bluuebunny/crossref_metadata_2025_split huggingface dataset:
Axotomy induces a different modulation of both low‐affinity nerve growth factor receptor and choline acetyltransferase between adult rat spinal and brainstem motoneurons
Authors: Rende Mario , Giambanco Ileana , Buratta Marina , Tonali Pietro 
Published: January 2005

AbstractAdult rat spinal and brainstem motoneurons reexpress low‐affinity nerve growth factor receptor (p75) after their axotomy. We have previously reported and quantified the time course of this reexpression in spinal motoneurons following several types of injuries of the sciatic nerve. Other studies reported the reexpression of p75 in axotomized brainstem motoneurons. Results of these previous studies differed regarding the type of the most effective triggering injury for p75 reexpression, the relative duration of this reexpression and the decrease of choline acetyltransferase (ChAT) immunoreactivity (‐IR) following a permanent axotomy of spinal or brainatem motoneurons. These differences suggest that these two populations of motoneurons respond to axotomy with a different modulation of p75 and ChAT expression. The aim of the present study was to determine whether differential modulation exists. We have analyzed and quantified the presence of p75‐ and ChAT‐IR motoneurone in the hypoglossal nucleus following the same types of injury and the same time course we previously used for sciatic motoneurons. The results show that a nerve crush is the most effective triggering injury for p75 and that it induces similar temporal patterns of p75 and ChAT expression for sciatic and hypoglossal motoneurons. In contrast, a cut injury of the sciatic and hypoglossal nerves resulted in distinct temporal courses of both p75 and ChAT expression between these two populations of motoneurons. In fact, a permanent axotomy of the hypoglossal motoneurons induced (i) a much longer maintenance phase for p75 than in aciatic motoneurons and (ii) a progressive loss of ChAT‐IR with a successive return to normal values in contrast to the modest decrease in the sciatic motoneurons. This evidence indicates that spinal and brainstem motoneurons respond to a permanent axotomy with a different modulation of p75 and ChAT expression. Altogether, the present data and the reported evidence of a differential post‐ axotomy cell death support the hypothesis that these two populations of motoneurons undergo different dynamic changes after axotomy. © 1995 Wiley‐Liss, Inc.
In situ labeling of apoptotic cell death in the cerebral cortex and thalamus of rats during development
Authors: Spreafico Roberto , Frassoni Carolina , Arcelli Paola , Selvaggio Mariateresa , De Biasi Silvia 
Published: January 2005

AbstractApoptosis is a form of naturally occurring cell death that plays a fundamental role during development and is characterized by internucleosomal DNA fragmentation. In this study we used specific in situ labeling of DNA breaks (Gavrieli et al. [1992] J. Cell. Biol. 119:493–501) to analyze the distribution of apoptotic cells in rat cerebral cortex and thalarnus at different developmental stages from embryonic day 16 to adulthood. Control experiments and electron microscopy confirmed that the reaction product was confined to the nucleus of selected cells. Plotting and counting of labeled nuclei in counterstained paraffin sections showed that apoptosis occurred mainly during the first postnatal week and was absent in embryonic and adult samples. In the cortex, the number of apoptotic cells progressively increased from birth to the first postnatal week, with a peak between postnatal (P) day 5 and P8, and subsequently decreased. At the time of maximal expression of apoptosis, labeled nuclei were present mainly in layer VIb and underlying white matter and at the border between cortical plate and layer I. Only a few apoptotic cells were found scattered in the thalamus, without a particular concentration in selected areas, but with a peak at P5. Differences in the number of apoptotic cells between cortex and thalamus suggest that apoptotic cell death may have a different functional significance in the two brain areas. © 1995 Wiley‐Liss, Inc.
Localization of α7 nicotinic receptor subunit mRNA and α‐bungarotoxin binding sites in developing mouse somatosensory thalamocortical system
Authors: Bina Keshavan G. , Guzman Patricia , Broide Ron S. , Leslie Frances M. , Smith Martin A. , O'Dowd Diane K. 
Published: January 2005

AbstractPrevious studies in rat, showing a transient pattern of expression of the α7 nicotinic acetylcholine receptor in the ventrobasal thalamus and barrel cortex during the first 2 postnatal weeks, suggest that these receptors may play a role in development of the thalamocortical system. In the present study, in situ hybridization and radiolabeled ligand binding were employed to examine the spatiotemporal distribution of α7 mRNA and α‐bungarotoxin binding sites in the thalamocortical pathway of mouse during early postnatal development. As in the rat, high levels Of α7 mRNA and α‐bungarotoxin binding sites are present in the barrel cortex of mouse during the first postnatal week. Both α7 mRNA and its receptor protein are observed in all cortical laminae, with the highest levels seen in the compact cortical plate, layer IV, and layer VI. When viewed in a tangential plane, α7 mRNA and α‐bungarotoxin binding sites delineate a whisker‐related barrel pattern in layer IV by P3–5. Quantitative analysis reveals a dramatic decrease in the levels of expression of α7 mRNA and α‐bungarotoxin binding sites in the cortex by the end of the second postnatal week. Unlike in the rat, only low levels of α7 mRNA or α‐bungarotoxin binding sites are present in the ventrobasal complex of the mouse thalamus. The broad similarities between the thulamocurticul development of rat and mouse taken together with the present results suggest that α7 receptors located on cortical neurons, rather than on thalamic neurons, play a role in mediating aspects of thalamocortical development. © 1995 Wiley‐Liss, Inc.
Expression of brain‐type creatine kinase and ubiquitous mitochondrial creatine kinase in the fetal rat brain: Evidence for a nuclear energy shuttle
Authors: Chen Lulu , Roberts Robert , Friedman David L. 
Published: January 2005

AbstractTo test the hypothesis that embryonic brain cells utilize a creatine phosphate energy shuttle, we examined the pattern of creatine kinase (CK) isoform expression and localization in the fetal rat brain. Moderate levels of CK activity are present at embryonic day 14 (7 U/mg protein) and decrease slightly until 3 days postpartum followed by a rapid, fourfold up‐ regulation to adult levels by 1 month (18 U/mg protein). In parallel with changes in enzyme activity, there is a biphasic and coordinate pattern of expression of brain‐type CK (BCK) and ubiquitous mitochondrial CK (uMtCK) determined by nondenaturing electrophoresis and immunoblot analysis. The localization of CK isoforms was examined by immunocytochemistry, and, during the fetal period, BCK and uMtCK immunoreactivity was detected throughout the central and peripheral nervous system, especially in neuroepithelial regions of the cerebral vesicles and spinal cord. In large cells within the olfactory neuroepithelium and ventral spinal cord, differential compartmentation of CK isoforms was evident, with BCK localized primarily in cell nuclei, whereas uMtCK immunoreactivity was present in the cell body (but not within nuclei). In olfactory bulb neuroepithelium, both isoforms were expressed in the middle zone of the germinal layer associated with DNA synthesis. In embryonic skeletal and cardiac muscle, which also express BCK, the same compartmentation of BCK was seen, with BCK localized primarily in the cell nucleus of cardiac and skeletal myoblasts. These results demonstrate a coordinate pattern of expression and compartmentation of BCK and uMtCK isoforms in the fetal brain that, in some cells, provides the anatomic basis for a nuclear energy shuttle. © 1995 Wiley‐Liss, Inc.
Analysis of unsteady pipe flow using the modified finite element method
Authors: Szymkiewicz Romuald , Mitosek Marek 
Published: January 2005

AbstractA modified finite element method is proposed to solve the unsteady pipe flow equations. This approach yields a six‐point implicit scheme with two weighting parameters. An accuracy analysis carried out using the modified equation approach showed that the proposed scheme has higher accuracy compared to other methods. A comparison of experimental data and the results of numerical solution showed that the required damping and smoothing of a pressure wave can be obtained when numerical diffusion is produced by the applied method. It suggests that the physical dissipation process observed in the water hammer phenomenon is not represented properly in its mathematical model. Therefore, the classical system of water hammer equations seems to be incomplete. Copyright © 2004 John Wiley & Sons, Ltd.
Anticonvulsant activity of a new 1,4‐benzodiazepine in rodents and the baboon Papio papio
Authors: Piper David C. , Meldrum B. S. , Gardner C. R. 
Published: January 2005

AbstractRU 31124, a new anticonvulsant 1,4‐benzodiazepine was compared with clonazepam in a series of tests in rats and mice. It demonstrated greater anticonvulsant potency whilst having equivalent sedative properties to clonazepam. This profile of activity was confirmed in the photosensitive baboon, Papio papio, in which RU 31124 provided long‐lasting protection against convulsions at doses having little or no sedative side effects.
Receptor binding and the discovery of psychotherapeutic drugs
Authors: Hamblin Mark , Creese Lan 
Published: January 2005

AbstractThe identification of useful new drugs, when not due entirely to serendipity, has often relied on in vivo techniques that are both difficult to interpret and to perform. The receptor binding technique, however, by allowing the direct study of the specific biochemical site of action of most psychotherapeutic drugs has provided a simple, selective, and sensitive method to study drug‐receptor interactions. The biochemical locus of action for a family of drugs can often be identified by comparing their absolute potencies in in vivo systems with their affinities at a number of drug and/or neurotrans mitter receptor binding sites. Once a particular binding site is identified as therapeutically relevant, affinity for this binding site can be used as a screen for novel compounds that may show similar in vivo activity. Detailed structure‐activity relationships can be determined in vitro without the problems of metabolism and differential absorption that complicate in vivo studies. Such studies allow the pinpointing of active sites within the drug molecule for further synthetic manipulations. Receptor binding studies have been essential in the elucidation of the therapeutic mechanisms of neuroleptics, tricyclic antidepressants, opiates, and benzodiazepines. Receptor binding studies are not only useful in the identification and quantification of therapeutically useful drug receptor interactions but have also been invaluable in the study of similar interactions that manifest themselves as drug‐induced side effects. Such studies may eventually allow the development of drugs that are not only more therapeutically potent but are also free of side effects. Radioreceptor assays have also been introduced to measureserum drug levels of neuroleptics, antidepressants, anticholinergics, benzodiazepines and P‐adrenergic antagonists. These methods have the advantage of being quick, sensitive, selective, and inexpensive.
The effect of fluoxetine on morphine analgesia, respiratory depression, and lethality
Authors: Hynes Martin D. , Fuller Ray W. 
Published: January 2005

AbstractThe analgesic effect of morphine in a mouse writhing assay was enhanced by the simultaneous administration of fluoxetine, an inhibitor of serotonin uptake. Fluoxetine reduced the ED50 for morphine and extended the duration of morphine analgesia. The potentiation of morphine analgesia was particularly striking in mice made tolerant by repeated morphine injections. Potentiation of morphine by fluoxetine was also observed in a rat tail jerk test for analgesia. The acute lethality of morphine in rats and mice was altered by fluoxetine, yet the therapeutic index of morphine (ratio of LD50 to ED50) was unchanged. The decrease in blood pO2 produced by morphine at doses of 1 and 4 mg/kg in rats was attenuated by fluoxetine, which by itself increased blood pO2. These findings strengthen earlier evidence for an involvement of serotoninergic neurons in the analgesic effects of morphine and support the idea that enhanced serotoninergic function might be a useful means of enhancing morphine's actions in clinical therapy.
Isoxsuprine‐induced changes in maternal and fetal hemodynamics and fetal electroencephalogram
Authors: Ayromlooi Jahangir , Desiderio Denise M. , Tobias Mitchell D. , Leff Richard 
Published: January 2005

AbstractIsoxsuprine has been used in obstetrics in the treatment of premature labor. Its maternal and fetal effects were studied in five ewes with dated gestations of 137 ± 1.25 days (term approximately 147 days).Isoxsuprine (1 mg/min) was infused over a 30‐minute period to the anesthetized ewes while maternal and fetal blood pressures, uterine and fetal cerebral blood flows, and fetal brain function were studied. In addition, fetal and maternal acid‐base values and fetal cerebral metabolism were measured at baseline, 10, 20, 30, 45, and 60 minutes.Isoxsuprine caused maternal hypotension, tachycardia, and metabolic acidosis and temporary reduction of PO2 without affecting oxygen saturation, O2 content, or uterine blood flow. In the fetus hypotension, tachycardia, temporary metabolic acidosis, transient reduction in PO2 and O2 saturation occurred while PCO2, cerebral blood flow, brain glucose consumption, and the electroencephalogram remained essentially unchanged. Fetal pH, PO2, and O2 saturation returned toward baseline values at the end of the experiment.
The effect of electrostimulation on barbiturate‐induced sleeping times in rats
Authors: Capel I. D. , Pinnock M. H. , Withey N. J. , Williams D. C. , Patterson M. A. 
Published: January 2005

AbstractFemale rats, anaesthetized with hexobarbital, regained their righting reflex more rapidly following electrostimulation than sham‐treated controls. The extent of the decreased sleeping times in these animals varied according to the frequency (cycles per second) of the electrostimulation applied. The frequency which produced the largest decrease in sleeping time was 10 Hz. Determination of the activity of some microsomal enzymes indicated that the decreased sleeping time was not the result of increased hepatic enzyme activity. Animals which had received prior treatment with naloxone exhibited increased sleeping times following barbiturate administration, but the effects of electrostimulation on the sleeping time at 10 Hz was diminished, while the effect of electrostimulation at high frequency (500 Hz) was enhanced. Although repeated daily administration of hexobarbital progressively decreased sleeping times for all the animals, electrostimulation decreased the sleeping times of the treated rats by a similar percentage of the control animals on each successive day. Electrostimulation at a frequency of 10 Hz produced a significant decrease in serum corticosterone levels, whereas 500 Hz resulted in an increase.
Naloxone‐induced reversal of clonidine, but not hydralazine, hypotension
Authors: Bennett Debra A. , DeFeo John J. , Elko Edward E. , Lal Harbans 
Published: January 2005

AbstractNormotensive rats of the Sprague‐Dawley strain were administered either the centrally acting hypotensive drug clonidine (0.16 mg/kg IP) or the peripherally acting hypotensive drug hydralazine (1.25 mg/kg IP) to induce reliable hypotension (blood pressure reductions of 60–90 mm Hg), as measured by a tail cuff procedure. The opiate antagonist, naloxone (10–20 mg/kg IP), reversed clonidine but not hydralazine hypotension. Naloxone also failed to reverse hydralazine's hypotensive action in rats made hypertensive by renal ligation. Naloxone's reversal of clonidine (0.01 mg/kg IV) hypotension was confirmed in experiments in which blood pressure was measured through direct cannulation of the carotid artery. It is suggested that naloxone's antagonism of clonidine hypotension is located at a central nervous system site, and that clonidine hypotension may be mediated through an interaction with the brain opiate systems.
The brain renin‐angiotensin system
Authors: Severs Walter B. , Summy‐Long Joan Y. , Keil Lanny C. 
Published: January 2005

AbstractConsiderable evidence suggests that angiotensin interacts with the central nervous system (CNS) to increase blood pressure and alter peripheral hydration. Blood‐borne angiotensin may affect circumventricular organs resulting in increased water intake and vasopressin release. In addition, current literature documents the presence of a complete renin‐angiotensin system (RAS) in the brain. Angiotensin, presumably of central origin, increases sodium excretion; an effect opposite to blood‐borne peptide. This effect, along with increased water turnover, could dilute body fluids. The relative activities of the peripheral (renal) and central RASs thus may be of considerable importance in both normal and pathophysiological control of blood pressure and hydration. Indeed, some models of spontaneous hypertension in rats are associated with an altered brain RAS; central administration of converting enzyme inhibitors or angiotensin receptor antagonists returns elevated blood pressure toward normal.
Renal vasodilators and hypertension
Authors: Ackerman Dennis M. , Weinstock Joseph , Wiebelhaus Virgil D. , Berkowitz Barry 
Published: January 2005

AbstractSK&F 82526 is a potent renal vasodilator in dogs, monkeys, and hypertensive rats. It is orally active and has a specificity for the renal vasculature greater than dopamine. Its activity is owing, at least in part, to stimulation of renal dopamine receptors and has no effect on α‐ or β‐adrenergic receptors. This compound should be valuable in further examining the importance of renal blood flow in essential hypertension.
Antihypertensive effect of a calcium antagonistic drug: Regression of hypertensive cardiac hypertrophy by nifedipine
Authors: Kazda Stanislav , Garthoff Bernward , Thomas Günther 
Published: January 2005

AbstractThe cardiac hypertrophy which develops in models of sustained hypertension in experimental animals cannot be prevented or reversed by all antihypertensive drugs. Clearly, blood pressure is only one of numerous factors which contribute to the development of hypertensive cardiomegaly. The ability of drugs to reduce cardiac hypertrophy depends primarily on their mode of action, rather than on the degree of blood pressure decrease. Vasodilators effectively control high blood pressure but enhance cardiac hypertrophy in rats. In currect experiments, minoxidil lowered blood pressure, but caused increases in heart weight and plasma‐renin activity (PRA) in spontaneously hypertensive rats (SHR). In contrast, the calcium antagonist, nifedipine, reduced blood pressure or prevented its increase in SHR concurrently reducing heart wight and decreasing PRA. Moreever, nifedipine prevented salt‐induced hypertension and heart hypertrophy in SD (sensitive)‐Dahl rats. It is suggested that in contrast to the vasodilator minoxidil, nifedipine reduces the high renovascular resistance in hypertensives thus enhancing sodium and water elimination. Thus, the action of the calcium antagonist, nifedipine, involve both renal vasodilation and reduction of renin‐angiotensin mediated renal vasoconstriction. In this way, the decreased volume load together with the decreased arterial afterload will contribute to the prevention or regression of hypertensive cardiac hypertrophy.
A double‐blind dose‐determination study with flutroline: A new neuroleptic
Authors: Wilson W. H. , Guy W. , Ban T. A. , Adelson L. M. , Perez‐Payan H. 
Published: January 2005

AbstractIn a 4‐wk double‐blind clinical trial four doses (1, 5, 10, and 20 mg) of flutroline were compared in newly admitted schizophrenic patients. Although there were few statistically significant differences among the four dosage groups, there were at least five indications of greater thereapeutic effectiveness in the higher dosages. The most favorable changes were seen in the 20‐mg group, which was the only group to show improvement in all five factors of the Brief Psychiatric Rating Scale and in which a significant elevation of serum prolactin level occurred at a 6‐hr post‐dose sampling. In a previous clinical trial in which three different daily doses of flutroline (1, 20, and 100 mg) were compared, 20 and 100 mg were found to be equal in their therapeutic effects and superior to 1 mg. Since no dosage between 1 and 20 mg were employed, the possibility that therapeutic effects with flutroline may already be present in daily doses below 20 mg could not be ignored. While the present findings are in favor of this contention, they also indicate that therapeutic efficacy with 20 mg is greater than with 1‐, 5‐, or 10‐mg daily doses.
Effect of neuromuscular blocking agents pancuronium bromide and its monoquaternary analogue Org NC 45 on regional blood flow and cardiac metabolism in pigs
Authors: Mohan Dhasmana K. , Verdouw Pieter D. , Prakash Om , Saxena Pramod R. 
Published: January 2005

AbstractThe effects of pancuronium bromide (60, 120, 300, and 600 μg.kg−1, i.v.) and its monoquaternary analogue Org NC 45 (300,750, and 1500 μg.kg−1, i.v.) on the systemic and regional hemodynamic variables were studied in the anesthetized pig. Pancuronium exhibited a dose‐dependent positive chronotropic and inotropic activity. The enhanced oxygen requirement of the myocardium was successfully met by a combination of higher blood supply to, and oxygen extraction by, the tissue. No changes were noticed in cerebral, renal or hepatic arterial blood flow. On the other hand, Org NC 45, which unlike pancuronium lacks vagolytic and sympathomimetic actions, did not cause an increase in heart rate or left ventricular dP/dtmax (LV dp/dtmax). Instead, in the two highest doses (750 and 1500 μg.kg−1) Org NC 45 decreased arterial blood pressure, LV dP/dtmax and the blood supply to the brain, kidneys, and liver. Neither compounds showed any effect on cardiac metabolism of glucose, lactate, or free fatty acids (FFA), although arterial blood glucose concentration did decrease following the two highest doses of each compound. Since Org NC 45, in a dose of 300 μg/kg−1, which is seven to ten times the ED90 for neuromuscular paralysis in man, is completely devoid of systemic and regional hemodynamic effects, and pancuronium in similar dose ratio is not, Org NC 45 might be preferred for use in cardiac anesthesia.
Studies on the profile of desmethylimipramine as a gastric antisecretory agent
Authors: Pendleton Robert G. , Miller Darlene A. 
Published: January 2005

AbstractDesmethylimipramine (DMI) and atropine were compared in a variety of organ system tests in rats involving parasympathetic function in order to evaluate the specificity of these compounds as gastric antisecretory agents. DMI was similar to atropine in its effects on the stomach; each markedly inhibited gastric acid secretion and stomach emptying and protected against restraint‐induced gastric ulceration. However, unlike atropine, DMI did not substantially increase pupil size, reduce fecal pellet output, cause urinary retention, or increase heart rate. From these data, it is possible that at least certain antidepressant type drugs could be developed for the treatment of peptic ulcer disease.