bluuebunny/crossref_metadata_2025_split huggingface dataset:
Acute effects of desmin mutations on cytoskeletal and cellular integrity in cardiac myocytes
Authors: Haubold Kurt , Herrmann Harald , Langer Stephen J. , Evans Robert M. , Leinwand Leslie A. , Klymkowsky Michael W. 
Published: January 2003

AbstractMutations in desmin have been associated with a subset of human myopathies. Symptoms typically appear in the second to third decades of life, but in the most severe cases can manifest themselves earlier. How desmin mutations lead to aberrant muscle function, however, remains poorly defined. We created a series of four mutations in rat desmin and tested their in vitro filament assembly properties. RDM‐G, a chimera between desmin and green fluorescent protein, formed protofilament‐like structures in vitro. RDM‐1 and RDM‐2 blocked in vitro assembly at the unit‐length filament stage, while RDM‐3 had more subtle effects on assembly. When expressed in cultured rat neonatal cardiac myocytes via adenovirus infection, these mutant proteins disrupted the endogenous desmin filament to an extent that correlated with their defects in in vitro assembly properties. Disruption of the desmin network by RDM‐1 was also associated with disruption of plectin, myosin, and α‐actinin organization in a significant percentage of infected cells. In contrast, expression of RDM‐2, which is similar to previously characterized human mutant desmins, took longer to disrupt desmin and plectin organization and had no significant effect on myosin or α‐actinin organization over the 5‐day time course of our studies. RDM‐3 had the mildest effect on in vitro assembly and no discernable effect on either desmin, plectin, myosin, or α‐actinin organization in vivo. These results indicate that mutations in desmin have both direct and indirect effects on the cytoarchitecture of cardiac myocytes. Cell Motil. Cytoskeleton 54:105–121, 2003. © 2003 Wiley‐Liss, Inc.
Centrosome and spindle pole body dynamics: A review of the EMBO/EMBL Conference on Centrosomes and Spindle Pole Bodies, Heidelberg, September 13–17, 2002
Authors: Palazzo Robert E. 
Published: January 2003

AbstractFive years after the first meeting held on Centrosomes and Spindle Pole Bodies, a second meeting was organized by Tano Gonzalez, Eric Karsenti, Kip Sluder, and Mark Winey in Heidelberg, Germany. Sponsored by the gracious European community (EMBO/EMBL), the meeting was both spectacular and exhausting. The wealth of information delivered, the plethora of model systems and unique approaches described, and the free exchange of information by a cooperative and excited community of scientists overwhelmed all participants. Even the best prepared scholars could not have anticipated the avalanche of data and insights that poured from the presentations from beginning to end. Daily posters by young and senior scientists added dimension to round out the well‐planned series of presentations. The meeting began with opening remarks by Eric Karsenti and Michel Bornens who reminded participants of the historical questions of the field. Where does the centrosome come from? What are the mechanisms that control centrosome assembly and duplication? How is duplication coordinated with the cell cycle? Why do some cells have centrosomes, while others do not? What are the components of the centrosome? Does the centrosome play an important role in disease?
EROICA: Exploring regions of interest with cluster analysis in large functional magnetic resonance imaging data sets
Authors: Jarmasz M. , Somorjai R.L. 
Published: January 2003

AbstractWe describe a divide and conquer strategy for an exploratory data analysis (EDA) of large functional magnetic resonance imaging (fMRI) data sets. The need for an EDA to precede and complement a confirmatory model‐based analysis is now well established. For complex fMRI experiments, where a prior model of the expected response cannot be posited, the sole option is to conduct an initial EDA. An EDA often discovers unanticipated behavior, allowing the experimenter to augment or even change the original hypothesis. In addition, the gross artifact behavior that EDA makes evident may aid the experimenter in deciding whether the data set is even usable, some additional preprocessing step is required, or the one used has introduced spurious effects. The proposed strategy, named EROICA for exploring regions of interest with cluster analysis, evolved from an empirical observation that a typical cluster of activation or artifact time series can be partitioned into three subsets: time series corrupted by significant trends and time series above and below some noise level. Moreover, the sought‐after common temporal behavior among the cluster time series can be extracted in an uncorrupted form from the above noise level time series alone. Thus, the key feature of EROICA is the initial partition of the data set into trendy and below the noise level time series, followed by the fuzzy cluster analysis (FCA) of the above the noise level time series to extract common cluster behavior patterns (centroids). The initial partition is based on a test statistic in the power spectrum domain. This step has significant ramifications: it greatly speeds up the FCA because of the much smaller number of time series to cluster; it makes the clustering results more robust because they are no longer affected by the trendy and noisy time series; the above the noise level time series can be further grouped according to the location of the spectral peak on the frequency axis, and these groups can be used to create a subset of initial centroids that greatly improves the convergence rate of the FCA; and the group of below the noise level time series (referred to as the noise pool) can be used as a data‐driven representation of the underlying noise source. In the final step, each time series is modeled as a linear combination of the closest centroid plus noise. The noise pool is very convenient for obtaining thresholds when testing the significance of the model parameter without having to model or assume the distributional properties of the underlying noise source. To limit the number of false positives in the activation maps, the significance test also tests the time series power spectrum values at the frequency locations determined by the cluster centroid. EROICA is one of the analysis options offered by the general image‐processing package EvIdent®. © 2003 Wiley Periodicals, Inc. Concepts Magn Reson 16A: 50–62, 2003
Activation and deactivation in blood oxygenation level dependent functional magnetic resonance imaging
Authors: Frankenstein Uta , Wennerberg Anders , Richter Wolfgang , Bernstein Charles , Morden Dara , Rémy Florence , Mcintyre Michael 
Published: January 2003

AbstractDecreases in the blood oxygenation level dependent signal are somewhat puzzling for several reasons. The first is the synaptic complexity in interactive networks, and the second involves the interplay between oxidative demand and perfusion in producing signal change. The third reason involves the relativity of both activation and deactivation to the choice of the baseline condition. The fourth is that deactivations could reflect passive shunting of blood to activating areas as easily as they reflect active inhibition. However, understanding deactivations is necessary to fully understand how excitation and inhibition affect functional images. We propose strategies using convergent experiments as a means of elucidating the nature of deactivations. © 2003 Wiley Periodicals, Inc. Concepts Magn Reson 16A: 63–70, 2003
Synaptic connections of distinct interneuronal subpopulations in the rat basolateral amygdalar nucleus
Authors: Muller Jay F. , Mascagni Franco , Mcdonald Alexander J. 
Published: January 2003

AbstractAlthough it is well established that the activity of pyramidal projection neurons in the basolateral amygdala (ABL) is controlled by γ‐aminobutyric acid (GABA)ergic inhibitory interneurons, very little is known about the connections of specific interneuronal subpopulations in this region. In the present study, immunohistochemical techniques were used at the light and electron microscopic levels to identify specific populations of interneurons and to analyze their connections with each other and with unlabeled presumptive pyramidal neurons. Double‐labeling immunofluorescence experiments revealed that antibodies to vasoactive intestinal peptide (VIP) and calbindin‐D28K (CB) labeled two separate interneuronal subpopulations in the ABL. Light microscopic double‐labeling immunoperoxidase experiments demonstrated that many VIP‐positive (VIP+) axon terminals formed intimate synaptic‐like contacts with the CB‐positive (CB+) neurons and that both CB+ and VIP+ terminals often contributed to the formation of pericellular baskets that surrounded unlabeled perikarya of pyramidal neurons. By using a dual immunoperoxidase/immunogold‐silver procedure at the ultrastructural level, it was found that 30% of VIP+ terminals in the anterior subdivision of the basolateral nucleus innervated interneurons that were either CB+ (25%) or VIP+ (5%). A smaller percentage (15%) of CB+ terminals formed synapses with labeled interneurons. Both VIP+ and CB+ terminals also innervated unlabeled perikarya, dendrites, and spines, most of which probably belonged to pyramidal neurons. The interconnections between interneurons may be important for disinhibitory mechanisms and the mediation of rhythmic oscillations in the ABL. J. Comp. Neurol. 456:217–236, 2003. © 2003 Wiley‐Liss, Inc.
Transient cochlear ischemia causes delayed cell death in the organ of Corti: An experimental study in gerbils
Authors: Koga Kenichiro , Hakuba Nobuhiro , Watanabe Futoshi , Shudou Masachika , Nakagawa Takayuki , Gyo Kiyofumi 
Published: January 2003

AbstractTo elucidate whether ischemia–reperfusion can cause delayed cell death in the cochlea, the effects of transient cochlear ischemia on hearing and on neuronal structures in the cochlea were studied in Mongolian gerbils. Ischemia was induced by bilaterally occluding the vertebral arteries for 5 minutes in gerbils, which lack posterior cerebral communicating arteries. In gerbils, the labyrinthine arteries are fed solely by the vertebral arteries. Occlusion of the vertebral arteries caused a remarkable increase in the threshold of compound action potentials (CAPs), which recovered over the following day. However, 7 days after the onset of reperfusion, the threshold began to increase again. Morphologic changes in the hair cell stereocilia were revealed by electron microscopy. The number of nuclear collapses was counted in cells stained for DNA and F‐actin to evaluate the degree of cell death in the organ of Corti. Changes in spiral ganglion cell (SGC) neuron number were detected, whether or not progressive neuronal death occurred in the SGC. These studies showed that sporadic fusion of hair cells and the disappearance of hair cell stereocilia did not begin until 4 days after ischemia. On subsequent days, the loss of hair cells, especially inner hair cells (IHCs), and the degeneration of SGC neurons became apparent. Ten days after ischemia, the mean percentage cell loss of IHCs was 6.4% in the basal turn, 6.4% in the second turn, and 0.8% in the apical turn, respectively, and the number of SGC neurons had decreased to 89% of preischemic status. These results indicate that transient ischemia causes delayed hearing loss and cell death in the cochlea by day 7 after ischemia. J. Comp. Neurol. 456:105–111, 2003. © 2002 Wiley‐Liss, Inc.
Molecular mapping of the origin of postnatal spinal cord ependymal cells: Evidence that adult ependymal cells are derived from Nkx6.1+ ventral neural progenitor cells
Authors: Fu Hui , Qi Yingchuan , Tan Min , Cai Jun , Hu Xuemei , Liu Zijing , Jensen Jan , Qiu Mengsheng 
Published: January 2003

AbstractRecent studies have suggested that the ependymal cells lining the central canal of postnatal spinal cord possess certain properties of neural stem cells. However, the embryonic origin and developmental potential of the postnatal spinal cord ependymal cells remain to be defined. In this report, we investigated the developmental origin of postnatal spinal ependymal cells by studying the dynamic expression of several neural progenitor genes that are initially expressed in distinct domains of neuroepithelium in young embryos. At later stages of development, as the ventricular zone of the embryonic spinal cord is reduced, expression of Nkx6.1 progenitor gene is constantly detected in ependymal cells throughout chick and mouse development. Expression of other neural progenitor genes that lie either dorsal or ventral to the Nkx6.1+ domain is gradually decreased and eventually disappeared. These results suggest that the remaining neuroepithelial cells at later stages of animal life are derived from the Nkx6.1+ ventral neuroepithelial cells. Expression of Nkx6.1 in the remaining neuroepithelium is closely associated with, and regulated by, Shh expression in the floor plate. In addition, we suggested that the Nkx6.1+ ependymal cells in adult mouse spinal cords may retain the proliferative property of neural stem cells. J. Comp. Neurol. 456:237–244, 2003. © 2003 Wiley‐Liss, Inc.
EphA family gene expression in the developing mouse neocortex: Regional patterns reveal intrinsic programs and extrinsic influence
Authors: Yun Mihae E. , Johnson Randall R. , Antic Anica , Donoghue Maria J. 
Published: January 2003

AbstractParcellation of the mammalian cerebral cortex into distinct areas is essential for proper cortical function; however, the developmental program that results in the genesis of distinct areas is not fully understood. We examined the expression of members of the EphA family—the EphA receptor tyrosine kinases and the ephrin‐A ligands—within the developing mouse cerebral cortex, with the aim of characterizing this component of the molecular landscape during cortical parcellation. We found that specific embryonic zones, such as the ventricular, subventricular, intermediate, subplate, and marginal zones, as well as the cortical plate, were positive for particular EphA genes early in corticogenesis (E12–E15). Along with this zone‐selective expression, several genes (EphA3, EphA4, EphA5) were evenly expressed along the axes of the developing cortex, whereas one family member (EphA7) was expressed in a distinct anteroposterior pattern. Later in corticogenesis (E16–E18), other EphA family members became selectively expressed, but only within the cortical plate: EphA6 was present posteriorly, and ephrin‐A5 was expressed within a middle region. At birth, patterning of EphA gene expression was striking. Thus, we found that the expression of a single EphA gene or a combination of family members can define distinct embryonic zones and anteroposterior regions of the neocortex during development. To examine whether cellular context affects the patterning of EphA expression, we examined gene expression in embryonic cortical cells grown in vitro, such that all cellular contacts are lacking, and in Mash‐1 mutant mice, in which thalamocortical connections do not form. We found that the expression patterns of most EphA family members remained stable in these scenarios, whereas the pattern of ephrin‐A5 was altered. Taken together, this work provides a comprehensive picture of EphA family expression during mouse corticogenesis and demonstrates that most EphA expression profiles are cell intrinsically based, whereas ephrin‐A5 is plastically regulated. J. Comp. Neurol. 456:203–216, 2003. © 2003 Wiley‐Liss, Inc.
Zonal organization of the vestibulocerebellum in pigeons (Columba livia): I. Climbing fiber input to the flocculus
Authors: Winship Ian R. , Wylie Douglas R.W. 
Published: January 2003

AbstractPrevious studies in pigeons have shown that the neurons in the medial column of the inferior olive respond best to patterns of optic flow resulting from self‐rotation. With respect to the axis of rotation, there are two functional groups: rVA neurons prefer rotation about the vertical axis, whereas rH45 neurons respond best to rotation about an horizontal axis oriented at 45 degrees ipsilateral azimuth. The rVA and rH45 neurons are located in the caudal and rostral margins of the medial column, respectively. These olivary neurons project as climbing fibers to the contralateral flocculus. In this study, injections of anterograde tracers into the medial column were used to investigate the zonal organization of the climbing fiber input to the flocculus of pigeons. Iontophoretic injections of either cholera toxin subunit‐B or biotinylated dextrin amine were made into the medial column of the inferior olive at locations responsive to rVA or rH45 rotational optic flow. Anterogradely labeled climbing fibers in the flocculus showed a clear zonal organization. There were four parasagittal bands spanning both folia IXcd and X consisting of two rVA zones interdigitated with two rH45 zones. These findings are compared with the zonal organization of the flocculus in mammalian species. J. Comp. Neurol. 456:127–139, 2003. © 2002 Wiley‐Liss, Inc.
Zonal organization of the vestibulocerebellum in pigeons (Columba livia): II. Projections of the rotation zones of the flocculus
Authors: Wylie Douglas R.W. , Brown Matthew R. , Barkley Ryan R. , Winship Ian R. , Crowder Nathan A. , Todd Kathryn G. 
Published: January 2003

AbstractPrevious neurophysiologic research in birds and mammals has shown that there are two types of Purkinje cells in the flocculus. The first type shows maximal modulation in response to rotational optokinetic stimulation about the vertical axis (rVA neurons). The second type shows maximal modulation in response to rotational optokinetic stimulation about a horizontal axis oriented 45 degrees to contralateral azimuth (rH45c neurons). In pigeons, the rVA and rH45c are organized into four alternating parasagittal zones. In this study we investigated the projections of Purkinje cells in the rVA and rH45c zones by using the anterograde tracers biotinylated dextran amine and cholera toxin subunit B. After iontophoretic injections of tracers into the rH45c zones, heavy anterograde labeling was found in the infracerebellar nucleus and the medial margin of the superior vestibular nucleus. Some labeling was also consistently observed in the lateral cerebellar nucleus and the dorsolateral vestibular nucleus. After injections into the rVA zones, heavy anterograde labeling was found in the medial and descending vestibular nuclei, the nucleus prepositus hypoglossi, and the central region of the superior vestibular nucleus. Less labeling was seen in the tangential nucleus, the dorsolateral vestibular nucleus, and the lateral vestibular nucleus, pars ventralis. These results are compared and contrasted with findings in mammalian species. J. Comp. Neurol. 456:140–153, 2003. © 2002 Wiley‐Liss, Inc.
Developmental relationship between cholinergic amacrine cell processes and ganglion cell dendrites of the mouse retina
Authors: Stacy Rebecca Colleen , Oi Lun Wong Rachel 
Published: January 2003

AbstractGanglion cells of the mammalian retina undergo structural remodeling before their dendrites are confined to functionally distinct laminas within the inner plexiform layer. It has been proposed that cholinergic amacrine cells provide laminar cues that remodel ganglion cell dendrites, because their processes stratify before those of the ganglion cells. To address this possibility, it is necessary to know whether cholinergic cells contact all or only some classes of ganglion cells during development. We, therefore, used two‐photon microscopy to simultaneously reconstruct the dendritic arbors of different classes of ganglion cells and terminal processes of cholinergic cells in neonatal mouse retina. We determined that, after birth, cholinergic cells contacted only a subset of ganglion cells. Large bistratified cells (LBCs), resembling direction selective ganglion cells in other species, had dendrites that fasciculated with the cholinergic plexuses. The LBCs received numerous presynaptic cholinergic contacts shortly after birth. In contrast, large monostratified cells (LMCs), ramifying outside the cholinergic plexuses at maturity, received few, if any, cholinergic contacts even at early stages when their dendrites overlapped with the cholinergic processes. These observations suggest that cholinergic cells provide laminar cues for only subsets of ganglion cells. They also indicate that the synaptic organization between amacrine and ganglion cells may be specified early in development. J. Comp. Neurol. 456:154–166, 2003. © 2002 Wiley‐Liss, Inc.
Unique developmental patterns of GABAergic neurons in rat spinal cord
Authors: Tran Tracy S. , Alijani Ata , Phelps Patricia E. 
Published: January 2003

Abstractγ‐aminobutyric acid (GABA)ergic neurons have been postulated to compose an important component of local circuits in the adult spinal cord, yet their identity and axonal projections have not been well defined. We have found that, during early embryonic ages (E12–E16), both glutamic acid decarboxylase 65 (GAD65) and GABA were expressed in cell bodies and growing axons, whereas at older ages (E17–P28), they were localized primarily in terminal‐like structures. To determine whether these developmental changes in GAD65 and GABA were due to an intracellular shift in the distribution pattern of GAD proteins, we used a spinal cord slice model. Initial experiments demonstrated that the pattern of GABAergic neurons within organotypic cultures mimicked the expression pattern seen in embryos. Sixteen‐day‐old embryonic slices grown 1 day in vitro contained many GAD65‐ and GAD67‐labeled somata, whereas those grown 4 days in vitro contained primarily terminal‐like varicosities. When isolated E14–E16 slices were grown for 4 days in vitro, the width of the GAD65‐labeled ventral marginal zone decreased by 40–50%, a finding that suggests these GABAergic axons originated from sources both intrinsic and extrinsic to the slices. Finally, when axonal transport was blocked in vitro, the developmental subcellular localization of GAD65 and GAD67 was reversed, so that GABAergic cell bodies were detected at all ages examined. These data indicate that an intracellular redistribution of both forms of GAD underlie the developmental changes observed in GABAergic spinal cord neurons. Taken together, our findings suggest a rapid translocation of GAD proteins from cell bodies to synaptic terminals following axonal outgrowth and synaptogenesis. J. Comp. Neurol. 456:112–126, 2003. © 2002 Wiley‐Liss, Inc.