bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hydrocortisone influences voltage‐dependent L‐type calcium channels in cultured human skeletal muscle
Authors: Braun S. , Sarkozi E. , McFerrin J. , Askanas V. 
Published: January 2005

AbstractThe glucocorticoid hydrocortisone (HC), applied for up to 2 weeks to either aneurally or innervated cultured human muscle, produced 2‐fold increase of the number of dihydropyridine ([3H]PN200‐110) binding sites. The K+ ‐induced, nifedipine‐inhibited Ca2+ uptake was increased 40%. The effect of HC was concentration‐ and time‐dependent. [3H]PN200‐110 affinity for its receptor was not affected by HC treatment. HC did not exert significant influence on the total amount of protein, CK activity, and the number of myotubes. These results indicate that voltage‐dependent L‐type Ca2+ channel expression in human muscle is regulated by glucocorticoid. © 1995 Wiley‐Liss, Inc.
Reinnervation of a denervated slow muscle triggers high extrajunctional expression of the asymmetric molecular forms of acetyicholinesterase
Authors: Črne‐Finderle N. , Toplišek J. , Sketelj J. 
Published: January 2005

AbstractExpression of acetylcholine receptor and of the asymmetric molecular forms of acetylcholinesterase (AChE) in the extrajunctional regions of rat muscles is suppressed during early postnatal development. In mature muscles, the extrajunctional synthesis of acetylcholine receptor, but not of the asymmetric molecular forms of AChE, becomes reactivated after denervation. The hypothesis that a denervated muscle needs reinnervation in order to revert transiently to an immature state characterized by high extrajunctional production of the asymmetric AChE forms, was examined in rat muscles recovering after nerve crush. Molecular forms of AChE were analysed by velocity sedimentation. Activity of the asymmetric A12 AChE form in the extrajunctional regions of the slow soleus (SOL) muscle increased during the first week after reinnervation to about 9 times its control level, remained high for about one week, and declined towards normal thereafter. If the nerve was crushed close to the muscle and reinnervation occured very rapidly, the extrajunctional increase of the A12 AChE form still occured but was less pronounced than after late reinnervation. In contrast, a transient paralysis of the SOL muscle due to acetylcholine receptor blockade by α‐bungarotoxin, followed by spontaneous recovery of muscle activity after 3–5 days, did not revert AChE regulation into an immature state. Disuse of the SOL muscle caused by leg immobilization, which is known to change the tonic pattern of neural stimulation of the SOL muscle into a phasic one, did not prevent the reversion of AChE regulation during reinnervation. This indicates that neural stimulation pattern is not crucial for this reversion. In contrast to slow SOL, the fast extensor digitorum longus muscle did not revert to an immature state in respect to AChE regulation after reinnervation. This muscle type‐specific response may be due to intrinsic differences between the myogenic cells of slow and fast muscle fibres. © 1995 Wiley‐Liss, Inc.
Inhibition of the ATP‐sensitive potassium channel in the guinea pig substantia nigra by BMS 181100 is not mediated by a sigma‐binding site
Authors: O'Callaghan J. F. X. , Greenfield S. A. 
Published: January 2005

AbstractQuantitative autoradiography of brain tissue has revealed a high density of binding sites for the K‐ATP channel antagonists, the sulphonylureas, and for σ‐ligands in the substantia nigra (SN). In view of the high density of the two binding sites in the SN the possibility has been investigated that the K‐ATP channel and the σ‐binding site are functionally linked. The K‐ATP channel‐mediated membrane hyperpolarisation and decrease in input resistance produced by hypoxia and by the metabolic inhibitor, cyanide, in rostral substantia nigra pars compacta neurons are antagonised by the σ‐ligand BMS 181100. In addition, BMS 181100 antagonises activation of the K‐ATP channel by diazoxide; cromakalim is found to be without effect in these neurons. Antagonism of the cyanide‐induced hyperpolarisation is dose dependent and is observed at concentrations of the drug which have no observable effect on the resting membrane properties of the neurons. By contrast, the nonselective sigma ligands 1,3‐di‐O‐tolylguanidine (10 μM) and ( +)‐3‐(3‐hydroxyphenyl)‐N‐(1 ‐propyl)piperidine (100 μM), and the selective σl‐ligand (+)‐pentazocine 5‐10 μM) have no effect on the cyanide‐induced hyperpolarisation. 5‐HT (50‐100 μM) and the selective 5‐HT1A receptor agonist 8‐OH‐DPAT (50 μM) also fail to antagonise the cyanideinduced hyperpolarisation. The antagonism of the cyanide‐induced hyperpolarisation by BMS 181100 persists in the presence of tetrodotoxin (1 μM) and in the presence of high concentrations of (+)‐3‐(3‐hydroxyphenyl)‐N‐(1‐propyl)piperidine, but not under conditions of reduced calcium (0.1‐0.2 mM) and raised magnesium (6 mM) concentrations, which block synaptic transmission. It is concluded that in substantia nigra phasic neurons the σ‐binding site does not regulate activation of the ATP‐sensitive channel. However, BMS 181100 antagonises K‐ATP channel activation in these neurons independently of σ‐binding sites and 5‐HT receptors. This action of BMS 181100 is TTX insensitive and Ca2+ dependent. © 1995 Wiley‐Liss, Inc.
Developmental regulation of Thy 1.2 rate of synthesis in the mouse cerebellum
Authors: Radrizzani M. , Carminatti H. , Pivetta O. H. , Vargas V. P. Idoyaga 
Published: January 2005

AbstractThy 1.2 is a well‐known major cell surface glycoprotein of the central nervous system (CNS). However, the regulation of the expression of this molecule as well as its function are yet to be determined. To approach these problems we studied the synthesis of the molecule in the developing cerebellum of wild‐type and staggerer mutant mice. We found the appearance of a [35S]‐methionine‐labeled band detected with specific Sepharose 4B‐bound monoclonal antibodies (Mabs). The Thy 1.2 activity increases progressively from postnatal day 9 (P9), reaching the highest rate at P12, subsequently decreasing sharply at P13, and remaining relatively low up to P16 in the wild type. Comparison of these data to the rates of total protein synthesis reveals a selective developmental regulation of Thy 1.2 expression, at least at the translational level. This correlates quite well with the timing of synaptic stabilization between parallel fibers and Purkinje cell dendritic spines. Furthermore, at P12 Thy 1.2 protein is preferentially located in the synaptosomal fraction. The parallel fiber:Purkinje cell synapsis is not stabilized in the staggerer mutant mouse. At P12 Thy 1.2 synthesis is 30% of the wild type, indicating that the translational regulation of Thy 1.2 is altered in the staggerer mutation. © 1995 Wiley‐Liss, Inc.
Characterization of synaptic vesicles and related neuronal features in nerve growth factor and ras oncogene differentiated PC12 cells
Authors: Tao‐Cheng J.‐H. , Dosemeci A. , Bressler J. P. , Brightman M. W. , Simpson D. L. 
Published: January 2005

AbstractPC12 cells can differentiate into neuron‐like cells after treatment with either nerve growth factor (NGF) or transduction with a retrovirus which expresses the K‐ras oncogene. The concomitant treatment of NGF plus ras differentiates PC12 cells further than either agent alone with respect to neurite outgrowth, acetylcholinesterase levels, and most strikingly, the number of synaptic vesicle (SV) clusters. These SV clusters in PC12 cell neurites closely resemble those in the presynaptic terminals of neurons. Such SV clusters have not been described in cell lines previously. The SV clusters from all three differentiated groups (NGF, ras, and NGF plus ras) were similar in size, shape, and configuration, except that the ones in the doubly treated group occur in higher frequency and have more vesicles. The synaptic nature of these vesicle clusters was demonstrated by their regulated depletion after potassium stimulation. Furthermore, these vesicle clusters stained positively for two SV‐associated proteins, synapsin I and synaptophysin, by EM immunocytochemistry (ICC). Such SV clusters in a cell line are very useful for characterizing the regulated release of SVs and the distribution of SV‐related antigens in intact cells. Analysis by SDS‐gel electrophoresis and immunoblotting indicated that synapsin I levels are higher in all three differentiated groups compared to untreated cells; whereas synaptophysin levels are lower in cells exposed to NGF alone or with NGF and ras double treatment. Possible convergence and/or divergence on the mechanisms of NGF and ras differentiation in PC12 cells are discussed. © 1995 Wiley‐Liss, Inc.This article is a US Government work and, as such, is in the public domain in the United States of America.
Response of olfactory Schwann cells to intranasal zinc sulfate irrigation
Authors: Chuah M. I. , Tennent R. , Jacobs I. 
Published: January 2005

AbstractThe response of olfactory Schwann cells was assessed at 2, 4, and 7 days following intranasal zinc sulfate irrigation in 1‐month‐old mice. Ultrastructural and immunohistochemical observations showed dramatic differences between experimental and control mice which had been washed with saline intranasally. Two days after zinc sulfate treatment, many olfactory nerve bundles contained patchy areas of axonal degeneration, while the cell bodies of the olfactory Schwann cells appeared to have increased in electron density and to have shifted peripherally. Some of the cell bodies protruded from the surface of the axon fascicle, suggesting that the olfactory Schwann cells were in the initial process of migrating away. On the fourth day when most of the olfactory axons had degenerated, some olfactory Schwann cells were aligned immediately beneath the basal lamina of the olfactory epithelium. These cells were immunopositive for the S‐100 protein and possessed an expanded perinuclear space. Many olfactory Schwann cells were present in the region beneath the cribriform plate, while some appeared to have passed through the gaps between the bony plates to reach the olfactory bulb. Hence, the results showed that many olfactory Schwann cells migrated towards the olfactory bulb following loss of axonal contact. Furthermore, on the seventh day following zinc sulfate treatment, some olfactory Schwann cells in the vicinity of the olfactory bulb appeared phagocytic, as indicated by their extension of processes around fragments of cell debris and the presence of lysosome‐like organelles in the perikaryon. The control mice which had been intranasally irrigated with saline did not demonstrate massive olfactory axonal degeneration, and the morphology of the nasal cavity region was similar to that of normal mice. © 1995 Wiley‐Liss, Inc.
Selective block of Ca2+‐dependent K+ current in crayfish neuromuscular system and chromaffin cells by sea anemone Bunodosoma cangicum venom
Authors: Araque A. , Urbano F. J. , Cerveñansky C. , Gandía L. , Buño W. 
Published: January 2005

AbstractThe effects of the nematocyst venom of the sea anemone Bunodosoma cangicum on depolarization‐activated currents were studied in opener crayfish muscle fibers and in cultured bovine chromaffin cells. The venom selectively and reversibly blocked the Ca2+ ‐dependent K+ current (IK(Ca)) present in crayfish muscle in a dose‐dependent manner without affecting voltage‐gated Ca2+ or K+ currents. Furthermore, the venom also reduced IK(Ca) in chromaffin cells, without modifying voltage‐gated Na+, Ca2+, or K+ currents. Synaptic transmission in crayfish muscle was also affected by the venom. Repetitive excitatory and inhibitory postsynaptic currents (each associated with a presynaptic action potential) were evoked by each nerve stimulus, suggesting that presynaptic IK(Ca) may control the electrical activity of excitatory and inhibitory presynaptic fibers. We conclude that B. cangicum venom includes a toxin that selectively and reversibly blocks Ca2+ ‐dependent K+ currents in crayfish muscle and in bovine chromaffin cells, and modifies excitatory and inhibitory synaptic transmission, probably abolishing a similar conductance at the presynaptic fibers. © 1995 Wiley‐Liss, Inc.
Seed reserves of chickpea in relation to molybdenum supply
Authors: Nautiyal Nirmala , Singh Soni , Chatterjee Chitralekha 
Published: January 2005

AbstractChickpea (Cicer arietinum L), cv K75 plants were grown till maturity at 0.00001, 0.0001, 0.001 (deficient), 0.02 (adequate), 0.2 (supranormal) and 2.0 (excess) mg dm−3 Mo in refined sand. The pod and seed yield of chickpea were at a maximum at 0.2 mg dm−3 Mo, which is ten times higher than the usual Mo requirement. The seed weight of chickpea was decreased more by low (<0.02 mg dm−3) than excess (2 mg dm−3) Mo. In chickpea seeds, the concentrations of starch, reducing, non‐reducing and total sugars were highest at 0.02 mg dm−3 Mo and decreased by Mo stress (<>0.02–0.2 mg dm−3). In comparison, the content of methionine, lysine, legumin, vicilin, total proteins, protein and non‐protein nitrogen in seeds of chickpea decreased variably both at low (<0.02 mg dm−3) and high (>0.2 mg dm−3) Mo. Both deficiency and excess of Mo deteriorated the quality of seeds by increasing the content of phenols, cysteine and albumin and decreasing that of methionine, lysine, legumin and vicilin protein fractions, apart from reducing the seed weight. The quality of seeds deteriorated more by deficiency than excess of Mo in chickpea. Copyright © 2004 Society of Chemical Industry
Parkinsonism following dystonia in three patients
Authors: Katchen Marc , Duvoisin Roger C. 
Published: January 2005

AbstractThree patients who presented initially with dystonia and subsequently developed typical idiopathic parkinsonism were evaluated: One patient presented with a writer's cramp, one with axial dystonia, and one with Meige syndrome. All three displayed amelioration of their dystonia with progression of their parkinsonism over a period of 2 to 15 years. Treatment with levodopa gave some relief of the parkinsonism symptoms in two patients but exacerbated or reactivated the dystonia. It is suggested that both the dystonia and the parkinsonism represent the changing clinical expression of the same disorder at different times in its evolution.
Sudden onset of confusion with severe exacerbation of parkinsonism during levodopa therapy
Authors: Sage Jacob I. , Duvoisin Roger C. 
Published: January 2005

AbstractTwo patients with Parkinson's disease presented with unprovoked, abrupt onset of hallucinations, confusion and the simultaneous worsening of parkinsonian symptoms. This clinical syndrome appears to be a rare complication of dopaminergic therapy since improvement occurred gradually with reduction of Sinemet dosage.
Acetazolamide responsive hereditary paroxysmal ataxia
Authors: Friedman J. H. , Hollmann P. A. 
Published: January 2005

AbstractThe fourteenth family with an apparently autosomal dominant paroxysmal ataxia is described. As in the seven families described since 1978, acetazolamide completely cured the attacks. A possible mechanism of action of acetazolamide is discussed.
Adrenergic beta2‐selective blocker in isoprenaline‐enhanced essential tremor
Authors: Teräväinen Heikki , Huttunen Juha 
Published: January 2005

AbstractA beta2‐selective adrenergic‐receptor‐blocking drug, ICI 118.551,150 mg/day, prevented almost as effectively as the nonselective antagonist propranolol, 240 mg/day, the isoprenaline enhancement of essential tremor amplitude.
Continous intracerebroventricular infusion of dopamine and dopamine agonists through a totally implanted drug delivery system in animal models of Parkinson's disease
Authors: De Yebenes J. G. , Fahn S. , Lovelle S. , Jackson‐Lewis V. , Jorge P. , Mena M. A. , Reiriz J. , Bustos J. C. , Magariños C. , Martinez A. 
Published: January 2005

AbstractWe studied the effect of intracerebroventricular infusion of dopamine and dopamine agonists in rat and primate models of Parkinson's disease as an experimental approach to the treatment of levodopa‐induced fluctuations. The infusion of dopamine, lisuride, and pergolide into the ventricle ipsilateral to the lesion, by 6‐hydroxydopamine, of the nigrostriatal pathway induced a contralateral rotation which was maximal 24–48 h after infusion and whose intensity progressively decreased over the period of 1 weak. [3H] Spiperone binding was decreased by the infusion of dopamine but the responses to subcutaneous apomomorphines were unchanged. The infusion of dopamine also restored the levels of monoamines in the rat brain. In chronic reserpized rats, the infusion of dopamine restored brain levels of dopamine but did not reverse akinesia unless monoamine oxidase inhibitors were simultaneously administered, either systemically or intracerebroventricularly. Lisuride and pergolide proved much weaker than dopamine in reversing the effects of reserpine. Intracerebroventricular infusion of dopamine plus deprenyl reversed MPTP induced akinesia in monkeys but the pump used for the delivery was not well tolerated, because of its size, by the animals.
Parkisonism induced by high‐dose cytosine arabinoside
Authors: Luque F. Antonio , Selhorst John B. , Petruska Paul 
Published: January 2005

AbstractWe report a severe parkinsonian condition following high dose, parenteral cytosine arabinoside (Cytosar) that persisted for 8 weeks. The durg was used in a patient with acute myelogenous leukemia that was refractory to all other treatment. The syndrome was partially responsive to antiparkinsonian durgs and fortunately remitted completely within 12 weeks.
Dystonia and tremor following exposure to 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin
Authors: Klawans Harold L. 
Published: January 2005

AbstractForty‐seven railroad workers who were exposed to polychlorinated phenols, including dioxin (TCDD), during 1979 while cleaning up the chemical spillage following damage to a tank car filled with these chemicals were followed medically for the subsequent 6 years. Two committed suicide. The initial neurological complaints included a sense of fatigue and muscle aching, both of which have been reported in other individuals following dioxin exposure. On detailed neurological examination in December, 1985, 24 of 45 had dystonic writer's cramp and/or other action dystonias of the hands. None of the involved individuals had a family history of dystonia, and all 24 dated the onset of the dystonia to the first 2 to 3 years subsequent to their toxic exposure. The dystonias varied in severity but were usually mild. No other types of dystonic involvement were recognized. Thirty‐five of the 45 individuals also manifested postural and terminal intention tremor which resembled benign essential tremor. None of the involved individuals had a family history of tremor, and all 35 of those affected dated the onset of the tremor to some time subsequent to their toxic exposure. Forty‐three of 45 patients had histories and findings suggestive of peripheral neuropathy. This is the first report relating and type of dystonia to prior dioxin exposure and the first report relating action dystonia, such as dystonic writer's cramp, and postural/terminal intention tremor, to toxic exposure of any type.
Blink reflex studies in focal dystonias: Enhanced excitability of brainstem interneurons in cranial dystonia and spasmodic torticollis
Authors: Tolosa Eduardo , Montserrat Luis , Bayes Angeles 
Published: January 2005

AbstractWe have studied the orbicularis oculi reflex to paired stimuli in patients with various forms of focal dystonia and in normal controls. In normals, the conditioning stimulus (CS) facilitated the test stimulus (TS) early response (R1), but markedly inhibited the TS polysynaptic late response (R2). In all types of dystonias studied the CS facilitated the TSR1 as in normals. However, in patients with blepharospasm (alone or associated with oromandibular dystonia), spasmodic torticollis, or spasmodic dysphonia, it inhibited the TSR2 significantly less than that of the controls, with marked enhancement of the recovery curve of the late response. The TSR2 recovery curve of patients with focal arm dystonia was normal. These results are indicative of increased brainstem interneuron excitability in the various dystonias mediated by the cranial nerves, but not in focal arm dystonias such as dystonic writer's cramp. This abnormality might be caused by an abnormal input possibly from the basal ganglia upon these brainstem cells. Our results also suggest that a similar pathophysiology underlies the various focal dystonias of the head and neck.
Isoniazid therapy in Parkinson's disease
Authors: Gershanik O. S. , Luquin M. R. , Scipioni O. , Obeso J. A. 
Published: January 2005

AbstractThe effect of isoniazid on levodopa‐induced dyskinesias has been evaluated in 20 patients with Parkinson's disease, following a serendipitous observation that choreic dyskinesias induced by levodopa in one parkinsonian patient were markedly reduced during treatment with isoniazid for tuberculous infection. A mean average isoniazid dose of 290 mg was given without any change in current antiparkinsonian treatment. “Benefit of dose” choreic dyskinesias were markedly reduced in 18 patients within the first few weeks of treatment. This effect was accompanied by an intolerable worsening of parkinsonian signs. All patients returned to their basal situation after isoniazid interferes with the therapeutic action of levodopa and dopamine agonists. The precise mechanism by which this action occurred is not known, but several possible explanations are discussed.
Delayed‐onset dystonia associated with corticospinal tract dysfunction
Authors: Factor Stewart A. , Sanchez‐Ramos Juan , Weiner William J. 
Published: January 2005

AbstractWe report a young man with delayed‐onset dystonia secondary to a cerebral infarction. The infarction was caused by an embolic event at the age of 18 months. Delay to onset of dystonia was 16 years and, prior to the onset of dystonia, the patient had profound corticospinal tract dysfunction manifested by a severe hemiparesis. Computed tomography scan revealed infarction of the lentiform nucleus and precentral gyrus. The profound involvement of the corticospinal tract both clinically and radiologically are features not previously described in symptomatic dystonia and contradict the concept that sparing of the corticospinal tract is an essential feature for the onset of acquired dystonia.
Dementia and treatment with L‐dopa in Parkinson's disease
Authors: Hietanen M. , Teräväinen H. 
Published: January 2005

AbstractWe compared the neuropsychological performance of patients with Parkinson's disease who were young at onset of the disease (mean age, 41.4 years) and had received prolonged L‐dopa treatment (mean, 52.1 months) with nontreated patients of the same age. A similar comparison was made for patients who were older at onset of the disease (mean, 62.1 years). There were no significant differences in cognitive and memory functions between the L‐Dopa‐treated and untreated young patients, whereas the L‐Dopa‐treated patients in the older age group performed more poorly than untreated patients in some memory tests (Wechsler Memory Scale I: logical and visula) and cognitive functions (Wechsler Adult Intelligence Scale: similarities, block design, and cognitive flexibility). Treatment duration, disease duration, and mean L‐Dopa dose were comparable for the two age groups. After linear effects of age and disease duration had been eliminated, the duration of L‐Dopa treatment did not correlate with the cognitive vaiables studied. These observations suggest that treatment with L‐Dopa may not be the cause of cognitive impairment in Parkinson's disease.