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PubMed1995

Alterations of brain levels of phosphoinositidase-C-linked Gq alpha/G11 alpha proteins and motor function in rats after cardiac arrest.

BACKGROUND AND PURPOSE: Phosphoinositidase-C-linked Gq alpha and G11 alpha proteins have only recently been characterized. Second messenger systems are known to be affected by hypoxia-ischemia. However, the effects of hypoxia-ischemia on the brain levels of Gq alpha and G11 alpha proteins are not known. Therefore, in the present studies, the effects of hypoxia-ischemia on Gq alpha and G11 alpha proteins in rats were investigated with quantitative immunoblot analysis. METHODS: Cardiac arrest was induced in male Sprague-Dawley rats by an intracardial injection of KCl. Resuscitation began 10 minutes afterwards. At various time points after resuscitation, animals were killed and the cerebral cortex, striatum, and cerebellum were dissected. Levels of Gq alpha and G11 alpha proteins were investigated by quantitative immunoblot analysis. RESULTS: At 1, 2, 4, and 6 hours after resuscitation, Gq alpha and G11 alpha protein levels remained unaltered. However, a significant reduction of these proteins was seen in the cerebral cortex and cerebellum of rats 3 and 14 days after cardiac arrest, with partial recovery by an average of 60 days. In contrast, no significant change was detected in the striatum. CONCLUSIONS: These observations indicate that phosphoinositidase-C-linked signal transduction pathways may be attenuated after hypoxic-ischemic insults to the brain, and that this phenomenon, together with many other factors, may contribute to the expression of motor dysfunction in rats after cardiac arrest.

Analysis of Variance↗

PubMed1989

Drug effects on active immobility responses: what they tell us about neurotransmitter systems and motor functions.

The literature reviewed indicates that active immobility can be promoted by systemic injections of various neurotransmitter systems, as follows: (1) Dopaminergic blockade of both D1 and D2 receptor subtypes. (2) Cholinergic agonism of both muscarinic and nicotinic receptors. (3) Noradrenergic agonism of both alpha-1 and alpha-2 receptors (but these agonists may interfere with haloperidol- and reserpine-induced catalepsy). (4) GABA agonism. (5) Histamine agonism, particularly at the H1 receptor. (6) Opiate agonism, including action of many endogenous opiate peptides, particularly those affecting mu and delta receptors. (7) Agonism by certain other peptides (neurotensin, cholecystokinin). Among the major interactions of neurotransmitter systems that regulate immobility, are the following: (1) Cholinergic-dopaminergic (cholinolytics disrupt catalepsy of dopaminergic blockade and dopaminergic agonists tend to disrupt cholinomimetic catalepsy). (2) Opiate-induced catalepsy is antagonized by the dopamine agonist, apomorphine, but is enhanced by amphetamine. It is also antagonized by certain alpha-2 adrenergic agonists, while it does not seem to be antagonized by anticholinergics. (3) Numerous other interactions have been reported, involving opiates and MSH, serotonin and dopamine mimetics, serotonin and ketamine, GABA and neuroleptics, neurotensin and anticholinergics and histamine. The significance of the multiple neurotransmitter systems is unknown. One possible explanation is that the various neurotransmitter systems participate in mediating the sensory inputs that are involved in triggering immobility and regulate the higher-order limbic and basal ganglia processing reactions that engage a final motor output pathway from the brainstem. The brain is assumed to contain two sets of systems, each with its own, or possibly overlapping, set of neurotransmitter systems, that promote either active immobility or locomotion. The systems reciprocally inhibit each other. Another view, not mutually exclusive, is that output from the locomotor-promoting system provides a negative feedback, via the active immobility pathways, to act as a "brake" on movement, while at the same time maintaining the muscular tonus that is characteristic of active immobility.

Animals↗

PubMed1994

Neuroleptic medication for dystonia. Reciprocal relationship between effects on motor function and mood.

BACKGROUND: The presence of dysphoric symptoms associated with neuroleptic medication is commonly reported. METHOD: Neuroleptic treatment of a segmental dystonia resulted in a disabling depressive illness, which when treated with antidepressants led to the return of the involuntary movements. RESULTS: The use of several different antidepressants and neuroleptics confirmed the association between drugs and symptoms. Genetic studies excluded "poor metaboliser status" as a reason for the patient's sensitivity to these drugs. CONCLUSIONS: The case illustrates a delicate imbalance between dose of neuroleptic medication and depressive symptoms. We should be aware of the possibility of mood changes in patients treated with neuroleptics for a variety of conditions.

Adult↗

PubMed2000

S18616, a highly potent spiroimidazoline agonist at alpha(2)-adrenoceptors: II. Influence on monoaminergic transmission, motor function, and anxiety in comparison with dexmedetomidine and clonidine.

The alpha(2)-adrenoceptor (AR) agonist, S18616 ((S)-spiro[(1-oxa-2-amino-3-azacyclopent-2-ene)-4,2'-(8'-chloro-1' , 2',3',4'-tetrahydronaphthalene)] accompanying article), suppressed electrical activity of adrenergic neurons in the locus ceruleus, an action reversed by the alpha(2)-AR antagonist, idazoxan, which itself enhanced their firing rate. Electrical activity of serotonergic neurons in the dorsal raphe nucleus was similarly suppressed, an action likewise blocked by idazoxan, which did not, itself, influence firing. In freely moving rats, S18616 decreased extracellular levels of norepinephrine (NE), serotonin (5-HT), and dopamine (DA) in frontal cortex and hippocampus. The selective alpha(2)- versus alpha(1)-AR antagonists, atipamezole and BRL-44408 (a preferential alpha(2A)-AR antagonist), elevated levels of NE and DA but not 5-HT. In their presence, the influence of S18616 on frontocortical levels of NE, DA, and 5-HT was blocked. In contrast, prazosin, a selective alpha(1)- versus alpha(2)-AR antagonist (which also preferentially blocks alpha(2B/2C)-ARs) dose dependently decreased levels of 5-HT, but not NE and DA, and failed to modify the actions of S18616. Ultrasonic vocalizations elicited by rats in an aversive environment were inhibited by S18616, which also suppressed aggressive and marble-burying behaviors in mice. Furthermore, S18616 (biphasically) enhanced punished responses in the Vogel conflict test and active social interaction tests in rats. At higher doses, S18616 displayed sedative/hypnotic properties. Both anxiolytic and motor actions of S18616 were inhibited by atipamezole and BRL-44408 but not prazosin. Dexmedetomidine mimicked the actions of S18616 at higher doses except for more potent sedative/hypnotic properties. Clonidine also mimicked S18616, but only at markedly higher doses. In conclusion, via activation of alpha(2)-ARs, S18616 potently inhibits corticolimbic adrenergic, serotonergic, and (frontocortical) dopaminergic transmission in parallel with the expression of its anxiolytic and sedative properties.

Adrenergic alpha-2 Receptor Agonists↗

PubMed1983

Differential effects of limbic versus striatal dopamine loss on motoric function.

Bilateral 6-hydroxydopamine injections into either the ventral tegmental area, or the substantia nigra pars compacta in rats, produced severe losses of dopamine in the nucleus accumbens-olfactory tubercle and striatum respectively. After 1 and 3 months postoperation, the depletion of limbic dopamine was associated with reduced spontaneous locomotor activity, which was enhanced by apomorphine (0.125 mg/kg), but not amphetamine (1.0 mg/kg). The severe loss of striatal dopamine had no persistent effect on spontaneous or D-amphetamine-induced locomotor activity, but did produce a persistent augmentation of rigidity. Although there was considerable recovery, both lesions chronically increased catalepsy scores. The results of this study suggested that limbic dopamine deficits may be important in initiation of movement; whereas, striatal dopamine deficits may contribute more to the rigidity aspects of Parkinsonism.

Animals↗

PubMed1998

The N-terminus of A1-type myosin essential light chains binds actin and modulates myosin motor function.

There are two isoforms (A1 and A2) of the myosin essential light chain (ELC) and consequently two isoenzymes of myosin subfragment 1 (S1), S1(A1) and S1(A2). The two isoenzymes differ in their kinetic properties with S1(A1) having a lower apparent Km for actin and a slower turnover of MgATP (k(cat)) than S1(A2). The two forms of the ELC differ only at their N-termini where A1 has an additional 40-odd amino acids that are not present in A2. The human atrial ELC (an A1-type ELC) was overexpressed in Escherichia coli and purified by ammonium sulphate fractionation and ion-exchange chromatography. The recombinant ELC had actin-activated MgATPase kinetics similar to those for rabbit skeletal S1(A1) under the same conditions. Deletion of the first 45 amino acid residues resulted in an ELC similar to the rabbit skeletal A2 isoform and, when hybridised into S1, in S1(A2)-like kinetic properties. Results obtained with an ELC mutant that lacks the first 11 residues were intermediate between these two extremes but tending towards the S1(A2)-like phenotype. The wild-type ELC (both hybridised into S1 or free in solution) could be cross-linked to F-actin, whereas the deletion mutant lacking the first 45 amino acids could not. The deletion mutant lacking the first 11 amino acids cross-linked only poorly under the same conditions, consistent with the MgATPase data. We therefore conclude that these N-terminal eleven amino acids predominantly encode an actin-binding site which modulates the kinetics of the myosin motor. Furthermore, while free A1-type ELC cross-linked to both polymeric F-actin and the monomeric G-actin:DNase-I complex, the same ELC in S1(A1) could only cross-link to F-actin. This suggests that the light chain binds to a different actin monomer than the heavy chain.

Actins↗

PubMed1983

Plasma concentrations of delta-9-tetrahydrocannabinol and impaired motor function.

Fifty-nine volunteer subjects were allowed to smoke marijuana cigarettes until a satisfactory level of 'high' was obtained. They then had blood samples taken 5, 30, 90 and 150 min following smoking after which they were tested with the roadside sobriety test. Attempts to correlate passing or failing on three coordination tests with plasma concentrations of delta-9-tetrahydrocannabinol (THC) showed that if concentrations measured at 5 min were ignored, failures were almost inevitably associated with plasma concentrations of THC above 25-30 ng/ml. Overall, 94% of subjects failed to pass the test 90 min after smoking and 60% after 150 min, despite the fact that by then plasma concentrations were rather low. It would seem that establishing a clear relation between THC plasma concentrations and clinical impairment will be much more difficult than it has been for alcohol.

Adult↗

PubMed2001

Motor function and regulation of myosin X.

Myosin X is a member of the diverse myosin superfamily that is ubiquitously expressed in various mammalian tissues. Although its association with actin in cells has been shown, little is known about its biochemical and mechanoenzymatic function at the molecular level. We expressed bovine myosin X containing the entire head, neck, and coiled-coil domain and purified bovine myosin X in Sf9 cells. The Mg(2+)-ATPase activity of myosin X was significantly activated by actin with low K(ATP). The actin-activated ATPase activity was reduced at Ca(2+) concentrations above pCa 5 in which 1 mol of calmodulin light chain dissociates from the heavy chain. Myosin X translocates F-actin filaments with the velocity of 0.3 microm/s with the direction toward the barbed end. The actin translocating activity was inhibited at concentrations of Ca(2+) at pCa 6 in which no calmodulin dissociation takes place, suggesting that the calmodulin dissociation is not required for the inhibition of the motility. Unlike class V myosin, which shows a high affinity for F-actin in the presence of ATP, the K(actin) of the myosin X ATPase was much higher than that of myosin V. Consistently nearly all actin dissociated from myosin X in the presence of ATP. ADP did not significantly inhibit the actin-activated ATPase activity of myosin X, suggesting that the ADP release step is not rate-limiting. These results suggest that myosin X is a nonprocessive motor. Consistently myosin X failed to support the actin translocation at low density in an in vitro motility assay where myosin V, a processive motor, supports the actin filament movement.

Actins↗

PubMed2005

The efficacy of diazepam in enhancing motor function in children with spastic cerebral palsy.

Muscle spasm and hypertonia limit mobility in children with spastic cerebral palsy. This double-blind, placebo-controlled, randomized controlled clinical trial studies the clinical efficacy of a low dose of diazepam in enhancing movement in children with spastic cerebral palsy. One hundred and eighty children fulfilled the criteria and were randomly allocated to receive one of two doses of diazepam or placebo at bedtime; 173 completed the study. There was a significant reduction of hypertonia, improvement in the range of passive movement, and an increase in spontaneous movement in the children who received diazepam. There was no report of daytime drowsiness. In developing countries, where cost factors often determine choice of drug, diazepam is a cheap and effective way of relieving spasm and stiffness, optimizing physical therapy and facilitating movement in children with spasticity.

Analysis of Variance↗

PubMed1981

Spinal monoaminergic systems: an aspect of somatic motor function.

A synopsis is made of the kinds of monoaminergic terminals that are found in the ventral horn of the spinal cord, and of the physiological effects these monoamines exert on interneurons (INs), alpha motoneurons (alpha-MNs), and gamma motoneurons (gamma-MNs). It is suggested that in addition to the usual transmitter mechanism involving the activation of fast ionic conductances, monoamines in the ventral horn may function as neuromodulators and as part of the neuronal control for a limb. Experiments are then described in which it is shown that the monoamines can exert selective effects on INs, alpha-MNs, and gamma-MNs. The activation of gamma-MNs in the spinal cord partly depleted of 5-hydroxytryptamine (5-HT) is a striking example of that selectivity. The neurochemical basis of the physiological effects of monoamines on the cord is briefly reviewed. It is suggested that after the administration of dihydroxyphenylalanine (DOPA), all three major monoamines--dopamine (DA), norepinephrine (NE), and 5-HT--could be involved in mediating the physiological effects of DOPA. The evidence for the presence of dopaminergic nerves in the cord is briefly described, and their possible physiological significance is discussed.

Animals↗

PubMed1991

Influence of cisapride on antroduodenal motor function in healthy subjects and diabetics with autonomic neuropathy.

Antroduodenal manometry was used to assess motility in 10 healthy volunteers and 15 diabetics with cardiac autonomic neuropathy whilst they received 20 mg cisapride orally or an apparently identical placebo. Interdigestive motility was recorded after an overnight fast and for 2 hours following a 500 kcal liquid meal. Active treatment did not influence the number or duration of interdigestive motility cycles in either group although antroduodenal co-ordination in both the fasting and the fed state was enhanced by cisapride (P less than 0.05). In diabetics the postprandial antral motility index was increased by cisapride, whereas in healthy subjects antral and duodenal motility indices were increased both fasting and in the fed state (P less than 0.05). These results suggest that impaired antroduodenal co-ordination is of importance in delaying gastric emptying by diabetic subjects.

Adult↗

PubMed1998

Adenosine A2A receptors modify motor function in MPTP-treated common marmosets.

Both adenosine A1 and A2 receptor populations are located in the striatum and can modify locomotor activity, and they may form a therapeutic target for Parkinson's disease (PD). Administration of the selective adenosine A2A antagonist (E)-1,3-diethyl-8-(3,4-dimethoxystyryl)-7-methyl-3,7-dihydro-1H-pu rine-2,6-dione (KW-6002) to MPTP-treated common marmosets increased locomotor activity. In contrast, administration of the selective A1 receptor antagonist 1,3-dipropyl-8-cyclopentylxantine (DPCPX) had no effect on locomotion. Administration of the adenosine A2A receptor agonist 2-[p-[2-(2-aminoethylamino) carbonylethyl] phenethyl amino]-5'-N-ethylcarboxamidoadenosine (APEC) dose dependently suppressed basal locomotor activity. A minimally effective dose of APEC (0.62 mg/kg, i.p) completely reversed the increase in locomotor activity produced by administration of KW-6002. The adenosine A2A receptor appears to be an important target for the treatment of basal ganglia disorders, particularly PD.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

PubMed2002

Rehabilitation of cognitive and motor functions in younger and older patients with vascular brain damage, rheumatologic illness and in post-surgery patients.

This study presents results of inpatient rehabilitation (as monitored by Functional Independence Measure (FIM)) of patients with vascular brain damage (n = 78), post surgery patients (n = 62) and of patients with rheumatologic illness (n = 45). These patients were divided into two age groups (cut off point 65 years). There were significant differences in the FIM scores in all three diagnosis groups between the younger and the older patients at discharge, the younger patients reaching a higher FIM score. However, there were no substantial differences between the two age groups in FIM gains the length of stay in any of the diagnosis groups. This study indicates that although younger patients reach higher FIM score at admission and at discharge the patients older than 65 improved in a comparable way during the same length of stay thus requiring comparable financial resources.

Activities of Daily Living↗

PubMed1996

Effects of dynorphin A (1-17) on motor function and spinal intracellular messenger systems in rat.

The effect of intrathecal injection of dynorphin A (1-17) on second messenger systems of spinal cord relative to behavioral change in rats was studied. Dynorphin A (1-17) 5, 10 (20 nmol) caused dose-dependent flaccid paralysis of hindlimbs. Dynorphin A (1-17) 10, 20 nmol dose-dependently decreased spinal adenylate cyclase (AC) activity, cyclic AMP production, calmodulin (CaM) level and cyclic-nucleotide phosphodiesterase (PDE) activity 10 min after intrathecal injection. They recovered to a varying extent two hours later. Pretreatment with selective kappa-opioid receptor antagonist nor-BNI 30 nmol 10 min before dynorphin A (1-17) markedly antagonized the effects of dynorphin A (1-17) at 20 nmol on hindlimb paralysis and inhibition of intracellular second messengers. The L-type calcium channel blocker verapamil (100 nmol) also played a role in blocking dynorphin neurotoxicity. The NMDA receptor antagonist APV could partially or completely block dynorphin inhibition of CaM level and PDE activity without affecting paralysis and decrease of AC-cAMP level induced by dynorphin A (1-17) 10 min after intrathecal injection.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed1991

Motor function of the monkey globus pallidus. 1. Neuronal discharge and parameters of movement.

In order to examine the role of the basal ganglia (BG) in the regulation of basic movement parameters, we recorded extracellularly from pallidal neurons in conscious monkeys during the performance of a sequential wrist movement task which was composed of a series of holds and ballistic jumps. The movement sequence was predictable and had to be performed within specified time restraints. We recorded the activity of 297 neurons whose discharges were related to the movement task. We included only neurons whose discharges were related to movements at or about the wrist joint by prior examination outside the behavioural paradigm. Each neuron discharged preferentially to one direction of movement at or about the wrist joint. No consistent correlation was found between neuronal discharge and initial joint position, static load application, amplitude of movement or velocity of movement. The mean onset of neuronal discharge was 2 ms after the onset of EMG activity. The findings implied little contribution from the pallidal neurons in the execution of the current movement or to the movement's parameters. The implications are that the basal ganglia are likely to be concerned with other aspects of movement control.

Animals↗

PubMed2004

Effects of a nonpeptide motilin receptor antagonist on proximal gastric motor function.

AIM: To assess the effects of the motilin receptor antagonist RWJ-68023 on basal and motilin-stimulated proximal gastric volume. METHODS: Eighteen healthy male volunteers received RWJ-68023 in two different doses or placebo for 135 min. After 45 min, subjects received a motilin infusion for 90 min. Proximal gastric volume was measured with a barostat at constant pressure and during isobaric distensions. Abdominal symptoms were scored using visual analogue scales. Motilin and RWJ-68023 concentrations were assessed by radioimmunoassay and liquid chromatography-mass spectrometry, respectively. RESULTS: Both dosages of RWJ-68023 were safe and well tolerated. The most common adverse events were of gastrointestinal origin. RWJ-68023 did not affect basal proximal gastric volume, but the high-dose RWJ-68023 reduced the contractile effect of motilin on the stomach. This antagonizing effect of RWJ-68023 was only significant (P = 0.014) during the distension procedure. CONCLUSIONS: The RWJ-68023 doses used in this study were selected to accomplish plasma concentrations that would block the motilin effect entirely. However, the antagonizing effect of RWJ-68023 was partial and only present when the tonic condition of the stomach was modulated by motilin.

Adolescent↗

PubMed1981

Effect of histamine on motor function of opossum sphincter of Oddi.

In this study, we evaluated the effect of histamine on phasic contractile activity in the opossum sphincter of Oddi (SO). SO manometry was done in 35 animals, using an infused catheter system with minimal compliance. In anesthetized animals, phasic SO contractions occurred at a frequency of 7.3 +/- 0.3 (SE) contractions/min with an amplitude of 83 +/- 4 mmHg. Intravenous histamine (5-80 micrograms/kg) invariably inhibited the frequency and amplitude of SO phasic contractions. At larger doses, the SO contractions were abolished for several minutes. The SO inhibitory effect of histamine was duplicated by the selective H1-agonist, 2-pyridylethylamine, and abolished by H1-blockade with pyrilamine or neural blockade with tetrodotoxin. After tetrodotoxin, histamine and 2-pyridylethylamine caused an increased frequency and amplitude of SO contractions. This excitatory effect was blocked by pyrilamine. The histamine effects on SO phasic contractions were not altered by metiamide, atropine, phentolamine, propranolol, hexamethonium, or a large dose of nicotine. We conclude that 1) histamine depresses phasic SO contractions in the opossum; 2) histamine's depressant SO effect is mediated by H1 stimulation of noncholinergic, nonadrenergic SO inhibitory nerves, overriding an H1 stimulatory effect on SO smooth muscle; and 3) histamine has no H2-mediated effect on the opossum SO.

Ampulla of Vater↗

PubMed1976

Cerebral palsy: predictive value of selected clinical signs for early prognostication of motor function.

A prospective longitudinal study involving 233 children with cerebral palsy was carried out to select signs useful for early prognostication of ambulation. All patients were followed from the time they were 12 months old and their progress was observed until they reached the age of 3 to 11 years. The population consisted of 61 children having congenital hemiplegia, 37 having diplegia, 85 having spastic quadriparesis and 28 having the spastic-athetoid clinical type of cerebral palsy. In addition, there were 14 children with athetoid, 6 with ataxic and 2 with hypotonic cerebral palsy. Of the total population, 78.7% achieved some degree of functional walking. Findings indicated that the probability of ambulation was related to the clinical type of cerebral palsy. In some the ultimate functional outcome was rather uniform, as in those with congenital hemiplegic and ataxic types where the prognosis was consistently favorable or in those with hypotonic cerebral palsy in whom the outlook was poor. In spastic diplegic, quadriparetic, spastic-athetoid and athetoid types, on the other hand, expectations varied considerably. For this group of patients, sitting by two years was found to be a predictive sign of high reliability since all children who sat by this age eventually walked. For the group of patients not sitting by two years which included more than half of the eventual ambulators, suppression of obligatory primitive reflex activity between 18 and 24 months provided a sensitive indicator to distinguish the children who ultimately walked from those who would not be expected to do so. These data offer a possibility for predicting future ambulatory status by two years of age in those clinical types of cerebral palsy where difficulties of early accurate prognostication are most likely to be encountered. Observations also suggested that the presence of mental retardation adversely affects ambulation.

Age Factors↗