bluuebunny/crossref_metadata_2025_split huggingface dataset:
Chemical alteration of poly(tetrafluoroethylene) Teflon induced by exposure to vacuum ultraviolet radiation and comparison with exposure to hyperthermal atomic oxygen
Authors: Everett Michael L. , Hoflund Gar B. 
Published: January 2005

AbstractThe chemical alteration of poly(tetrafluoroethylene) Teflon by vacuum ultraviolet radiation (VUV) (115–400 nm) has been examined with X‐ray photoelectron spectroscopy (XPS). The initial F/C atom ratio of 1.98 decreases to 1.65 after a 2‐h exposure. The F/C atom ratio is further reduced to a steady‐state value of 1.60 after a 74‐h exposure. The high‐resolution XPS C1s data indicate that new chemical states of carbon form as F is removed and that the relative amounts of these states depend on the F content of the near‐surface region. The states are most likely due to C bonded only to one F atom, C bonded only to other C atoms, and C that has lost a pair of electrons through the emission of F−. The exposure of the VUV‐damaged surface to research‐grade O2 results in the chemisorption of a very small amount of O, and this indicates that large quantities of reactive sites are not formed during the chemical erosion by VUV. Further exposure to VUV removes this chemisorbed oxygen. A comparison of the XPS data indicates that the mechanisms of chemical alteration by VUV radiation and hyperthermal (∼5 eV) atomic oxygen are different, as expected, because the excitation sources are quite different. © 2004 Wiley Periodicals, Inc. J Polym Sci Part A: Polym Chem 43: 552–561, 2005
Cyanoxyl‐mediated free‐radical polymerization of acrylic acid: Its scope and limitations
Authors: Grande Daniel , Guerrero Ramiro , Gnanou Yves 
Published: January 2005

AbstractThis work examines the scope and limitations of the cyanoxyl (·OCN)‐mediated free‐radical polymerization of acrylic acid (AA) with respect to the criteria of livingness. Cyanoxyl persistent radicals were generated in situ through the reaction between arenediazonium salts (XC6H4NN⊕BF, where X is H, OCH3, Cl, or NO2) and sodium cyanate (NaOCN). This article thoroughly discusses the role played by such oxygen‐centered radicals in the polymerization process; it particularly focuses on the influence of the concentration and nature of the diazonium salt, the solvent, and the temperature on features such as the variations of ln([M]0/[M]) versus time (where [M]0 is the initial monomer concentration and [M] is the monomer concentration), the number‐average molar mass versus conversion, and the polydispersity versus conversion in cyanoxyl‐mediated free‐radical polymerizations of AA. Cyanoxyl‐terminated samples were used as macroinitiators for the polymerization of methyl methacrylate to generate poly(acrylic acid)‐b‐poly(methyl methacrylate) block copolymers. © 2004 Wiley Periodicals, Inc. J Polym Sci Part A: Polym Chem 43: 519–533, 2005
Identification of motor neurons for accessory muscles of inspiration and expiration, pectoralis, trapezius and external oblique: Comparison with non‐respiratory skeletal muscle
Authors: Charlton Clivel G. , Crowell Bernard , Benson Richard 
Published: January 2005

AbstractThe motor neurons for the accessory muscles of respiration, pectoralis, trapezius, external oblique, and the rectus abdominis were studied in the spinal cord. The objective was to determine if the localization and morphology of the motor neurons for these muscles bear any distinct relationship to the specialized function of these muscles, serving both as supportive skeletal muscles and as accessory respiratory muscles. In addition, it was of interest to know if the inspiratory role of the pectoralis and trapezius muscles and the expiratory role of the external oblique and rectus abdominis are related to the spatial organization of the motor neurons; this knowledge may be important in the discrimination of influences from afferent connections. The motor neurons for these muscles were retrogradely labeled with true blue and were compared with the triceps motor neurons. All neurons occurred ipsilateral and most labeling occurred in C6–7. The motor neurons for the accessory muscles were mainly confined to the ventrolateral tip of the ventral gray matter. The triceps neurons were dorsolateral to the respiratory related neurons in C6–7. Within the confines of the ventrolateral area, the majority of neurons for the pectoralis were localized medial to ventromedial, those for the trapezius were ventrolateral, and those for the external oblique were in the extreme ventrolateral to ventral sections of C7. No neurons were observed in C2 to T2 for the rectus abdominis. A second neuronal column occurred medioventrally in the ventral gray of C4–6 for the trapezius, and is distinct and separated from the C6–7 cell column. The motor neurons for the accessory muscles were oval in shape and of medium size (≈︁ 35 microns). Those for the triceps were small to large 18–45 microns, elongated in shape with distinctly labeled processes and well defined perimeter. The neurons within each column often occurred in clumps and are probably separated by densely packed dendrites that may cause the insulation of one cellular column from another to achieve discriminatory afferent influences to individual neuronal columns. The localization of the motor neurons for the accessory respiratory muscles in C7 superimposed the localization of a high density of substance P receptors (Charlton and Helke, 1986) that also occurred in the phrenic nucleus. The overlapping of the substance P receptors with the motor neurons for the accessory respiratory muscles is supportive of a role for substance P in respiratory control. Finally, the accesory respiratory muscles were innervated by dorsal root sensory neurons that occurred throughout the cervical segments and the first and second thoracic segments. This was in contrast to the innervation of the triceps by sensory neurons located in just one or two segments from its motor neurons of innervation.
Asymptomatic striatal dopamine depletion: PET scans in unilateral MPTP monkeys
Authors: Guttman M. , Yong V. W. , Kim S. U. , Calne D. B. , Martin W. R. W. , Adam M. J. , Ruth T. J. 
Published: January 2005

AbstractIn cynomolgus monkeys, 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MRTP) produces irreversible clinical, chemical, and pathological alterations that are similar to those found in Parkinson's disease. Unilateral carotid injections of this toxin produce ipsilateral nigrostriatal dopamine depletion while sparing the contralateral dopaminergic pathways. In order to study the damage to the nigrostriatal dopamine system in asymptomatic animals after unilateral MPTP administration, positron emission tomography (PET) scans were performed with [18F]fluoro‐L‐dopa (6‐FD). This study demonstrates that clinically asymptomatic MPTP lesions may be assessed in vivo using 6‐FD and PET.
Electrophysiological and pharmacological characterization of identified nigrostriatal and mesoaccumbens dopamine neurons in the rat
Authors: Clark David , Chiodo Louis A. 
Published: January 2005

AbstractExtracllular single‐unit recording techniques were used to compare the basal activity and pharmacological responsiveness of identified nigrostriatal and mesoaccumbens dopamine (DA)‐containing neurons. The projection area of each DA cell was determined by antidromic activation techniques. The forebrain stimulation used for the cell identification procedure did not alter the pharmacological responsiveness of DA neurons; the inhibitory effect of apomorphine (and d‐amphetamine) was identical when stimulation was applied either prior to or following drug administration. Analysis of the spike discharge pattern revealed that a higher proportion of mesoaccumbens DA cells exhibited burst‐firing activity. Although the firing pattern of the two populations of burst‐firing DA cells was similar in many regards, mesoaccumbens DA cells exhibited a longer postburst inhibition than did nigrostriatal DA cells. Each of the DA agonists, apomorphine, pergolide, B‐HT 920, and d‐amphetamine, inhibited nigrostriatal and mesoaccumbens DA neuronal activity in a similar fashion. However, there was a marked population difference in the recovery of cell firing in the 10 minutes following apomorphine‐induced inhibition; the recovery of mesoaccumbens spike discharges was considerably slower. Although this population difference was apparent to some extent following administration of pergolide or B‐HT 920 (but not d‐amphetamine), it was considerably less marked. The present findings are discussed with respect to the known regulatory control of midbrain DA neurons.
[3H]vesamicol binding in brain: Autoradiographic distribution, pharmacology, and effects of cholinergic lesions
Authors: Altar C. Anthony , Marien Marc R. 
Published: January 2005

AbstractAn autoradiographic analysis of high‐affinity binding sites for the vesicular acetylcholine transport blocker [3H]vesamicol (2‐(4‐phenylpiperidino) cyclohexanol; AH 5183) was conducted in rat brain. [3H]Vesamicol binding was displaced 52–99% by DPPN ([2,3,4,8]‐decahydro‐3‐(4‐phenyl‐1‐piperidinyl)‐2‐napthalenol) (IC50=14nM) and by ketanserin (500 nM), haloperidol (43 nM), and vesamicol analogs, but not by drugs selective for adenosine, adrenergic, amino acid, calcium channel, monoaminergic, opioid, PCP, sigma, or several other receptor classes. [3H]Vesamicol binding was most concentrated in the interpeduncular nucleus and fifth and seventh cranial nerve nuclei. Moderate binding was found in the lateral caudate‐putamen, medial nucleus accumbens, olfactory tubercle, vertical and horizontal diagonal bands of Broca, and basolateral amygdala. The distribution of [3H]vesamicol binding was similar to distributions of acetylcholine (r = 0.88), acetylcholine esterase (r = 0.97), choline acetyltransferase (ChAT) (r = 0.97), and [3H]hemicholinium‐3 binding sites (r = 0.95−0.99). Lower correlations were obtained between [3H]vesamicol and muscarinic receptor densities (r = 0.50−0.70). Few exceptions to the match between binding and cholinergic neuronal markers were found, e.g., the molecular layer of the cerebellum and the thalamus. Lesions of cholinergic neuronal projections to the neocortex or hippocampus reduced [3H]vesamicol binding in each of these regions, but to a lesser extent than reductions in ChAT. [3H]Vesamicol binding sites appear to be anatomically associated with brain cholinergic neurons, a locus that is consistent with the control by this site of vesicular acetycholine uptake.
Chloral hydrate anesthesia alters the responsiveness of identified midbrain dopamine neurons to dopamine agonist administration
Authors: Kelland Mark D. , Freeman Arthur S. , Chiodo Louis A. 
Published: January 2005

AbstractSingle‐unit electrophysiological recording techniques were used to sample the basal activity of antidromically identified nigrostriatal and mesoaccumbens dopamine (NSDA and MADA, respectively) neurons and to examine the responsiveness of these cells to dopamine agonist‐induced inhibition of cell firing rate in either chloral hydrate‐anesthetized or paralyzed rats. Paralyzed rats exhibited a greater percentage of burst‐firing cells (69%) than did anesthetized animals (37%). Furthermore, paralyzed rats were less sensitive to the mixed D1/D2 DA receptor agonist apomorphine and the selective D2 DA receptor agonist quinpirole. However, significantly higher doses of d‐amphetamine were required in paralyzed animals only with respect to inhibiting MADA neurons. The abilities of apomorphine and quinpirole to inhibit NSDA cell firing were rate‐dependent in both anesthetized and paralyzed rats, whereas d‐amphetamine‐induced inhibition was rate dependent only in anesthetized animals. In contrast, apomorphine‐ and quinpirole‐induced inhibition of MADA neurons were rate‐dependent only in anesthetized rats, whereas d‐amphetamine‐induced inhibition was rate‐dependent only in paralyzed animals. These results suggest that general anesthesia exerts subtle effects on the basal activity and pharmacological responsiveness of midbrain dopamine neurons.
Afferent axons from the antenna influence the number and placement of intrinsic synapses in the antennal lobes of Manduca sexta
Authors: Tolbert Leslie P. 
Published: January 2005

AbstractThe present study compares the placement and frequency of occurrence of synapses in normally developing antennal lobes of the brain of the moth Manduca sexta and in lobes developing in the absence of afferent axons from the antenna. The antennal lobes develop during the metamorphosis from larva to moth, and require antennal afferent input to develop their characteristic knots of synaptic neuropil, the glomeruli, that are arrayed around a central core of coarse neuropil. Synapses begin to form throughout the neuropil of the antennal lobe before ingrowth of antennal axons into the lobe. During normal development, almost all synapses (those among intrinsic neurons as well as those made by antennal afferent axons) become segregated into glomeruli as the glomeruli are established. Thus, in normal mature lobes, the radial segregation between synaptic (glomerular) and nonsynaptic (central) regions is virtually complete. In lobes that have never been allowed to receive antennal axons, an outer ring of “protoglomerular” neuropil develops in place of the glomeruli. A similar segregation of synaptic and nonsynaptic regions occurs, with two major differences: the frequency of synapses that develops in the outer ring of fine‐textured neuropil is almost 50% higher than in normal glomeruli, and the small number of synapses that occur in the coarse central neuropil now occur on aberrant fine processes in that neuropil. Apparently, in the absence of their normal massive input from the antenna, elements intrinsic to the antennal lobe are induced to form extra synapses with each other, and to send aberrant fine branches to synapse in a region of neuropil normally containing predominantly large‐caliber neurite trunks and few synapses.
Antagonism of ethanol effects by Ro 15‐4513: An electrophysiological analysis
Authors: Marrosu Francesco , Carcangiu Giampaolo , Passino Nicola , Aramo Stefano , Mereu Giampaolo 
Published: January 2005

AbstractEthanol (ETH) and general anesthetics have been reported to facilitate the chloride channel opening, possibly, or at least partly, through an interaction with the GABA‐benzodiazepine (BZ) receptor‐gated chloride ionophore “supramolecular complex”. Recently Ro 15‐4513, a novel BZ ligand, has been indecated as a potent and selective antagonist of various ETH‐induced behavioral and biochemical effects. However, since its precise characterization is still a matter of debate, we have tested and compared the effect of Ro 15‐4513, as well as its antagonism against ETH, in two objective electrophysiological parameters, i.e., the electroencephalograph (EEG) pattern in freely moving rats and single unit activity of reticulata neurons.Ro 15‐4513 produced an EEG state of alertness and antagonized the behavioral impairment and the EEG deterioration by ETH. However, while its protective action was consistent against moderate doses (2 g/kg) of ETH, it was much less evident versus higher doses. (4 and 8 g/kg).On reticulata cells, Ro 15‐4513 potently stimulated their spontaneous firing and reversed the depression by both ETH and Na‐pentobarbital. Moreover, the ß‐carboline DMCM also had similar effects.The “pure” BZ antagonist Ro 15‐1788 was completely inefective against ETH, yet fully cancelled the reversing actions of Ro 15‐4513 and DMCM upon ETH or Na‐pentobarbital effects.It is concluded that Ro 15‐4513 behaves as a BZ inverse agonist, so that its opposition to ETH and Na‐pentobarbital is probably the result of its “negative” coupling with the BZ recognition site that triggers the closing of chloride channels. It suggests that BZ inverse agonists might constitute, in the near future, a new class of analeptic drugs.
Primary afferent excitatory transmission recorded intracellularly in vitro from rat medial vestibular neurons
Authors: Lewis Michael R. , Phelan Kevin D. , Shinnick‐Gallagher Patricia , Gallagher Joel P. 
Published: January 2005

AbstractIntracellular recordings were made from rat medial vestibular nucleus (MVN) neurons in transverse brain slices containing the root of the vestibular nerve (N. VIII). Electrical stimuli applied to the N. VIII tract evoked an orthodromic excitatory postsynaptic potential (EPSP) that lasted about 50 ms following a 0.5 to 1.5 ms delay between the stimulus artifact and synaptic potential. These orthodromic EPSPs were insensitive to the following antagonists: atropine, hexamethonium, dephenhydramine, and caffeine. Based on these results we conclude that the primary afferent excitatory transmitter is not acetylcholine, histamine, or adenosine, respectively. However, kynurenic acid, a general excitatory amino acid receptor antagonist, blocked the orthodromic EPSP while having no effect on the resting membrane potential, input resistance, or action potential configuration of MVN neurons. Our data suggest that an excitatory amino acid, or amino acid‐like substance, is responsible for primary afferent excitatory transmission in the rat medial vestibular nucleus.
Age‐dependent effects of 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP): Correlation with monoamine oxidase‐B
Authors: Walsh Sharon L. , Wagner George C. 
Published: January 2005

AbstractThe effects of 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP) administration on whole brain dopamine content and monoamine oxidase subtype B (MAO‐B) activity were assessed in Swiss‐Webster male mice. Groups of mice at six different ages (1,2,4,8,16, and 52 weeks) were treated with either MPTP(12.5 mg/kg) every 2 hours for four subcutaneous injections or with the saline vehicle in the same injection volume. A third group of subjects was untreated and sacrificed at the same ages. The animals were sacrificed 1 week following treatment. The brains were removed and divided into right and left halves. The right brain halves from all subjects of a given age were assayed for MAO‐B activity. The left brain halves were assayed for dopamine content using high performance liquid chromatography.The results revealed a significant age‐dependent increase in both dopamine content and MAO‐B activity in the untreated controls. It was also found that the toxic effect of MPTP as measured by whole brain dopamine depletion was increased at each successive age tested. There was a significant correlation (r = + 0.96) between the baseline levels of MAO‐B activity and the degree of lesion induced by MPTP treatment. These results indicate that the increased sensitivity to MPTP reported in aged animals may, in part, be attributable to the increase in MAO‐B activity in older animals.
Fade of the response to prolonged glutamate application in the rat hippocampal slice
Authors: Cole Alison E. , ffrench‐Mullen Jarlath M. H. , Fisher Robert S. 
Published: January 2005

AbstractThe effect of prolonged glutamate (GLU) application was examined on 60 CA1 pyramidal neurons in the in vitro rat hippocampal slice preparation. Continuous application of L‐GLU, either by bath perfusion (0.5–2mM) of the slices or iontophoresis (200 mM) into the dendritic region of the neurons, elicited a transient depolarization which faded to a mean of 53% of the initial peak amplitude despite continued exposure to the agonist. Membrane depolarization to aspartate (ASP) and the d‐isomer of GLU also faded with time. In contrast, the depolarizing response to the excitatory amino acid agonists N‐methyl‐D, L‐aspartate (NMA), quisqualate (QUIS), and kainate (KA) did not fade significantly during continuous application. The fade of the GLU depolarization was not affected by the NMDA antagonist D‐2‐amino‐5‐phosphonovalerate (APV) or by blocking synaptic transmission with tetrodotoxin. At the time of maximum fade of the GLU depolarization, there was no change in input resistance or GLU reversal potential. In addition, fade of the response was not a consequence of changes in extracellular potassium concentration, GLU uptake mechanisms, or the electrogenic pump. The most likely explanation for fade is postsynaptic receptor desensitization.
Colocalization of taurine‐ and cysteine sulfinic acid decarboxylase‐like immunoreactivity in the hippocampus of the rat
Authors: Magnusson Kathy Ruth , Clements Jane Reichert , Wu Jang‐Yen , Beitz Alvin James 
Published: January 2005

AbstractIt is proposed that taurine is an inhibitory neurotransmitter/neuromodulator in the CNS. The present study localized taurine‐containing neurons within the rat hippocampus with the use of a monoclonal antibody against conjugated taurine (Tau2) in conjuction with an antiserum against cysteine sulfinic acid decarboxylase (CSADC), a synthesizing enzyme for taurine. Taurine‐like immunoreactivity (Tau‐LI) and CSADC‐LI were colocalized in neurons of the dentate gyrus, CA1(/CA2), CA3, and CA4. Of all the cells examined, pyramidal basket cells within the granule cell layer of the dentate gyrus were most intensely stained with both Tau2 and CSADC. Granule cells were also double‐labeled with Tau‐LI and CSADC‐LI Cell nuclei and dendrites in the CA1 region stained more intensely with Tau2 than somata. CSADC‐LI was colocalized with Tau‐LI within these neurons. Light staining with both Tau2 and the CSADC antiserum was inconsistently present in CA3 and CA4 neurons and was found to be highly dependent on the type of fixation and delay to fixation. Tau‐LI was more consistently present in increased numbers of neurons in CA3 when glutaraldehyde was added to the paraformaldehyde fixative solution. Hippocampi which were immersion‐fixed in paraformaldehyde following a 0‐, 6‐, or 24‐hour postmortem delay exhibited a lack of Tau2 staining in the CA3 region in the majority of animals studied, similar to some paraformaldehyde perfusion‐fixed rats. These studies suggest that taurine was present in the majority of neurons within the major cell layers of the rat hippocampus, but Tau‐LI was more easily lost from neurons in the CA3 region following delay to fixation. The localization of Tau‐LI in excitatory neurons such as granule cells and pyramidal cells is not consistent with its proposed inhibitory transmitter role. However, the prominent Tau2 staining in dendrites of the CA1 region provides anatomical support for the hypothesis that taurine may be released from dendrites in the CA1 region and may function as a neuromodulator of calcium flux in these pyramidal neurons.
Motor effects of two sigma ligands mediated by nigrostriatal dopamine neurons
Authors: Goldstein Susanne R. , Matsumoto Rae R. , Thompson Tina L. , Patrick Robert L. , Bowen Wayne D. , Walker J. Michael 
Published: January 2005

Abstract(+)‐Pentazocine, a potent sigma ligand that lacks affinity for PCP receptors, produced dose‐dependent contralateral circling behavior following microinjections in the substantia nigra of rats. This effect was attenuated by 6‐hydroxydopamine (6‐OHDA) lesions of ascending dopamine neurons and enhanced by systemic injections of amphetamine. 6‐OHDA lesions also attenuated the circling produced by another selective sigma ligand, 1,3‐di‐o‐tolylguanidine (DTG). These findings suggest that sigma receptors are involved in the neural control of movement and the regulation of the ascending dopamine system. Since all typical antipsychotic drugs tested bind to sigma receptors with Ki values less than 1 μM, these findings further suggest that sigma receptors may mediate some of the motor side effects of antipsychotic drug therapy.