frequency and intensity evoked no MSRR amplitude asymmetry during subsequent bilateral testing of the same nerves. But in decerebrated rats the MSRR asymmetry has frequently appeared after such stimulation. Asymmetry of the reticular descending influence is supposed to play a major role in the trace stable changes of excitability of the spinal cord neuronal substrate as well as different capacities of different neurons (or their elements) for fixation and retention of such changes.

Animals↗
PubMed2000

Modulation of synaptic transmission from segmental afferents by spontaneous activity of dorsal horn spinal neurones in the cat.

We examined, in the anaesthetised cat, the influence of the neuronal ensembles producing spontaneous negative cord dorsum potentials (nCDPs) on segmental pathways mediating primary afferent depolarisation (PAD) of cutaneous and group I muscle afferents and on Ia monosynaptic activation of spinal motoneurones. The intraspinal distribution of the field potentials associated with the spontaneous nCDPs indicated that the neuronal ensembles involved in the generation of these potentials were located in the dorsal horn of lumbar segments, in the same region of termination of low-threshold cutaneous afferents. During the occurrence of spontaneous nCDPs, transmission from low-threshold cutaneous afferents to second order neurones in laminae III-VI, as well as transmission along pathways mediating PAD of cutaneous and Ib afferents, was facilitated. PAD of Ia afferents was instead inhibited. Monosynaptic reflexes of flexors and extensors were facilitated during the spontaneous nCDPs. The magnitude of the facilitation was proportional to the amplitude of the 'conditioning' spontaneous nCDPs. This led to a high positive correlation between amplitude fluctuations of spontaneous nCDPs and fluctuations of monosynaptic reflexes. Stimulation of low-threshold cutaneous afferents transiently reduced the probability of occurrence of spontaneous nCDPs as well as the fluctuations of monosynaptic reflexes. It is concluded that the spontaneous nCDPs were produced by the activation of a population of dorsal horn neurones that shared the same functional pathways and involved the same set of neurones as those responding monosynaptically to stimulation of large cutaneous afferents. The spontaneous activity of these neurones was probably the main cause of the fluctuations of the monosynaptic reflexes observed under anaesthesia and could provide a dynamic linkage between segmental sensory and motor pathways.

Action Potentials↗
PubMed1984

Crossed and uncrossed central effects of muscle spindle afferents from the lateral pterygoid muscle of the guinea pig.

Physiological evidence is presented for the presence of stretch reflexes in the lateral pterygoid (Pt) muscle of the guinea pig. The central reflex effects of excitation of Pt stretch reflex afferents were also investigated. Passive lateral jaw displacement, which resulted in stretch of the Pt muscle on the side of jaw movement and stretch of the zygomatico-mandibularis (Z) muscle on the side contralateral to the movement, evoked increased EMG activity in these muscles. Stimulation of the trigeminal mesencephalic nucleus (mes V) evoked monosynaptic reflexes in both the Pt and Z nerves. Tonic stretch of the Pt muscle facilitated the monosynaptic reflex in the Pt nerve evoked by stimulation of mes V. Tonic vibration of the Pt muscle facilitated the mes V evoked monosynaptic reflex in the nerves to the ipsilateral Pt and contralateral Z muscles. Conversely, tonic vibration of the Z muscle facilitated the monosynaptic reflex evolved by mes V stimulation in the contralateral Pt and ipsilateral Z nerve. The results support the view that muscle spindles exist in the Pt and Z muscles and that there is a monosynaptic stretch reflex for both the Pt and Z muscles with cell bodies located in the mes V nucleus. It was also shown that the ipsilateral Pt muscle and the contralateral Z muscle act as synergists in the production of lateral jaw movements and that the organization of the stretch reflexes originating from the Pt and Z muscles support their synergistic action.

Animals↗
PubMed2000

Stretch and H reflexes in triceps surae are similar during tonic and rhythmic contractions in high decerebrate cats.

During locomotion in decerebrate and spinal cats the group Ia afferents from hind leg muscles are depolarized rhythmically. An earlier study concluded that this locomotor-related primary afferent depolarization (PAD) does not contribute to modulation of monosynaptic reflex pathways during locomotion. This finding indicated that the neural network generating the locomotor rhythm, the central pattern generator (CPG), does not presynaptically inhibit monosynaptic reflexes. In this investigation we tested this prediction in decerebrate cats by measuring the magnitude of reflexes evoked in ankle extensor muscles during periods of tonic contractions and during sequences of rhythmic contractions. The latter occurred when the animal was induced to walk on a treadmill. At the similar levels of activity in the soleus muscle there was no significant difference in the magnitude of the soleus H reflex in these two behavioral situations. Similar results were obtained for reflexes evoked by brief stretches of the soleus muscle. We also examined the reflexes evoked by ramp-and-hold stretches during periods of rhythmic and tonic activity of the isolated medial gastrocnemius (MG) muscle. At similar levels of background activity, the reflexes evoked in the MG muscle were the same during rhythmic and tonic contractions. Our failure to observe a reduction in the magnitude of H reflexes and stretch reflexes during rhythmic contractions, compared with reflexes evoked at the same level of background activity during tonic contractions, is consistent with the notion that the CPG for stepping does not presynaptically inhibit monosynaptic reflexes during the extension phase of locomotor activity. Our results indicate that presynaptic inhibition of the monosynaptic reflex associated with normal locomotion in cats or humans arises from sources other than the extensor burst generating system of the central pattern generator.

Animals↗
PubMed1977

Modulation of hindlimb reflexes by tonic neck positions in cats.

In cats with the head fixed in a stereotactic frame a slight facilitation of the gastrocnemiussoleus (GS) monosynaptic reflexes in the ipsilateral hindlimb, accompanied by an inhibition of the monosynaptic reflex of the antagnostic deep peroneal nerve (DP), occurs following lateral flexion and rotation around the body axis at an angle of 25 degrees. Following dorsiflexion of the body a moderate inhibition of the extensor reflexes (GS) up to 10% and a reciprocal slight excitation in the same range of the monosynaptic reflexes of flexor muscles (DP) is recorded. On the other hand after ventriflexion of the body there is a marked inhibition in the range of 50% of all the monosynaptic extensor and flexor reflexes for all the stimulus intensities used. This inhibition can already be demonstrated in ventriflexion of 10 degrees-15 degrees. All these patterns of reflex modulation are similar in cortically intact, ischemically decorticated and precollicularly decerebrated cats. Furthermore these patterns are not essentially influenced by cerebellectomy, although all reflex amplitudes are reduced. However, the spinal reflexes can not be modulated by these body movements after acute spinalization.

Afferent Pathways↗
PubMed1991

Substance P and NMDA receptors mediate a slow nociceptive ventral root potential in neonatal rat spinal cord.

Substance P and glutamate actions have separately been implicated in the generation of nociceptive-related slow ventral root potentials (slow VRPs). We report that slow VRPs are dependent on both substance P and NMDA receptor-mediated neurotransmission. Slow VRPs of 10-40 s duration were evoked by electrically stimulating a lumbar dorsal root and recorded at the corresponding ipsilateral ventral root in spinal cords isolated from 1- to 5-day-old rats; the monosynaptic reflex was also recorded. The NMDA receptor antagonist APV (5-20 microM) and the substance P antagonist spantide (10-20 microM) both reversibly depressed the slow VRP without affecting the monosynaptic reflex; spantide and APV applied together nearly abolished the slow VRP. The quisqualate-kainate receptor antagonist CNQX (1-5 microM) reduced the monosynaptic reflex and an early component of the slow VRP. A slow VRP could be elicited by brief (0.1-1.0 s) focal applications of either substance P (2-20 microM) or NMDA (10 microM), and also by CGRP (2-20 microM). Substance P-evoked and NMDA-evoked responses were blocked by their respective antagonists spantide and APV. Each was also cross-sensitive to the other antagonist. Both excitatory amino acids, acting on an NMDA receptor, and substance P, acting on a tachykinin receptor, thus appear to be involved in generating this slow potential. Both NMDA and tachykinin receptors are necessary to generate a full response.

2-Amino-5-phosphonovalerate↗
PubMed1958

Early post-tetanic potentiation and low frequency depression of some group I reflex actions.

Group I reflex functions, namely monosynaptic reflex transmission, facilitation of synergists, and direct and disynaptic inhibition, show early post-tetanic potentiation following conditioning with a brief, high frequency, tetanus. Of these reflex functions, monosynaptic transmission always shows low frequency depression. Direct inhibitory pathways, and therefore inhibitory junctions, are insensitive to low frequency depression. The fact that direct inhibition can be potentiated shows it to be sufficiently labile that a decrease in efficacy at inhibitory junctions during repetitive activity should be revealed. Disynaptic inhibition often shows low frequency depression. As it is likely that inhibitory junctions in the direct and disynaptic pathways are similar, the low frequency depression of disynaptic inhibition is probably due to the properties of the excitatory relay between afferent fibers and interneurons in that pathway. Facilitation between synergists is often more depressed when the conditioning and testing volleys are nearly simultaneous than when they are separated by 1 to 1.5 msec. This result indicates that an early and rapid phase of action, responsible for homonymous and heteronymous transmission, is more sensitive to low frequency depression than is residual facilitation. In general, reflex transmission is more sensitive than are other aspects of action by group I fibers to events concurrent with and following repetitive activation.

Reflex↗
PubMed1971

Effects of initial conditions on the Hoffman reflex.

The Hoffmann reflex is a monosynaptic reflex elicited by electrical stimulation of afferent nerve fibres. The amplitude of the reflex response may be measured both by EMG recording from the muscle and by sensing the muscle twitch. These two effects are dependent, not only on the amplitude of the stimulus, but on the state of excitability of the afferent-efferent synaptic pools and on the mechanical state of the muscle. Voluntary control of the stimulated muscle influences these conditions but the effects on the EMG are quite different from those on the twitch. This paper discusses these effects under isometric conditions.

Adult↗
PubMed1979

Abolition of a viscerosomatic reflex during oxygen deprivation.

Effect of hypoxia was studied on the J reflex, a term used for the reflex inhibition of muscular exercise by activation of type J pulmonary endings. Hypoxia was induced by ventilating the animal with gas mixtures varying from 18 to 9% oxygen in nitrogen. The blood gas tensions of the arterial blood (PaO2) were measured before, during, and after hypoxia. It was found that the J reflex is sensitive to a reduction in oxygen. A fall in PaO2 between 67 and 47 Torr abolished this reflex. Studies were also undertaken to exclude the possibility that the effect of hypoxia was predominantly exerted on monosynaptic reflex itself. A similar fall in PaO2 also depressed the monosynaptic reflex. Minimum time required for the significant depression was 32 s. On the contrary the J reflex was abolished within this period suggesting that the abolition of J reflex is independent of the changes in monosynaptic reflex during hypoxia.

Action Potentials↗
PubMed1994

Correlates of anesthetic properties in isolated spinal cord: cyclobutanes.

Two halogenated cyclobutanes, one anesthetic and one not, were compared on receptor-specific pathways in isolated neonatal rat spinal cord. The anesthetic 1-chloro-1,2,2-trifluorocyclobutane depressed the monosynaptic reflex (glutamate non-NMDA receptors) and abolished a slow ventral root potential (glutamate NMDA, non-NMDA and tachykinin receptors). This compound slightly enhanced the muscimol-evoked dorsal root potential (GABAA) but reversibly depressed the dorsal root potential elicited by dorsal root stimulation. The non-anesthetic 1,2-dichlorohexafluorocyclobutane increased monosynaptic reflex, depressed slow ventral root potential approximately 50%, had little effect on muscimol-evoked dorsal root potential, and irreversibly depressed dorsal root-evoked dorsal root potential. Hypoxia accounts for slow ventral root potential depression, but not monosynaptic reflex enhancement. In this preparation and for this pair of compounds, anesthetic properties are related to blockade of transmission at glutamate synapses, with a small component of GABAA enhancement. Monosynaptic reflex increase may be related to the non-anesthetic cyclobutane's convulsant and anti-anesthetic properties.

Anesthesia↗
PubMed1999

The effects of calcium channel blocker, flunarizine on spinal reflexes in the cats.

Effects of calcium channel blocker flunarizine on spinal monosynaptic reflexes were investigated in spinal cats. Flunarizine was administered locally into the spinal cord (10, 50, 100 microM) and intraperitoneally (5, 10, 20 mg/kg). Adult cats (n = 10), weighing 1.5-3 kg were anesthetized with ketamine (50 mg/kg, i.m.) and artificially ventilated. Animals were spinalized at C1 level. A laminectomy was performed in the lumbosacral region. The ventral and dorsal roots of segment L5 were isolated and a pouch of skin was formed at the site of the dissection to allow the exposed tissues to be covered with liquid paraffin. The temperature was kept at 38.5 degrees C with a heating pad. A polyethylene cannula was introduced into the left carotid artery to monitor blood pressure, which was kept above 100 mmHg. The dorsal root of segment L5 was placed on a silver-silver chloride wire electrode for stimulation through an isolation unit. The reflex potentials were recorded from the ipsilateral L5 ventral root, mounted on a silver-silver chloride wire electrode. The systemic (5, 10, 20 mg/kg) and local (50 and 100 microM) dosages of cinnarizin derivative flunarizine significantly decreased the amplitude of reflex response (p < 0.05). Moreover, the latency of the monosynaptic reflexes was increased after administration of the drug (p < 0.05). Voltage-dependent calcium channels in the spinal cord may play an important role to regulate reflex respond.

Animals↗
PubMed1982

Effect of nitrous oxide alone or its combination with fentanyl on spinal reflexes in cats.

The effects of nitrous oxide alone and combination of nitrous oxide and fentanyl on spinal reflexes were studied in cats with transected spinal cord at the thoracic level. Nitrous oxide 33, 50 and 75% in oxygen depressed the amplitude of monosynaptic reflexes in a dose-dependent manner, but exerted little effect on polysynaptic reflexes. The addition of fentanyl 2.5 microgram kg-1 during the administration of 75% nitrous oxide in oxygen depressed monosynaptic reflexes further. These results suggest that nitrous oxide or its combination with fentanyl has a depressant action on the transmission of monosynaptic reflexes in the spinal cord, but nitrous oxide might exert less effect on the spinal interneurones which mediate polysynaptic reflexes.

Animals↗
PubMed2004

Xenon suppresses nociceptive reflex in newborn rat spinal cord in vitro; comparison with nitrous oxide.

Although analgesic action of xenon has been reported, little is known about the effect of xenon at the spinal cord, which plays a crucial role in nociceptive transmission. We studied the effect of xenon on nociceptive reflex (the slow ventral root potential) and the monosynaptic reflex in neonatal rat spinal cord in vitro in comparison with nitrous oxide. Xenon (30%) and nitrous oxide (30%) were applied for 17 min through superfusing artificial cerebrospinal fluid. Xenon and nitrous oxide significantly reduced the amplitude of nociceptive reflex by approximately 70% and approximately 25%, respectively. Xenon and nitrous oxide also significantly reduced the amplitude of the monosynaptic reflex by approximately 35% and approximately 15%, respectively. These results indicate that xenon suppressed the synaptic transmission at the spinal cord, especially those of the slow ventral root potential, which reflect nociceptive transmission.

Animals↗
PubMed1982

Ventral root depolarization and spinal reflex augmentation by a TRH analog in rat spinal cord.

The experiments were performed on spinal rats transected at the C 1 level. Intravenous administrations of TRH and its analog DN-1417 (gamma-butyrolactone-gamma-carbonyl-L-histidyl-L-prolinamide), which has less endocrine activity, produced a marked increase in the monosynaptic reflex (MSR) and depolarization of the ventral root, without affecting the dorsal root reflex (DRR) and the resting potential of the dorsal root. Excitation of the monosynaptic reflex was not antagonized by chlorpromazine, haloperidol, atropine or cyproheptadine, and was not influenced by pretreatment with reserpine. The depolarization of the ventral root persisted in the presence of baclofen or tetrodotoxin. These findings suggest that depolarization of the ventral root induced by TRH and DN-1417 is due to a direct action on motoneuronal membranes, and that an increase in the monosynaptic reflex is in part due to a depolarization of motoneurones. The effect of DN-1417 were longer lasting than those of TRH.

Animals↗
PubMed1976

[Pharmacological comparison between enflurane and halothane].

General pharmacological properties of enflurane (E) and halothane (H) were investigated. Maximum blood concentrations of both drugs reached 30 min after inhalation. E showed lower maximum blood concentration, initial velocity of uptake and shorter half life than H. Neither drug had any effect on neuromuscular junction, but E increased N-M effect of succinylcholine. Both drugs decreased tension of uterine and intestine muscles. Poly- and monosynaptic reflexes were inhibited more by H. ED50's of E and H for intestine muscles. Poly- and monosynaptic reflexes were inhibited more by H. ED50's of E and H for righting reflux were 1.25 and 1.40%, respectively. Tonic and clonic convulsions and death induced by electric shock were inhibited more by E. Almost equal anticonvulsive potency was observed for chemoshocks. Death due to electric and chemoshock was remarkably inhibited by both drugs. Spontaneous EEG was altered in a different manner, although flattened with spikes at 4% concentration of both drugs. E altered rhythmicity of recruiting response and both drugs inhibited this response. H inhibited more remarkably the augmenting response and E inhibited the arousal response. E increased negative potentials of the primary response evoked by sensory stimulation, while H decreased these potentials. Both drugs completely inhibited the secondary response.

Animals↗
PubMed1985

Effects of IDPN-induced axonal swellings on conduction in motor nerve fibers.

Paranodal demyelination produces a reduction of conduction velocity and conduction block. The relative proportions of these changes appear to vary among different demyelinating disorders. In this study we have examined the effects on conduction of paranodal demyelination produced by giant axonal swellings. The axonal swellings were induced in rats by administration of beta, beta'-iminodipropionitrile (IDPN). In this experimental model synchronous axonal swellings occur in the proximal region of virtually every alpha-motorneuron without evidence of segmental demyelination or fiber loss. Conduction across the motor neuron was evaluated by two methods: a monosynaptic reflex pathway and intracellular recording from single motor neurons. Increases in the delay across the central region of the monosynaptic reflex pathway began between 2 and 4 days after toxin administration. Intracellular studies confirmed that the slowing occurred across the proximal regions of the motor axons; more distal regions of the motor axons were unaffected. The substantial reduction in conduction velocity over the swollen segment occurs with only moderate evidence of conduction block, as assayed by a reduction in the H-reflex/M-response amplitude ratio. Parallel morphological studies showed that in the enlarged fibers the myelin terminal loops maintained contact with the axon but were displaced from the paranodal region into the internode. The appearance of this "passive" paranodal demyelination correlated closely with the increase in conduction delay. We suggest that the contact maintained by the displaced myelin terminal loops with the axolemma allows saltatory conduction to continue, and explains the paucity of conduction block in this model despite the prominent conduction slowing.

Animals↗
PubMed1978

Presynaptic and long-lasting postsynaptic inhibition during penicillin-induced spinal seizures.

In experiments on seven cats we tested the hypothesis that the epileptogenic effect of penicillin (PCN) on the spinal cord is mediated by a reduction of presynaptic inhibition. PCN-induced spinal hyperactivity was not associated with changes in either the presynaptic inhibition of extensor monosynaptic reflexes by conditioning volleys in flexor muscle nerves, or in evoked dorsal root potentials. Long-lasting inhibition of monosynaptic reflexes by repetitive cutaneous nerve volleys, shown by intracellular recording to be associated with prolonged inhibitory postsynaptic potentials (IPSPs), was also not changed by PCN. Antagonism of either pre- or postsynaptic spinal inhibition is not a necessary condition for induction of spinal seizures by PCN.

Animals↗