Biomedical subjects

E Lorenc-Koci

Publications and source records attributed to E Lorenc-Koci.

At least 19 recordsLinked to original sources

PubMed2006

2,9-Dimethyl-beta-carbolinium, a neurotoxin occurring in human brain, is a potent inducer of apoptosis as 1-methyl-4-phenylpyridinium.

The causes of neurodegeneration are not well understood. However, the role of environmental and endogenous toxins is receiving much attention. In this study, we compared the synthetic neurotoxin 1-methyl-4-phenyl-pyridinium with beta-carbolines occurring in human brain. Methylation of both nitrogens is necessary to convert a beta-carboline into a potent inhibitor of mitochondrial complex I. The respective beta-carboline, 2,9-dimethyl-beta-carbolinium ion is neurotoxic in rats. To investigate the underlying mechanisms, we incubated mouse neuroblastoma 2A cells with 2,9-dimethyl-beta-carbolinium ion, and compared the findings with effects of norharman, the precursor beta-carboline of methylated derivatives, and with 1-methyl-4-phenyl-pyridinium. 2,9-Dimethyl-beta-carbolinium ion caused a significant increase of reactive oxygen species (higher efficiency than 1-methyl-4-phenyl-pyridinium) and of mitochondrial membrane potential within the first minutes. After 60 min, the membrane potential dissipated. Concomitantly, the levels of glutathione increased in 2,9-dimethyl-beta-carbolinium ion but not in 1-methyl-4-phenyl-pyridinium treated cells. After 24 h effector caspases 3 and 7 were activated and the number of apoptotic cells increased as revealed by fluorescence-activated cell sorting cytometry. When incubated longer (48 h), cells underwent late apoptosis/secondary necrosis as shown by fluorescence-activated cell sorting analysis and confirmed qualitatively by an electron microscopy study. The effects of 2,9-dimethyl-beta-carbolinium ion on apoptotic changes were similar to those induced by 1-methyl-4-phenyl-pyridinium(,) while norharman showed only a weak potency at the very high doses. To investigate whether 2,9-dimethyl-beta-carbolinium ion is neurotoxic under in vivo conditions and whether only dopaminergic neurones are affected we conducted a dose-response study. Three weeks after injection of 2,9-dimethyl-beta-carbolinium ion in the substantia nigra we found a dose-dependent decrease of dopamine and its metabolites in the striatum of rats. The levels of 5-hydroxytryptamine were diminished although the decrease was less. The levels of noradrenaline increased after some doses. The findings strongly suggest an important role of endogenous beta-carbolines in neurodegeneration with apoptosis as the predominant mechanism.

1-Methyl-4-phenylpyridinium↗

PubMed2003

Contribution of the serotonin 5-HT1A receptor agonism of 8-OH-DPAT and EMD 128130 to the regulation of haloperidol-induced muscle rigidity in rats.

The aim of the present study was to find out whether (+/-)-8-hydroxy-2(di-n-propylamino)tetralin (8-OH-DPAT), a prototypical 5-HT1A agonist, and (R)-(-)-2-[5-(4-fluorophenyl)-3-pyridylmethylaminomethyl]-chromane HCl (EMD 128130), a compound with serotonin 5-HT1A-agonist and dopamine D2-like antagonist properties, are able to attenuate the haloperidol-induced (1 mg/kg) muscle rigidity in rats. Muscle tone was examined using a combined mechano- and electromyographic (EMG) method that simultaneously measured the mechanical muscle resistance (MMG) of the rat's hind foot to passive movements in the ankle joint, and the EMG activity of two antagonist muscles. Both 8-OH-DPAT (0.125-0.5 mg/kg i.p.) and EMD 128130 (1-10 mg/kg i.p.) dose-dependently decreased the haloperidol-enhanced MMG to passive movements, as well as the tonic and the long-latency reflex EMG activities. Provided these results can be extrapolated to humans, the efficacy of EMD 128130 in relieving the haloperidol-induced muscle rigidity supports the concept that novel antipsychotics with 5-HT1A agonist and dopamine D2 antagonist activities should have a favourable extrapyramidal side-effect profile.

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

PubMed2001

Decline in motor functions in aging is related to the loss of NMDA receptors.

The aim of the study was to assess the contribution of central dopaminergic and glutamatergic systems to the age-dependent loss of motor functions in rats. Rats of three age groups were compared: young (3-5-month-old), middle-aged (20-21-month-old) and old (29-31-month-old). The obtained results showed an age-dependent decline in the electromyographic (EMG) resting and reflex activities in the gastrocnemius and tibialis anterior muscles, as well as in the T-maze performance. Although these disturbances were accompanied with significant age-dependent decreases in the binding to NMDA, AMPA and dopamine D2 receptors, and a decline in the number of nigral dopamine neurons, they were significantly correlated with the loss of the binding to NMDA receptors only. The reduction in T-maze performance with aging was additionally correlated with a decrease in motor functions (EMG activity). The study suggests a crucial role of the loss of NMDA receptors in age-dependent motor disabilities, as well as in disturbances measured in the T-maze.

Aging↗

PubMed2001

(S)-4C3HPG, a mixed group I mGlu receptor antagonist and a group II agonist, administered intrastriatally, counteracts parkinsonian-like muscle rigidity in rats.

The aim of the present study was to determine whether S-4-carboxy-3-hydroxyphenylglycine (S)-4C3HPG, a mixed group I glutamate metabotropic receptor antagonist and a group II agonist, attenuated parkinsonian-like muscle rigidity in rats. Muscle tone was examined using a combined mechano and electromyographic method, which measured simultaneously the muscle resistance (MMG) of the rat's hind foot to passive extension and flexion in the ankle joint and the electromyographic activity (EMG) of the antagonistic muscles of that joint: gastrocnemius and tibialis anterior. Muscle rigidity was induced by pretreatment with haloperidol (1 mg/kg i.p.). (S)-4C3HPG injected in doses of 5 and 15 microg/0.5 microl bilaterally, into the rostral region of the striatum, decreased both the haloperidol-induced muscle rigidity (MMG) and the enhanced electromyographic activity (EMG). The present results suggest that blockade of mGluR1 receptors and/or activation of mGluR2 ones, localized in the rostral part of the striatum, may be responsible for the anti-parkinsonian effect of (S)-4C3HPG.

Animals↗

PubMed2001

SCH 58261, an A(2A) adenosine receptor antagonist, counteracts parkinsonian-like muscle rigidity in rats.

The aim of the present study was to find out whether blockade of adenosine A(2A) receptors by a selective antagonist, SCH 58261, influenced parkinsonian-like muscle rigidity. Muscle tone was examined using a combined mechano- and electromyographic method which simultaneously measured muscle resistance (MMG) of a rat hindfoot to passive extension and flexion in the ankle joint and electromyographic activity (EMG) of the antagonistic muscles of that joint: gastrocnemius and tibialis anterior. Muscle rigidity produced by reserpine (5 mg/kg + alpha-methyl-p-tyrosine, 250 mg/kg) was antagonized by SCH 58261 (0.1-5 mg/kg). SCH 58261 (5 mg/kg) also reduced reserpine-enhanced tonic and reflex EMG activities in both the gastrocnemius and the tibialis muscles. Moreover, SCH 58261 in doses of 1 and 5 mg/kg abolished muscle resistance induced by haloperidol (0.5 mg/kg). However, only the highest dose of SCH 58261 (5 mg/kg) decreased tonic EMG activity enhanced by haloperidol. Administration of L-DOPA (75 and 100 mg/kg) dose-dependently decreased the muscle resistance as well as tonic EMG activity evoked by haloperidol. Combined administration of SCH 58261 (0.1 mg/kg) and L-DOPA (50 mg/kg) in doses which did not affect the haloperidol-induced muscle rigidity produced a pronounced synergistic effect. The ability of SCH 58261 to diminish the parkinsonian-like muscle rigidity and to potentiate the effect of L-DOPA in this model seems to indicate a therapeutic value of this compound in the treatment of Parkinson's disease.

Adrenergic Uptake Inhibitors↗

PubMed2001

Effect of acute administration of 1,2,3,4-tetrahydroisoquinoline on the levels of glutathione and reactive oxygen species, and on the enzymatic activity of gamma-glutamyl transpeptidase in dopaminergic structures of rat brain.

The effect of acute administration of 1,2,3,4-tetrahydroisoquinoline, an endogenous substance suspected of producing Parkinsonism in humans, on the levels of glutathione and reactive oxygen species and on the enzymatic activity of gamma-glutamyl transpeptidase was investigated in the substantia nigra, striatum and cortex of rat brain. Four hours after a single dose of 1,2,3,4-tetrahydroisoquinoline (100 mg/kg i.p.), a significant increase in tissue glutathione level was found in the dopaminergic structures studied. The most pronounced effect was observed in the substantia nigra and cortex, and the weakest in the striatum. At the same time, significant inhibition of gamma-glutamyl transpeptidase was observed in the substantia nigra, cortex and striatum whose extent strictly corresponded to the increase in glutathione levels in those structures. Moreover, in 1,2,3,4-tetrahydroisoquinoline-treated rats, the production of reactive oxygen species was significantly reduced in the substantia nigra, whereas it was markedly enhanced in the striatum.Our results suggest that the increase in tissue glutathione level in the dopaminergic structures studied results from inhibition of gamma-glutamyl transpeptidase and refers to the extracellular pool of this peptide. Moreover, it is likely that both the 1,2,3,4-tetrahydroisoquinoline-induced alterations in glutathione level and the enhanced production of reactive oxygen species in the striatum may have implications for the pathogenesis of Parkinson's disease.

Animals↗

PubMed2001

Different action on dopamine catabolic pathways of two endogenous 1,2,3,4-tetrahydroisoquinolines with similar antidopaminergic properties.

The effect of single and multiple 1-methyl-1,2,3,4-tetrahydroisoquinoline (1MeTIQ) and 1-benzyl-1,2,3,4-tetrahydroisoquinoline (1BnTIQ) administration on concentrations of dopamine and its metabolites: homovanillic acid (HVA) and 3,4-dihydroxyphenylacetic acid (DOPAC) and 3-methoxytyramine (3MT) in three brain areas was studied HPLC with electrochemical detection in Wistar rats. The rate of dopamine catabolism in the striatum along the N-oxidative and O-methylation pathways was assessed by calculation of the ratio of appropriate metabolites to dopamine concentration. In addition, the spontaneous and apomorphine-stimulated locomotor activity, and muscle rigidity was studied after acute administration of 1MeTIQ and 1BnTIQ. We have found that 1MeTIQ did not change the level of dopamine and HVA in all investigated structures both after a single and chronic administration. However, the levels of intermediary dopamine metabolites, DOPAC and 3MT, were distinctly affected. The level of DOPAC was strongly depressed (by 60-70%) while the level of extraneuronal matabolite 3MT was significantly elevated (by 170-200%). In contrast to 1MeTIQ, 1BnTIQ depressed the level of dopamine (by approximately 60%) and increased the level of total metabolite, HVA, (by 40%) especially in the striatum, but the levels of DOPAC and 3MT remained unchanged. The paper has shown that 1MeTIQ and 1BnTIQ produced different effects on dopamine catabolism. Potential neuroprotective compound 1MeTIQ did not change the rate of total dopamine catabolism, it strongly inhibited the monoamine oxidase (MAO)-dependent catabolic pathway and significantly activated the catechol-O-methyltransferase (COMT)-dependent O-methylation. In contrast 1BnTIQ, a compound with potential neurotoxic activity, produced the significant increase of the rate of dopamine metabolism with strong activation of the oxidative MAO-dependent catabolic pathway. Interestingly, both compounds produced similar antidopaminergic functional effects: antagonism of apomorphine hyperactivity and induction of muscle rigidity. The results may explain the biochemical basis of the neuroprotective and of the neurotoxic properties endogenous brain tetrahydroisoquinoline derivatives.

3,4-Dihydroxyphenylacetic Acid↗

PubMed2000

The role of metabotropic glutamate receptor (mGluR) ligands in parkinsonian muscle rigidity.

It has been shown that the primary striatal dopaminergic hypofunction which is at the origin of Parkinson's disease, results in a secondary hyperactivity of glutamatergic neurotransmission. In the search for a therapy of Parkinson's disease, ionotropic, mainly NMDA, receptor antagonists were found to have moderately beneficial, yet also some undesirable side-effects. Therefore the present study was aimed at determining whether some metabotropic glutamate receptor (mGluR) ligands may have antiparkinsonian effects in the haloperidol-induced muscle rigidity. To this end three mGluR ligands were used: the potent and selective mGluR I antagonist (RS)-1-aminoindan-1,5-dicarboxylic acid (AIDA), the mixed group II agonist/ group I antagonist (S)-4-carboxy-3-hydroxyphenyl-glycine ((S)-4-C3HPG), and the potent group II agonist (+)-2-aminobicyclo[3.1.0.]hexane-2,6,-dicarboxylic acid (LY354740). Only LY354740 penetrated the brain from the periphery; for this reason other drugs were injected bilaterally into the rostral striatum or nucleus accumbens. The muscle tone was recorded by a mechanomyographic/electromyographic (MMG/EMG) method which measured the resistance of a rat's hind foot and the EMG reflex response of its muscles to passive movements. (S)-4C3HPG (5 and 15 microg/0.5 microl) and LY354740 (5 and 10mg/kg i.p.) diminished the muscle rigidity induced by haloperidol (1 mg/kg i.p.). AIDA (0.5-15 microg/0.5 microl) injected into the striatum was only slightly effective in the highest dose used. However, when injected into the nucleus accumbens AIDA (15microg/0.5microl) significantly and strongly counteracted the haloperidol-induced muscle rigidity. Our results suggest that stimulation of group II striatal mGluRs seems to play a major role in diminution of parkinsonian-like muscle rigidity. However, it seems that the antagonism of group I mGluRs located in the nucleus accumbens may also be of importance to the antiparkinsonian effect.

Animals↗

PubMed2000

Effect of acute and chronic administration of 1,2,3,4-tetrahydroisoquinoline on muscle tone, metabolism of dopamine in the striatum and tyrosine hydroxylase immunocytochemistry in the substantia nigra, in rats.

The effects of acute and chronic administration of 1,2,3,4-tetrahydroisoquinoline, an endogenous substance suspected of producing parkinsonism in humans, on the muscle tone and metabolism of dopamine in the striatum, and on the number of tyrosine hydroxylase-immunoreactive cells in the substantia nigra were investigated in rats. Muscle tone was examined using a combined mechanomyographic and electromyographic method which measured simultaneously the muscle resistance of the rat's hind foot to passive extension and flexion in the ankle joint and electromyographic activity of the antagonistic muscles of that joint: gastrocnemius and tibialis anterior. 1,2,3,4-Tetrahydroisoquinoline administered at doses of 50 and 100 mg/kg intraperitoneally for 19 days increased muscle resistance 1 h after the first injection (acute treatment), 1 h after the last injection (chronic treatment) and three days after compound withdrawal. Rigidity observed on the third day of 1,2,3,4-tetrahydroisoquinoline withdrawal was accompanied by an increased tonic (resting) electromyographic activity of the gastrocnemius and tibialis anterior muscles. At the same time, a significant reduction in the number of tyrosine hydroxylase-immunoreactive neurons in the substantia nigra and a decrease in the dopamine level in the striatum were also found. A declining number of tyrosine hydroxylase-immunoreactive neurons in the whole substantia nigra showed a significant negative correlation with the enhanced muscle resistance, as well as with the tonic electromyographic activity recorded at rest, i.e. before the start of movements, from the gastrocnemius and tibialis anterior muscles. Our results suggest that 1,2,3,4-tetrahydroisoquinoline may be one of the endogenous substances involved in the progress of Parkinson's disease.

Animals↗

PubMed1999

The role of striatal adenosine A2A receptors in regulation of the muscle tone in rats.

The aim of the present study was to assess contribution of striatal adenosine A2A receptors to regulation of the muscle tone in rats. The muscle tone was examined by a combined mechano- and electromyographic method, which measured simultaneously muscle resistance (MMG) of a rats hind foot to passive extension and flexion in the ankle joint and the electromyographic activity (EMG) of the antagonistic muscles: gastrocnemius and tibialis anterior. CGS 21680 (1 and 2 microg/0.5 microl), injected bilaterally into the rostral part of the striatum, dose-dependently increased both MMG and the EMG. The present results show that stimulation of striatal adenosine A2A receptors by CGS 21680 evokes parkinsonian-like muscle rigidity which may be due to activation of the GABAergic strio-pallidal pathway.

Adenosine↗

PubMed1999

Efficacy of pramipexole, a new dopamine receptor agonist, to relieve the parkinsonian-like muscle rigidity in rats.

The aim of the present study was to assess the efficacy of pramipexole (2-amino-4,5,6, 7-tetrahydro-6-propyl-amino-benzthiazole-dihydrochloride), a new dopamine D(2)/D(3) receptor agonist, to attenuate parkinsonian-like muscle rigidity in rats. Muscle tone was examined using a combined mechano- and electromyographic (EMG) method, which simultaneously measured the muscle resistance of a rat's hindlimb to passive extension and flexion at the ankle joint, and the EMG acitivity of the antagonistic muscles of that joint: gastrocnemius and tibialis anterior. Muscle rigidity was produced by reserpine (5 mg/kg) injected in combination with alpha-methyl-p-tyrosine (250 mg/kg) or by haloperidol (0.5 mg/kg). Pramipexole in doses of 0.5-5 mg/kg antagonized both reserpine+alpha-methyl-p-tyrosine- and haloperidol-induced muscle rigidity. Pramipexole also reduced reserpine-enhanced tonic and reflex EMG activities in the gastrocnemius muscle. The present results suggest that stimulation of the postsynaptic dopamine receptor may be chiefly responsible for the antiparkinsonian action of pramipexole. The ability of pramipexole to diminish the parkinsonian-like muscle rigidity seems to indicate a therapeutic value of this compound in the treatment of Parkinson's disease.

Animals↗

PubMed1998

Contribution of the glycine site of NMDA receptors in rostral and intermediate-caudal parts of the striatum to the regulation of muscle tone in rats.

The aim of the present study was to assess the contribution of the glycine site of NMDA receptors in the striatum to the regulation of muscle tone. Muscle tone was examined using a combined mechanoand electromyographic method, which measured simultaneously the muscle resistance (MMG) of the rat's hind foot to passive extension and flexion in the ankle joint and the electromyographic activity (EMG) of the antagonistic muscles of that joint: gastrocnemius and tibialis anterior. Muscle rigidity was induced by haloperidol (2.5 mg/kg i.p.). 5,7-dichlorokynurenic acid (5,7-DCKA), a selective glycine site antagonist, injected in doses of 2.5 and 4.5 microg/0.5 microl bilaterally, into the rostral region of the striatum, decreased both the haloperidol-induced muscle rigidity (MMG) and the enhanced electromyographic activity (EMG). 5,7-DCKA injected bilaterally in a dose of 4.5 microg/0.5 microl into the intermediate-caudal region of the striatum of rats not pretreated with haloperidol had no effect on the muscle tone. The present results suggest that blockade of the glycine site of NMDA receptors in the rostral part of the striatum may be mainly responsible for the antiparkinsonian action of this drug.

Animals↗

PubMed1998

The role of striatal glutamate receptors in models of Parkinson's disease.

The aim of the study was to examine the effect of antagonists of the NMDA receptor on the parkinsonian-like muscle rigidity in rats. Reserpine and haloperidol increased the muscle resistance of the hind foot to passive movements, as well as the reflex electromyographic (EMG) activity in the gastroenemius and tibialis anterior muscles. MK-801 (0.32-1.28 mg/kg s.c.), an uncompetitive antagonist of the NMDA receptor, and L-701,324 (5-40 mg/kg i.p.), an antagonist of the glycine site, reduced the muscle tone and the reflex EMG activity enhanced by reserpine or haloperidol. AP-5 (2 and 5 micrograms/0.5 microliter), a competitive antagonist of the NMDA receptor, and 5,7-dichlorokynurenic acid (1.0-4.5 micrograms/0.5 microliter), the glycine site antagonist injected bilaterally into the rostral striatum, inhibited the muscle rigidity induced by haloperidol. In contrast, AP-5, injected alone bilaterally into the intermediate-caudal striatum induced muscle rigidity. The present results suggest that: (1) the inhibitory effect of the NMDA receptor antagonists on the parkinsonian-like muscle rigidity depends, at least partly, on their action on the rostral striatum; (2) the blockade of NMDA receptors in the intermediate-caudal striatum may reduce the beneficial impact of these compounds.

Animals↗

PubMed1998

Muscle rigidity induced by fluphenazine in rats is antagonized by L-DOPA, an antiparkinsonian drug.

The aim of the present study was to find out whether the classic neuroleptic fluphenazine is a good model compound for inducing parkinsonian-like muscle rigidity in rats. The muscle tone was measured as resistance developed by the rat's hind foot to passive flexion and extension. Fluphenazine in doses of 0.4-3.0 mg/kg i.p. induced a dose-dependent increase in the hind foot resistance to passive movements. The muscle rigidity induced by fluphenazine 1.5 mg/kg i.p.) was counteracted in a dose-dependent manner by the main antiparkinsonian drug L-DOPA (25-75 mg/kg i.p.). The present results suggest that the fluphenazine-induced muscle rigidity may be a useful model of parkinsonian rigidity.

Animals↗

PubMed1997

Age-related muscle stiffness: predominance of non-reflex factors.

This study was aimed at assessing the contribution of reflex and non-reflex factors to the muscle tone of old female Wistar rats. The hind foot of a rat was flexed or extended at the ankle joint by 25 degrees over 250 ms. The resistance of the foot to passive movements (torque, mechanomyogram), as well as the reflex electromyographic activity in the gastrocnemius and tibialis anterior muscles, were recorded simultaneously. Moreover, the impact of the blockade of the reflex activity caused by the local anesthetic lignocaine (1-2 ml of a 2% solution, injected in the vicinity of the sciatic nerve) on the muscle tone was investigated. Additionally, old rats' hind leg muscle samples were analysed using fluorescent microscopy for the expression of fibronectin, which is an early marker of connective tissue formation. It has been shown that old rats are characterized by (i) a substantially increased resistance of flexor muscle stiffness (measured during extension) and unchanged resistance of extensors (measured during flexion), (ii) the loss of a major part of the reflex electromyographic activity and (iii) the increased content of fibronectin in muscles. Moreover, it has been shown that lignocaine, which completely blocked the electromyographic reflex activity in the gastrocnemius and tibialis anterior muscles in young animals, was unable to counteract the resistance of these muscles to passive movements in old rats. The present results suggest that the muscle stiffness seen in old rats is not due to a reflex response, but depends mainly on non-reflex factors--chiefly on a large overgrowth of non-elastic connective tissue replacing degenerated active muscle fibers.

Aging↗

PubMed1996

The influence of dizocilpine (MK-801) on the reserpine-enhanced electromyographic stretch reflex in rats.

The electromyographic (EMG) stretch reflex in the gastrocnemius and tibialis anterior muscles was elicited by passive bending and stretching of the rat's hind foot in the ankle joint. The EMG stretch reflex was increased by pretreatment with reserpine (10 mg/kg ip) which is a model compound commonly used to induce parkinsonian rigidity in laboratory animals. Dizocilpine (MK-801) (0.32, 0.64 and 1.28 mg/kg sc) inhibited long-latency supraspinal components of the reserpine-increased EMG stretch reflex, whereas a short-latency spinal component was not diminished. The present results suggest that MK-801 exhibits an antiparkinsonian action against reserpine-induced rigidity.

Animals↗

PubMed1996

Haloperidol-increased muscle tone in rats as a model of parkinsonian rigidity.

The aim of the present study was to find out whether haloperidol-induced rigidity was similar to that seen in parkinsonism. Simultaneous measurements of the muscle resistance (mechanomyogram, MMG) of the hind foot to passive flexion and extension in the ankle joint, as well as determination of the electromyographic (EMG) activity of the gastrocnemius and tibialis anterior muscles of rats were carried out. Haloperidol was injected in doses of 0.5-10 mg/kg 1 h before the start of measurements. Haloperidol increased, in a dose-dependent manner, the muscle resistance of the rat's hind leg to passive movements. Muscle rigidity was accompanied with an increase resting, as well as in the stretch-induced long-latency EMG activity (in which supraspinal reflexes are most probably involved) in both those muscles, whereas the short-latency EMG activity (first large bursts of EMG activity, beginning ca. 9 ms after the start of a movement, probably of a spinal origin) was significantly decreased. The obtained results suggest that the haloperidol-increased MMG/EMG activity might be a good model of parkinsonian rigidity.

Animals↗

PubMed1996

The role of reflex activity in the regulation of muscle tone in rats.

The aim of the study was to assess the contribution of reflex activity to the regulation of muscle tone in rats. The experiment was carried out on young Wistar male and female rats. The hindfoot of a rat was flexed or extended at the ankle joint by 25 deg over 250 ms. The resistance of the foot to passive movements, as well as the electromyographic (EMG) activity in the gastrocnemius and the tibialis anterior muscles, were recorded simultaneously. During passive movements, reflex EMG activity developed simultaneously in both antagonistic muscles of the foot. Three components were distinguished: a short-latency EMG-A (within the first 0-20 ms of a movement), long-latency EMG-B (within 60-160 ms), and EMG-C (within 220-340 ms). When the amplitudes of EMG-B and EMG-C components of the gastrocnemius muscle reflex response were greater than 50 microV, a significant correlation was found between them and the maximum resistance of the hindfoot (MMGmax) during flexion, whereas no such correlation was observed for the tibialis anterior muscle. No correlation was found when the amplitudes of the log-latency components of the gastrocnemius muscle were less than 50 microV. Moreover, no correlation was observed between the EMG-A and the MMG(max). The above results suggest that: (1) the muscle tone of the gastrocnemius muscle in rats seems to be regulated by long-latency (supraspinal) reflexes only when the level of EMG activity exceeds a critical threshold of ca 50 microV; (2) when the level of EMG activity is lower, a major role in the resistance of hindlimb muscles is played by some non-neuronal factors; and (3) the proposed animal model emphasizes new aspects of the reflex which may be useful in a search for basic mechanisms underlying changes in the muscle tone.

Animals↗