bluuebunny/crossref_metadata_2025_split huggingface dataset:
Features of mono‐ and multinucleated bone resorbing cells of the zebrafish Danio rerio and their contribution to skeletal development, remodeling, and growth
Authors: Witten P. Eckhard , Hansen Anne , Hall Brian K. 
Published: October 2004

AbstractTo provide basic data about bone resorbing cells in the skeleton during the life cycle of Danio rerio, larvae, juveniles, and adults (divided into six age groups) were studied by histological procedures and by demonstration of the osteoclast marker enzyme tartrate‐resistant acid phosphatase (TRAP). Special attention was paid to the lower jaw, which is a standard element for fish bone studies. The presence of osteoclasts at endosteal surfaces of growing bones of all animals older than 20 days reveals that resorption is an important part of zebrafish skeletal development. The first bone‐resorbing cells to form are mononucleated. They appear in 20‐day‐old animals concurrently in the craniofacial skeleton and vertebral column. Mononucleated osteoclasts are predominant in juveniles. Regional differences characterize the appearance of osteoclasts; at thin skeletal elements (neural arches, nasal) mononucleated osteoclasts are predominant even in adults. Multinucleated bone‐resorbing cells were first observed in 40‐day‐old animals and are the predominant osteoclast type of adults. Both mono‐ and multinucleated osteoclasts contribute to allometric bone growth but multinucleated osteoclasts are also involved in lacunar bone resorption and repeated bone remodeling. Resorption of the dentary follows the pattern described above (mononucleated osteoclasts precede multinucleated cells) and includes the partial removal of Meckel's cartilage. Bone marrow spaces created by resorption are usually filled with adipose tissue. In conclusion, bone resorption is primarily subjected to the demands of growth, the appearance of mono‐ and multinucleated osteoclasts is site‐ and age‐related, and bone remodeling occurs. The results are discussed in relation to findings in other teleosts and in mammals. J. Morphol. 250:197–207, 2001. © 2001 Wiley‐Liss, Inc.
In vivo cellular uptake of glutamate is impaired in the rat hippocampus during and after transient cerebral ischemia: A microdialysis extraction study
Authors: Bruhn Torben , Christensen Thomas , Diemer Nils Henrik 
Published: October 2004

AbstractUsing microdialysis in CA1 of the rat hippocampus, we studied the effect of transient cerebral ischemia on in vivo uptake and on extracellular levels of glutamate during, and at different time points after ischemia. 3H‐D‐aspartate (test substance), and 14C‐mannitol (reference substance), were added to the dialysis perfusate, and the cellular extraction of 3H‐D‐aspartate was calculated from scintillation analysis of fractionated dialysate samples. The extraction of 3H‐D‐aspartate was studied both in a tracer like condition with a perfusate concentration of 0.2 μM, and in a condition of high saturation level, with 1.0 mM D‐aspartate added to the perfusate. In between radioisotope perfusions, dialysate was sampled for analysis of amino acid content by HPLC. During ischemia, extraction of 3H‐D‐aspartate (0.2 μM) declined to a maximum reduction of 68%. In the hours after ischemia, extraction of 3H‐D‐aspartate (0.2 μM) was decreased by 32%. In the days after ischemia, there was a progressive decline in extraction of 3H‐D‐aspartate (1.0 mM), reaching a reduction of 89% on Day 4 after ischemia. Extracellular glutamate remained at control levels at all time points after ischemia. The present study is the first to investigate uptake of glutamate in the intact rat brain in relation to cerebral ischemia. Evidence is provided that uptake of Glu is restrained during ischemia, and that in the hours after ischemia, the extracellular turnover of glutamate is decreased. In the course of the days after ischemia, degeneration of CA1 pyramidal cells occurs concomitantly with a progressive decline in glutamate transport ability, possibly of pathogenetic importance to CA1 pyramidal cell loss. J Neurosci. Res. 66:1118–1126, 2001. © 2001 Wiley‐Liss, Inc.
Polyamine metabolism and glutamate receptor agonists‐mediated excitotoxicity in the rat brain
Authors: Camón L. , de Vera N. , Martínez E. 
Published: October 2004

AbstractPutrescine (PUT) increases have been seen in a range of models of neuropathological disturbances. The present study was designed to compare the ability of various types of glutamate receptor agonist to promote excitotoxic brain damage and to examine whether a PUT increase is a general marker of excitotoxic brain damage. To that end, we evaluated features of brain damage associated with the excitotoxicity induced by both ionotropic glutamate receptor (iGluR) and metabotropic glutamate receptor (mGluR) agonists in the conscious rat and the changes produced in the regulation of polyamine metabolism. Intracerebroventricular infusion of N‐methyl‐D‐aspartate (NMDA; 80 nmol), α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid (AMPA; 15 nmol), kainic acid (KA; 2.3 nmol), (R,S)‐3,5‐dihydroxyphenylglycine (3,5‐DHPG; 1.5 μmol), and (1S,3R)‐1‐aminocyclopentane‐1,3‐dicarboxylic acid (1S,3R‐ACPD; 2 μmol) produced similar seizure incidences (76–84%) in the rat. The convulsant episodes appeared sooner after iGluR (13–22 min) than after mGluR agonists (50–179 min). Histological analysis of the hippocampus 24 hr after seizures indicated several degrees of excitotoxic injury after equiconvulsive doses of the iGluR and mGluR agonists assayed. The agonists can be placed in the following order, according to the degree of damage they produce: AMPA > 3,5‐DHPG ≃ KA > NMDA > 1S,3R‐ACPD. In the frontal cortex, moderate to low levels of damage were observed after all GluR agonists. Both iGluR‐ and mGluR‐induced seizures produced an overshoot in the hippocampal and cortical PUT concentration, whereas spermidine and spermine levels were similar to control. Moreover, a concurrence of increased PUT levels and brain damage was observed, indicating that PUT is a general marker of excitotoxic brain damage. J Neurosci. Res. 66:1101–1111, 2001. © 2001 Wiley‐Liss, Inc.
Temporospatial sequence of cellular events associated with etoposide‐induced neuronal cell death: Role of antiapoptotic protein Bcl‐XL
Authors: Kim Ji‐Eun , Han Baek S. , Choi Won‐Seok , Eom Dae‐Seok , Lee Eun‐Hee , Oh Tae H. , Markelonis George J. , Saido Takaomi C. , Lee Gun‐Eui , Chung In‐Kwon , Oh Young J. 
Published: October 2004

AbstractEtoposide‐induced death comprises such nuclear events as the formation of topoisomerase II‐DNA cleavable complex and cytosolic events including caspase activation. By first establishing the temporospatial death sequence triggered by etoposide in a neuronal cell line, MN9D overexpressing Bcl‐XL (MN9D/Bcl‐XL) or control vector (MN9D/Neo), we examined whether formation of this complex is primarily responsible for cell death and at which strategic points and how Bcl‐XL blocks etoposide‐induced neuronal death. Etoposide induced death that was dependent on caspase, cycloheximide, and calpain in MN9D/Neo cells. Etoposide also induced death in enucleated MN9D/Neo cells, although this was less severe. The level of topoisomerase II‐DNA cleavable complex reached at a maximum of 2 hr after etoposide treatment was identical in MN9D/Neo and MN9D/Bcl‐XL cells. In MN9D/Neo cells, cytochrome c release into the cytosol and caspase activation occurred as early as 2 hr and 3–6 hr after etoposide treatment, respectively. Etoposide‐induced DNA laddering potentially via caspase appeared as early as 12 hr after drug treatment, followed by nuclear swelling in MN9D/Neo cells (>18–20 hr). Subsequently, nuclear condensation started by 24–28 hr and became apparent thereafter. All of these events except for nuclear swelling were substantially blocked in MN9D/Bcl‐XL. At the later stage of cell death (<32–36 hr), a specific cleavage of Bax and fodrin appeared that was completely blocked by calpain inhibitor or by Bcl‐XL. Taken together, our data suggest that Bcl‐XL prevents etoposide‐induced neuronal death by exerting its anticaspase and anticalpain effect on cellular events after the formation of topoisomerase II‐DNA cleavable complex that may not be a major contributor to cell death. J Neurosci. Res. 66:1074–1082, 2001. © 2001 Wiley‐Liss, Inc.
Structure–function correlation in transient amacrine cells of goldfish retina: Basic and multifractal analyses of dendritic trees in distinct synaptic layers
Authors: Djamgoz M.B.A. , Krasowska M. , Martinoli O. , Sericano M. , Vallerga S. , Grzywna Z.J. 
Published: October 2004

AbstractAmacrine cells generating light‐evoked transient ON–OFF responses were stained by intracellular injection of horseradish peroxidase after determining their input–output (voltage response vs. light intensity) profiles. Ten cells specifically having bistratified dendritic trees were analyzed. The cross‐sectional area of the dendrites in each sublamina (a and b) of the inner plexiform layer was initially measured. Although some variability was observed, there was no statistically significant overall difference in the cross‐sectional areas of the dendritic trees in sublaminae a and b. Also, the amplitudes of the ON and OFF responses, generated by a midrange criterion stimulus, could not be correlated with the cross‐sectional areas or the number of branches of the dendrites in sublaminae b and a, respectively. On the other hand, determination of the generalized fractal spectra revealed that the negative (up to –3) and zero‐order fractal dimensions of the dendritic trees in sublamina a were consistently higher than those for sublamina b. Furthermore, there was a positive correlation between response amplitude and some part of the generalized fractal dimension in the respective parts of the dendritic trees. It is concluded that dendritic tree characteristics differ in the two halves of the inner plexiform layer and that these can be related to the cells' light‐evoked response amplitudes. Furthermore, generalized fractal analysis appears to be a useful method for correlating structure and function in retinal amacrine cells with complex dendritic trees. J Neurosci. Res. 66:1208–1216, 2001. © 2001 Wiley‐Liss, Inc.
Distribution of high‐voltage‐activated calcium channels in cultured γ‐aminobutyric acidergic neurons from mouse cerebral cortex
Authors: Timmermann Daniel B. , Westenbroek Ruth E. , Schousboe Arne , Catterall William A. 
Published: October 2004

AbstractThe localization of voltage‐gated calcium channel (VGCC) α1 subunits in cultured GABAergic mouse cortical neurons was examined by immunocytochemical methods. Cav1.2 and Cav1.3 subunits of L‐type VGCCs were found in cell bodies and dendrites of GABA‐immunopositive neurons. Likewise, the Cav2.3 subunit of R‐type VGCCs was expressed in a somatodendritic pattern. Cav2.2 subunits of N‐type channels were found exclusively in small varicosities that were identified as presynaptic nerve terminals based on their expression of synaptic marker proteins. Two splice variants of the Cav2.1 subunit of P/Q‐type VGCCs showed widely differing expression patterns. The rbA isoform displayed a purely somatodendritic staining pattern, whereas the BI isoform was confined to axon‐like fibers and nerve terminals. The nerve terminals of these cultured GABAergic neurons express Cav2.2 either alone or in combination with Cav2.1 (BI isoform) but never express Cav2.1 alone. The functional association between VGCCs and the neurotransmitter release machinery was probed using the FM1‐43 dye‐labeling technique. N‐type VGCCs were found to be tightly coupled to exocytosis in these cultured cortical neurons, and P‐type VGCCs were also important in a fraction of the cells. The predominant role of N‐type VGCCs in neurotransmitter release and the specific localization of the BI isoform of Cav2.1 in the nerve terminals of these neurons distinguish them from previously studied central neurons. The complementary localization patterns observed for two different isoforms of the Cav2.1 subunits provide direct evidence for alternative splicing as a means of generating functional diversity among neuronal calcium channels. © 2002 Wiley‐Liss, Inc.
Vestibular compensation after ganglionectomy: Ultrastructural study of the tangential vestibular nucleus and behavioral study of the hatchling chick
Authors: Aldrich Eric M. , Peusner Kenna D. 
Published: October 2004

AbstractThe tangential nucleus is a major part of the avian vestibular nuclear complex, and its principal cells are structurally distinctive neurons participating in the vestibuloocular and vestibulocollic reflexes. After unilateral peripheral vestibular lesion, a behavioral recovery of function defined as vestibular compensation is observed. Because sprouting and hypertrophy of synapses have been reported in other regions of immature animals after central nervous system injury, we investigated whether this also occurs in the vestibular nuclei during compensation. To test this hypothesis, unilateral vestibular ganglionectomy was performed on 4–6‐day‐old hatchlings and vestibular function was tested during the next 2 months. Degeneration and evidence for regeneration of synapses were studied in the tangential nucleus at 1, 3, 7, and 56 days after surgery. Spoon endings, large vestibular terminals on the principal somata, degenerated 1–3 days after surgery. However, the small synaptic terminals showed no significant change in the percentage or number covering the soma or in mean terminal lengths in the deafferented or contralateral tangential nucleus. Furthermore, there was no evidence of neuron death in the tangential nucleus. Vestibular compensation occurred in three stages: 0–3 days, when vestibular synapses degenerated and severe behavioral deficits were seen; 4–9 days, when primary vestibular fibers degenerated centrally and marked improvement in both the static and the dynamic symptoms were observed; and 10–56 days, when changes in neuronal morphology were not detected but the dynamic symptoms gradually improved. Accordingly, after unilateral vestibular ganglionectomy, vestibular compensation proceeded without ultrastructural evidence of sprouting or hypertrophy of axosomatic synapses in the hatchling tangential nucleus. This rapid behavioral recovery of function distinguishes the vestibular system from other sensory systems, which, in general, exhibit much less robust recovery after injury to their peripheral receptors. © 2002 Wiley‐Liss, Inc.
p27Kip1 Enhances myelin basic protein gene promoter activity
Authors: Miskimins Robin , Srinivasan Rekha , Marin‐Husstege Mireya , Miskimins W. Keith , Casaccia‐Bonnefil Patrizia 
Published: October 2004

AbstractThe process of oligodendrocyte differentiation is a complex event that requires cell cycle withdrawal, followed by the activation of a specific transcriptional program responsible for the synthesis of myelin genes. Because growth arrest precedes differentiation, we sought to investigate the role of cell cycle molecules in the activation of myelin gene promoters. We hypothesized that the cell cycle inhibitor p27Kip1, which is primarily responsible for arresting proliferating oligodendrocyte progenitors, may be involved in the transcriptional regulation of myelin genes. In agreement with this hypothesis, overexpression of p27Kip1 in the CG4 cell line, but not in 3T3 fibroblasts, enhances the expression of luciferase driven by the myelin basic protein (MBP) promoter. Interestingly, this effect is specific for p27Kip1; overexpression of other cell cycle inhibitors had no effect. Additionally, this effect is independent of halting the cell cycle; treatment with the cell cycle blocker roscovitine did not affect MBP promoter usage. We conclude that p27Kip1 contributes to oligodendrocyte differentiation by regulating transcription of the MBP gene. © 2002 Wiley‐Liss, Inc.
Upregulation of the HLH Id gene family in neural progenitors and glial cells of the rat spinal cord following contusion injury
Authors: Tzeng Shun‐Fen , Bresnahan Jacqueline C. , Beattie Michael S. , de Vellis Jean 
Published: October 2004

AbstractSpinal cord injury (SCI) leads to a complex sequence of cellular responses, including astrocyte activation, oligodendrocyte death, and ependymal cell proliferation. Inhibitors of DNA binding (Id1, Id2, Id3) belong to a helix‐loop‐helix (HLH) gene family. Id genes have been implicated in playing a vital role in the proliferation of many cell types, including astrocytes and myoblasts. In the present study, the expression of Id family members in spinal cord after contusion injury was investigated by in situ hybridization. Id1, Id2, and Id3 mRNA expression was upregulated 5 mm rostral and caudal to the lesion center, and reached maximal levels 3 days after SCI. In addition, cell populations expressing Id1, Id2, and Id3 mRNA were maximally increased 3 days after SCI. The increase in Id2 and Id3 mRNA expression and Id2 and Id3 mRNA+ cells was still observed at 8 days. The Id mRNA expressing cells were phenotyped by combining immunostaining of cell‐specific markers with in situ hybridization. Glial fibrillary acidic protein (GFAP)+ astrocytes were found to express all three Id mRNA, whereas S‐100α+ astrocytes only expressed high levels of Id2 and Id3 mRNA. Cells having a neural progenitor morphology and the marker nestin appeared after SCI and they expressed Id1, Id2, and Id3 mRNA. Interestingly, some Rip+ oligodendrocytes located in the areas close to the central canal expressed Id3 mRNA after injury. In conclusion, Id genes are upregulated in a time‐dependent manner in astrocytes, oligodendrocytes, and neural progenitor subpopulations after SCI, suggesting that they play major roles in cellular responses following SCI. J Neurosci. Res. 66:1161–1172, 2001. © 2001 Wiley‐Liss, Inc.
Auditory processing of interaural timing information: New insights
Authors: Bernstein Leslie R. 
Published: October 2004

AbstractDifferences in the time‐of‐arrival of sounds at the two ears, or interaural temporal disparities (ITDs), constitute one of the major binaural cues that underlie our ability to localize sounds in space. In addition, ITDs contribute to our ability to detect and to discriminate sounds, such as speech, in noisy environments. For low‐frequency signals, ITDs are conveyed primarily by “cycle‐by‐cycle” disparities present in the fine‐structure of the waveform. For high‐frequency signals, ITDs are conveyed by disparities within the time‐varying amplitude, or envelope, of the waveform. The results of laboratory studies conducted over the past few decades indicate that ITDs within the envelopes of high‐frequency are less potent than those within the fine‐structure of low‐frequency stimuli. This is true for both measures of sensitivity to changes in ITD and for measures of the extent of the perceived lateral displacement of sounds containing ITDs. Colburn and Esquissaud (1976) hypothesized that it is differences in the specific aspects of the waveform that are coded neurally within each monaural (single ear) channel that account for the greater potency of ITDs at low frequencies rather than any differences in the more central binaural mechanisms that serve these different frequency regions. In this review, the results of new studies are reported that employed special high‐frequency “transposed” stimuli that were designed to provide the high‐frequency channels of the binaural processor with envelope‐based information that mimics waveform‐based information normally available only in low‐frequency channels. The results demonstrate that these high‐frequency transposed stimuli (1) yield sensitivity to ITDs that approaches, or is equivalent to, that obtained with “conventional” low‐frequency stimuli and (2) yield large extents of laterality that are similar to those measured with conventional low‐frequency stimuli. These findings suggest that by providing the high‐frequency channels of the binaural processor with information that mimics that normally available only at low frequencies, the potency of ITDs in the two frequency regions can be made to be similar, if not identical. These outcomes provide strong support for Colburn and Esquissaud's (1976) hypothesis. The use of high‐frequency transposed stimuli, in both behavioral and physiological investigations offers the promise of new and important insights into the nature of binaural processing. J Neurosci. Res. 66:1035–1046, 2001. © 2001 Wiley‐Liss, Inc.
Calcium/calmodulin‐dependent protein kinase IIβ isoform is expressed in motor neurons during axon outgrowth and is part of slow axonal transport
Authors: Lund Linda M. , McQuarrie Irvine G. 
Published: October 2004

AbstractPreviously, we identified calcium/calmodulin‐dependent protein kinase IIβ (CaMKIIβ) mRNA in spinal motor neurons with 372 bp inserted in what corresponds to the “association” domain of the protein. This was interesting because known additions and deletions to CaMKIIβ mRNA are usually less than 100 bp in size and found in the “variable” region. Changes in the association domain of CaMKIIβ could influence substrate specificity, activity or intracellular targeting. We show that three variations of this insert are found in CNS neurons or sciatic motor neurons of Sprague–Dawley rats. We used PCR and nucleic acid sequencing to identify inserts of 114, 243, or 372 bases. We also show that addition of the 372 bases is associated with outgrowth of the axon (the standard CaMKIIβ downregulates when axon outgrowth occurs). Radiolabeling, immunoblots, and 2D PAGE identified this larger CaMKIIβ as part of the group of soluble proteins moving at the slowest rate of axonal transport (SCa) in sciatic motor neurons (∼1 mm/day). This group is composed mainly of structural proteins (e.g., tubulin) used to assemble the cytoskeleton of regrowing axons. Published 2002 Wiley‐Liss, Inc.
Glial transporters for glutamate, glycine, and GABA III. Glycine transporters
Authors: Gadea Ana , María López‐Colomé Ana 
Published: October 2004

AbstractGlial cells possess transport systems for the three major amino acid neurotransmitters glutamate, γ‐aminobutyric acid (GABA) and glycine, involved in the arrest of neurotransmission mediated by these compounds. Two glycine transporters have been cloned: GLYT1, mainly expressed by glial cells and shown to colocalize with NMDA receptors, and GLYT2, exclusively expressed by neurons and colocalized with the inhibitory glycine receptors. The way in which the regulation of extracellular glycine concentration by glial glycine transporters affects physiological and pathological conditions is discussed. The presence, differential pharmacology and specific regulation of glycine transporters in glial cells strongly support an important role for glia in the modulation of both, excitatory and inhibitory neurotransmission. J. Neurosci. Res. 64:218–222, 2001. © 2001 Wiley‐Liss, Inc.
Absence of hippocampal mossy fiber sprouting in transgenic mice overexpressing brain‐derived neurotrophic factor
Authors: Qiao Xiaoxi , Suri Chitra , Knusel Beat , Noebels Jeffrey L. 
Published: October 2004

AbstractExcess neuronal activity upregulates the expression of two neurotrophins, nerve growth factor (NGF) and brain‐derived neurotrophic factor (BDNF) in adult hippocampus. Nerve growth factor has been shown to contribute the induction of aberrant hippocampal mossy fiber sprouting in the inner molecular layer of the dentate gyrus, however the role of prolonged brain‐derived neurotrophic factor exposure is uncertain. We examined the distribution and plasticity of mossy fibers in transgenic mice with developmental overexpression of brain‐derived neurotrophic factor. Despite 2–3‐fold elevated BDNF levels in the hippocampus sufficient to increase the intensity of neuropeptide Y immunoreactivity in interneurons, no visible changes in mossy fiber Timm staining patterns were observed in the inner molecular layer of adult mutant hippocampus compared to wild‐type mice. In addition, no changes of the mRNA expression of two growth‐associated proteins, GAP‐43 and SCG‐10 were found. These data suggest that early and persistent elevations of brain‐derived neurotrophic factor in granule cells are not sufficient to elicit this pattern of axonal plasticity in the hippocampus. J. Neurosci. Res. 64:268–276, 2001. © 2001 Wiley‐Liss, Inc.