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PubMed1989

[The impulse activity of the motor units of the human soleus muscle in the tonic vibration reflex].

The tonic vibration reflex was evoked in the human soleus muscle, the range of vibration frequencies was 30-180 Hz. The potentials of single motor units (MUs) were picked up. At low frequencies (to 70-80 Hz) the potentials of all MUs under study correlated with vibration stimuli. This showed the existence of ripples in the excitatory inflow to motoneurons. With an increase of the vibration frequency the correlation disappeared. In the voluntarily contracted muscle the correlation was revealed at higher vibration frequencies than in the relaxed muscle. Since the vibration is known to depress monosynaptic reflexes from primary spindle endings, it is suggested that the correlation of motoneuron discharges and vibration stimuli at low vibration frequency is, apparently, a result of the activation of secondary spindle endings which via short synaptic pathways evoked discrete EPSPs in motoneurons.

Action Potentials↗
PubMed1999

Hoffmann-reflex is delayed during 6 degree head-down tilt with balanced traction.

BACKGROUND: Increased spinal height due to the lack of of axial compression on spinal structures in microgravity may stretch the spinal cord, cauda equina, nerve roots, and paraspinal tissues. HYPOTHESIS: Exposure to simulated microgravity causes dysfunction of nerve roots so that the synaptic portion of the Achilles tendon reflex is delayed. METHODS: Six healthy male subjects were randomly divided into two groups with three in each group. The subjects in the first group underwent horizontal bed rest (HBR) for three days. After a two week interval they underwent bed rest in a position of head-down tilt with balanced traction (HDT). So that each subject could serve as his own control, the second group was treated identically but in opposite order. Bilateral F waves and H-reflexes were measured daily (18:30-20:30) on all subjects placed in a prone position. RESULTS: By means of ANOVA, differences between HDT and HBR were observed only in M-latency and F-ratio, not in F-latency, central latency, and H-latency. Differences during the course of the bed rest were observed in M-latency and H-latency only. Tibial H latency was significantly lengthened in HDT group on day 2 and 3, although no significant difference between HDT and HBR was observed. CONCLUSION: The monosynaptic reflex assessed by H-reflex was delayed during 6 degree HDT with traction. The exact mechanism of this delay and whether the change was due to lengthening of the lower part of the vertebrae remain to be clarified.

Action Potentials↗
PubMed1981

[Retuning of segmental responses to peripheral stimulation during fictive locomotion in cats].

Segmental reflex responses of the lumbosacral spinal cord to peripheral afferent stimulation were investigated in immobilized decorticated cats before and during fictitious locomotion. Appearance of fictitious locomotion was accompanied by an increase of the N1 component of the dorsal cord potential and of the dorsal root potential. Modulation of these responses depending on the phase of fictitious locomotion was observed against a background of their tonic increase. The N1 component and dorsal root potential had larger amplitudes when they appear at the end of the "extensor" phase and at the beginning of the "flexor" phase and smaller amplitudes when they were evoked at the end of the "flexor" phase and at the beginning of the "extensor" phase. Poly- and monosynaptic reflex responses of motoneurons revealed the same phase dependence during fictitious locomotion. Mechanisms and physiological significance of the revealed retuning of segmental reflex responses are discussed on the basis of the obtained data.

Animals↗
PubMed1980

[Characteristics of presynaptic inhibition of monosynaptic spinal cord reflexes after removal of the anterior lobe of the cerebellum].

In experiments on cats the antidromic responses from Ia fibres of n. gastrocnemius and n. peroneus profundus (Wall's technique) and monosynaptic discharges from VRL7 were recorded in norm and after removal of the cerebellum anterior lobe. The reduction of the amplitude of antidromic responses in the Ia afferents of n. gastrocnemius ad their increase in the Ia afferents of n. peroneus profundus were observed together with the reduction of the amplitude of both monosynaptic extensor and flexor responses. It is suggested that there exists a separate background control from the anterior lobe of the cerebellum over the spinal motoneurons and interneurons mediating presynaptic inhibition.

Animals↗
PubMed1990

Pharmacologic analysis of inhibition produced by last-order intermediate nucleus interneurons mediating nonreciprocal inhibition of motoneurons in cat spinal cord.

1. The aim of this study was to investigate the effects of drugs blocking glycinergic and GABAergic transmission on the postsynaptic inhibition of hindlimb motoneurons produced by activation of last-order laminae V-VI interneurons, which are coexcited by muscle and cutaneous afferents and have axonal branches projecting to the Clarke's column. 2. In anesthetized cats with right spinal cord hemisected and both dorsal columns cut between L4 and L5 segments, stimulation of the Clarke's column (CC) at L3-L4 level produced a short-latency, presumably monosynaptic, inhibitory potential that could be recorded either from L7 or S1 ventral rootlets by means of the sucrose-gap technique (iVRP) or intracellularly from hindlimb motoneurons (IPSP). These potentials have been attributed to antidromic activation of a population of last-order interneurons mediating nonreciprocal inhibition of motoneurons. 3. The early iVRP and IPSP produced by CC stimulation was practically abolished 10-20 s after the intravenous injection of strychnine (0.1 mg/kg) and replaced by an excitatory synaptic potential followed by delayed, slow, strychnine-resistant inhibitory potential. 4. Monosynaptic reflexes (MSR) elicited by stimulation of group I gastrocnemius (GS) afferents were inhibited during the occurrence of the CC-iVRP. This inhibition was significantly reduced after intravenous strychnine. On the other hand, the inhibition of the GS-MSR, produced by conditioning stimulation of the posterior biceps and semitendinosus (PBSt) nerve with trains of pulses applied 25-35 ms before the test stimulus, was practically unchanged after the intravenous injection of strychnine. 5. The CC-iVRP and the associated inhibition of GS-MSRs were not significantly affected after the intravenous injection of 0.1 mg/kg of picrotoxin, which clearly reduced the dorsal root potentials (DRP), the late component of the iVRP, and the inhibition of MSRs produced by PBSt volleys. 6. The effect of strychnine and picrotoxin was tested on the monosynaptic iVRP elicited by single intermediate nucleus interneurons that were antidromically activated from the CC and responded both to low-threshold cutaneous fibers and to group I or group II afferents. In three experiments where the interneuronal activity could be kept after the drug injection, it was possible to show that strychnine abolished the interneuronally elicited iVRP, which was replaced by an excitatory synaptic potential with onset preceding the interneuronal activity. In another experiment, it was possible to show that the interneuronally elicited iVRP was not affected by an intra-aortic injection of picrotoxin (0.5 mg/kg) that reduced to one-half the DRP and the iVRP produced by group I PBSt volleys.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2005

Reflex contribution of spindle group Ia and II afferent input to leg muscle spasticity as revealed by tendon vibration in hemiparesis.

OBJECTIVE: Foot dorsiflexion evokes a short- (SLR) and a medium-latency EMG response (MLR) in the soleus of standing subjects. SLR is mediated by spindle group Ia, while group II fibres contribute to MLR through an oligosynaptic circuit. We studied the effects of Achilles' tendon vibration on both responses in spastic patients to disclose any abnormal excitability of these pathways. METHODS: SLR and MLR were evoked in 11 hemiparetics and 11 normals. The vibration-induced changes in both responses were correlated to the Ashworth score of the affected leg. RESULTS: There were no differences between normals and patients in the size of control SLR or MLR. Vibration decreased SLR to 70% in normal subjects, but increased it to 110% in patients, in both affected and unaffected leg. Vibration did not affect MLR in normals, but increased it to 165% on the affected and 120% on the unaffected side of patients. Ashworth score was solely correlated with the degree of vibration-induced increase of MLR. CONCLUSIONS: While the lack of inhibitory effect of vibration on SLR confirms a reduced inhibitibility of the monosynaptic reflex, the increased MLR indicates a disinhibition of group II pathway in patients, connected to the loss of descending control on group II interneurones. Spastic hypertonia depends on release of group II rather than group Ia reflex pathways. SIGNIFICANCE: These findings give a neurophysiological support for the pharmacological treatment of spastic hypertonia and suggest a method for the assessment of its effects.

Adult↗
PubMed1984

[Action of benzodiazepines on spinal dorsal root reflex potentials in cats].

Effects of benzodiazepines on spinal reflex potentials, especially on the dorsal root reflex potentials (DRR), were studied in the spinal preparation of cats. All benzodiazepines used in this study (diazepam, chlordiazepoxide, bromazepam, flurazepam, medazepam, nitrazepam, oxazepam, oxazolazepam, lorazepam, estazolam and triazolam) were administered into the duodenum via a rubber tube implanted previously. These drugs consistently increased the amplitude of DRR. Presynaptic inhibition was increased, but postsynaptic inhibition was not affected by the drugs. DRR was decreased gradually by intravenous administration of semicarbazide, and pretreatment with semicarbazide completely blocked the spinal effect of diazepam. Pyridoxine given intravenously recovered the amplitude of DRR and restored the effect of diazepam on the spinal cord. Pretreatment of AOAA potentiated the increasing effect of diazepam on DRR. Occlusion of the thoracic aorta for 47 min with simultaneous clamping of the mammary arteries produced permanent hind-limb rigidity in cats (Murayama-type rigid cats). The ischemic spinal rigidity is characterized by an enhanced monosynaptic reflex and markedly reduced polysynaptic reflex potentials. Furthermore, DRR was not grossly detectable in the preparation. In these ischemic spinal rigid cats, diazepam administered intravenously or intraduodenally did not enhance DRR at all. These results suggest that the effect of diazepam is closely related with GABA content. Normal levels of GABA in the spinal cord are required for the increasing effect of diazepam on DRR and presynaptic inhibition. These benzodiazepines may act on the releasing mechanism of GABA from the spinal interneuron, or they presumably enhance the sensitivity of the GABA receptor in the spinal cord.

Action Potentials↗
PubMed1990

Enhancement of recurrent inhibition by intravenous administration of L-acetylcarnitine in spastic patients.

The recurrent inhibition of the soleus alpha-motoneurons at rest, evaluated by a specially designed method of paired H reflexes, was estimated in 10 patients with spastic paraparesis. In three of these patients, Renshaw cell activity produced inhibition of the corresponding alpha-motor neurons comparable to that obtained in normal subjects, while the inhibition was reduced in five and absent in two. The effects of intravenously administered L-acetylcarnitine on the activity of Renshaw cells were studied in these patients. In all patients except the two with no evidence of recurrent inhibition, L-acetylcarnitine was found to significantly increase the amount of recurrent inhibition. Its effect became evident at about 30 minutes, reached a maximum around 50 minutes and vanished about 70 minutes from the onset of administration. A significant correlation was found between Renshaw cell activity and the ability of the drug to increase it. L-acetylcarnitine appeared to act specifically by enhancing recurrent inhibition, since no variation in the excitability of the monosynaptic reflex arc was observed.

Acetylcarnitine↗
PubMed2000

Inputs from intrinsic primary afferent neurons to nitric oxide synthase-immunoreactive neurons in the myenteric plexus of guinea pig ileum.

Nitric oxide synthase (NOS) immunoreactivity occurs in two groups of neurons in the guinea pig small intestine: descending interneurons that are also immunoreactive for choline acetyltransferase (ChAT), and inhibitory motor neurons that lack ChAT immunoreactivity. Interneurons that are involved in local reflexes would be expected to have inputs from intrinsic primary afferent (sensory) neurons, most of which are calbindin-immunoreactive. We examined this possibility using triple staining for NOS, ChAT and calbindin immunoreactivity and investigated the relationships between calbindin-immunoreactive varicosities and the cell bodies of NOS-immunoreactive neurons, using high-resolution confocal microscopy and electron microscopy. By confocal microscopy, we found that the cell bodies of ChAT/NOS interneurons received 84 +/- 23 (mean +/- SD) direct appositions from calbindin-immunoreactive varicosities and that the cell bodies of NOS-inhibitory motor neurons received 82 +/- 20 appositions. Electron-microscopic examination of the relations of 265-calbindin-immunoreactive varicosities, at distances within the resolution of the confocal microscope (300 nm), to 30 NOS-immunoreactive nerve cells indicated that 84% formed close contacts or synapses and 16% were separated from neurons by thin glial cell processes. Thus, each NOS-immunoreactive nerve cell receives about 70 synaptic inputs or close contacts from the calbindin-immunoreactive varicosities of intrinsic primary afferent neurons. It is concluded that there are monosynaptic reflex connections in which intrinsic primary afferent neurons synapse directly with motor neurons and di- or poly-synaptic reflexes in which ChAT- and NOS-immunoreactive neurons are interneurons, interposed between intrinsic primary afferent neurons and NOS-inhibitory neurons.

Afferent Pathways↗
PubMedDate not supplied

Antidromic discharges of dorsal root afferents in the neonatal rat.

Presynaptic inhibition of primary afferents can be evoked from at least three sources in the adult animal: 1) by stimulation of several supraspinal structures; 2) by spinal reflex action from sensory inputs; or 3) by the activity of spinal locomotor networks. The depolarisation in the intraspinal afferent terminals which is due, at least partly, to the activation of GABA(A) receptors may be large enough to reach firing threshold and evoke action potentials that are antidromically conducted into peripheral nerves. Little is known about the development of presynaptic inhibition and its supraspinal control during ontogeny. This article, reviewing recent experiments performed on the in vitro brainstem/spinal cord preparation of the neonatal rat, demonstrates that a similar organisation is present, to some extent, in the new-born rat. A spontaneous activity consisting of antidromic discharges can be recorded from lumbar dorsal roots. The discharges are generated by the underlying afferent terminal depolarizations reaching firing threshold. The number of antidromic action potentials increases significantly in saline solution with chloride concentration reduced to 50% of control. Bath application of the GABA(A) receptor antagonist, bicuculline (5-10 microM) blocks the antidromic discharges almost completely. Dorsal root discharges are therefore triggered by chloride-dependent GABA(A) receptor-mediated mechanisms; 1) activation of descending pathways by stimulation delivered to the ventral funiculus (VF) of the spinal cord at the C1 level; 2) activation of sensory inputs by stimulation of a neighbouring dorsal root; or 3) pharmacological activation of the central pattern generators for locomotion evokes antidromic discharges in dorsal roots. VF stimulation also inhibited the response to dorsal root stimulation. The time course of this inhibition overlapped with that of the dorsal root discharge suggesting that part of the inhibition of the monosynaptic reflex may be exerted at a presynaptic level. The existence of GABA(A) receptor-independent mechanisms and the roles of the antidromic discharges in the neonatal rat are discussed.

Animals↗
PubMed1975

Human masseter muscle: H- and tendon reflexes. Their paradoxical potentiation by muscle vibration.

We developed a method for direct electrical stimulation of the masseter nerve in man. Both direct M-reponses and genuine H-reflexes were recorded from the ipsilateral masseter muscle. Muscle vibration that inhibits the Achilles tendon reflex and the soleus H-reflex was found to potentiate the masseter tendon reflex and also the masseter H-reflex. This unexpected contrast may be related to peculiar brain stem circuitry of the masseter reflex mechanism.

Achilles Tendon↗
PubMed1989

Protirelin (thyrotropin-releasing hormone) in amyotrophic lateral sclerosis. The role of androgens.

Protirelin (thyrotropin-releasing hormone) appears to be a neuromodulator in the extrahypothalamic nervous system and has been suggested as an adjunct in the treatment of amyotrophic lateral sclerosis (ALS). Clinical studies have been divided on the efficacy of protirelin (TRH) despite strong experimental findings that are consistent with a role for the peptide in ALS. Recent findings provide evidence of a gender-related specificity in the ability of protirelin to potentiate the monosynaptic reflex. While castration in male neonatal rats lowered the sensitivity to protirelin, testosterone treatment restored that sensitivity. An examination of the clinical studies reveals a failure either to identify patients' sex or to separate the results on the basis of sex. These findings provide convincing evidence for the potential efficacy of protirelin in ALS if the patient's sex and underlying hormonal status are taken into account.

Amyotrophic Lateral Sclerosis↗
PubMed2000

Computerized posturography analysis of progressive supranuclear palsy: a case-control comparison with Parkinson's disease and healthy controls.

BACKGROUND: Progressive supranuclear palsy (PSP) is a neurodegenerative disorder that is frequently mistaken for Parkinson's disease (PD) in its early stages. OBJECTIVE: To compare balance measures using computerized posturography in patients with early PSP and early PD. METHODS: We performed computerized posturography (SMART Balance Master; NeuroCom International, Inc, Clackamas, Ore) in 20 patients with clinically diagnosed mild to moderate PSP (ambulatory) and compared results with those from 20 patients with PD of similar age and disease duration who were not receiving medications, and from 20 healthy age- and sex-matched controls. Sensory organization testing (SOT), limits of stability (LOS), and toes-up perturbations (4 degrees at 50 degrees per second) were tested while receiving and not receiving a combination of oral carbidopa (25 mg) and levodopa (250 mg) in the PSP group. Clinical assessment included Unified Parkinson's Disease Rating Scale, Performance-oriented assessments, and functional reach. RESULTS: When compared with the PD and control groups, total LOS time (P < .001) and path sway (P < .001) were significantly prolonged in PSP. Total SOT showed significantly worse scores in PSP compared with PD and control groups (F(2,57) = 29.6; P < .001). Univariate follow-up tests comparing PSP and PD showed differences in the following conditions: eyes open and visual sway (P = .003), eyes open and platform sway (P = .003), eyes closed and platform sway (P < .001), and eyes open and platform and visual sway (P < .001). Medium- and long-latency responses to perturbation were similar, but a larger number in the PSP group lacked short-latency responses (chi(2) = 11.3; P = .002). Levodopa administration did not significantly improve any aspect of posturography testing in PSP. In differentiating PSP from PD, LOS time and SOT condition of eyes open and platform and visual sway were nearly 100% sensitive and 100% specific (canonical correlation, 0.91). CONCLUSIONS: Computerized posturography testing reliably differentiated early PSP from early PD and age-matched controls. The PSP group demonstrated severely contracted limits of stability with probable deficits in motor programming. Results of SOT in PSP suggested a vestibular pattern and overreliance on visual cues, even when incorrect. The absence of short-latency responses (monosynaptic reflex arch) suggests an additional disturbance in the spinal cord or peripheral nervous system. Arch Neurol. 2000;57:1464-1469

Aged↗
PubMed1978

Attenuated dynamic responses of primary endings of muscle spindles: a basis for depressed tendon responses in acrylamide neuropathy.

Depressed or lost tendon reflexes commonly observed in patients with peripheral neuropathies may result partly from attenuation of the dynamic discharge from the primary endings of muscle spindles. This possibility was investigated in cats with an experimental neuropathy induced with acrylamide (30 mg/kg/day intramuscularly). Achilles tendon reflexes and the dynamic discharge from primary muscle spindles were evaluated after five or ten injections of acrylamide. After five injections the animals were moderately impaired neurologically, the Achilles tendon reflex was difficult to elicit in 2 of 5 animals, and the dynamic responses of primary endings of soleus muscle spindles to stretch were depressed. Following ten injections of acrylamide the cats were severely impaired neurologically; tendon responses were either absent or difficult to elicit, and the dynamic responses of their muscle spindles to stretch were reduced by 50% (p less than 0.01). Additionally, the spindels responded to stretch with only 20 to 30% the normal number of afferent impulses. These data suggest that lost tendon responses in acrylamide neuropathy result in part from inadequate activation of motoneurons by spindle afferent discharge.

Acrylamides↗
PubMed1987

The peripheral distribution and central projections of the sensory rami of the facial nerve in goldfish, Carassius auratus.

Taste buds in goldfish and other cyprinids are found not only within the oropharyngeal cavity but also scattered over the external body surface. The external taste buds are innervated by branches of the facial nerve that terminate centrally in an enlargement of the medulla termed the facial lobe. The peripheral distribution and areas of innervation of the rami of the facial sensory nerve were determined by using a modification of the Sihler technique and by examination of a Bodian-stained head series. The central projections of individual rami of the facial sensory nerve were traced by means of the horseradish peroxidase (HRP) technique. Fibers of the facial sensory nerve distribute over the head and trunk via nine rami. The supraorbital ramus distributes fibers to taste buds above the eye. The palatine, maxillary, and mandibular rami innervate taste buds of the rostral palate, upper lip, and lower lip, respectively. The three rami of the hyomandibular trunk innervate taste buds on the operculum, branchiostegal rays, and in the lower cheek region. A facial recurrent ramus was also found that distributes fibers to taste buds on the trunk and pectoral fin via two rami, the lateral recurrent ramus and pectoral recurrent ramus. The facial sensory rami map somatotopically on the facial lobe. Overall, the projections follow an anteroposterior orientation with the long axis of the body tilted slightly ventrally. The lips and rostral palate make up a disproportionately large portion of the map, taking up nearly the entire ventral extent of the lobe. The trunk and pectoral fin regions map broadly across the dorsal portion of the lobe. Further, projections to the nucleus of the descending trigeminal tract were observed with labeling of the supraorbital, maxillary, and mandibular rami, and the rami of the hyomandibular trunk. Projections to the facial motor nucleus were also observed with labeling of maxillary and mandibular rami, perhaps indicating a monosynaptic reflex are. These projections have not been reported in previous studies on the teleostean facial taste system.

Animals↗
PubMed1986

Correlation of 1a afferent conduction with the ataxia of Fisher syndrome.

The pathophysiology of the ataxia in Fisher syndrome (the syndrome of acute ophthalmoplegia, ataxia, and areflexia) has been attributed to both peripheral nervous system pathology and cerebellar system dysfunction. Pathologic studies have demonstrated no consistent central nervous system abnormalities. We present a case in which abnormalities of 1a sensory conduction were found to correlate directly with the degree of ataxia, without impairment of motor or cutaneous sensory conduction. We propose that the ataxia seen in typical Fisher syndrome may be due to demyelination of 1a afferent fibers.

Adult↗