bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ni0‐Catalyzed Cyclotrimerization of 1,3‐Butadiene: A Comprehensive Density Functional Investigation on the Origin of the Selectivity
Authors: Tobisch Sven 
Published: February 2003

AbstractA comprehensive theoretical investigation of the mechanism for the Ni0‐catalyzed cyclotrimerization of 1,3‐butadiene by the [Ni0(η2‐butadiene)3] active catalyst complex is presented by employing a gradient‐corrected DFT method. All critical elementary processes of the catalytic cycle have been scrutinized, namely, oxidative coupling of two butadienes, butadiene insertion into the allyl–NiII bond, allylic isomerization in both octadienediyl–NiII and dodecatrienediyl–NiII species, and reductive elimination under ring closure. For each of these elementary steps several conceivable routes and also the different stereochemical pathways have been probed. The favorable route for oxidative coupling start from the prevalent [Ni0(η2‐butadiene)3] form of the active catalyst through coupling between the terminal non‐coordinated carbon atoms of two reactive η2‐butadiene moieties; this is assisted by an ancillary butadiene in η2‐mode. The initial η3,η1(C1)‐octadienediyl–NiII product is the active precursor for subsequent butadiene insertion, which preferably takes place into the η3‐allyl–NiII bond. The insertion is driven by a strong thermodynamic force. Therefore, the dodecatrienediyl–NiII products, with the most favorable bis(η3‐allyl),Δ‐trans isomers in particular, represent a thermodynamic sink. Commencing from a preestablished equilibrium between the various bis(η3‐allyl),Δ‐trans forms of the [NiII(dodecatrienediyl)] complex, the major cyclotrimer products, namely all‐t‐CDT, c,c,t‐CDT and c,t,t‐CDT, are formed along competing paths by reductive elimination under ring closure, which is shown to be rate‐controlling. The all‐c‐CDT‐generating path is completely precluded by both thermodynamic and kinetic factors, giving rise to negligibly populated bis(η3‐allyl),Δ‐cis precursor isomers. The regulation of the selectivity of the CDT formation as well as the competition between the two reaction channels for generation of C12‐ and C8‐cycloolefins is elucidated.
Acetylenic Quinoxalinoporphyrazines as Photosensitisers for Photodynamic Therapy
Authors: Mitzel Frieder , FitzGerald Simon , Beeby Andrew , Faust Rüdiger 
Published: February 2003

AbstractA range of lipo‐ and hydrophilic derivatives of the new class of octaalkynyl tetra‐[6,7]‐quinoxalinoporphyrazines (TQuiPors), analogues of the naphthalocyanines, were prepared in two steps starting from functionalised hexa‐1,5‐diyne‐3,4‐diones. Divalent zinc and magnesium ions were introduced into the macrocyclic core. Whereas the triisopropylsilyl‐, 3,5‐di‐tert‐butylphenyl‐ and 4‐triisopropylsilyloxyphenyl‐terminated acetylenic TQuiPors are lipophilic and hence soluble in standard organic solvents, a polyethylene glycol‐substituted derivative was found to dissolve in DMSO as well as in ethanol/water mixtures. The new chromophores are characterised by intense UV/Vis/NIR absorptions, most notably by bands at 770 nm with extinction coefficients exceeding 500 000 M−1 cm−1. With a view to possible photodynamic therapy applications, the potency of the chromophores to sensitise the formation of singlet oxygen was examined, both qualitatively using a 1,3‐diphenylisobenzofuran assay, and quantitatively by the determination of the singlet oxygen quantum yields. It was found that all TQuiPors produce singlet oxygen when irradiated in the presence of air. In particular, the octaalkynyl Zn‐TQuiPor generates singlet oxygen with a quantum yield of 56 %, thereby rivalling, and, in conjunction with its absorption profile, even exceeding the standards set by established PDT agents. The photostabilities of the TQuiPors were assessed and generally found to be satisfactory, but dependent on the solvent and the wavelength of the incident light.
Coordinated development of identified serotonergic neurons and their target ciliary cells in Helisoma trivolvis embryos
Authors: Koss Ron , Diefenbach Thomas J. , Kuang Shihuan , Doran Shandra A. , Goldberg Jeffrey I. 
Published: February 2003

AbstractEmbryonic neuron C1s (ENC1s) are bilateral serotonergic neurons that function as cilioexcitatory motor neurons in embryonic development of the pond snail, Helisoma trivolvis. Recent experiments demonstrated that these neurons stimulate cilia‐driven embryo rotation in response to hypoxia. In the present study, a comprehensive anatomic analysis of these cells and their target ciliary structures was done to address the following questions: (1) Does ENC1 have a morphology consistent with an oxygen‐sensitive sensory cell; (2) Is the development of ENC1's neurite outgrowth pathway coordinated with the development of its target effectors, the pedal and dorsolateral ciliary bands; and (3) What is the anatomic basis of ENC1–ciliary communication? By using an array of microscopic techniques on live and serotonin‐immunostained embryos, we found that each ENC1 possessed an apical dendrite that was capped with an integral dendritic knob penetrating the embryo surface. The dendritic knobs contained both microvilli and nonmotile cilia that suggested a sensory transduction role. Each ENC1 also possessed a descending projection, whose development was characterized by the rapid formation of the primary neurite pathway between stages E13 and E15, with the primary neurite of the right ENC1 developing in advance of its contralateral homologue. Secondary neurite branches formed between stages E15 and E30 in a spatiotemporal pattern that closely matched the development of the dorsolateral and pedal bands of cilia. Both dorsolateral and pedal ciliated cells formed basal processes that contacted ENC1 neurites. Finally, gap junction profiles were observed at neurite–neurite, neurite–ciliary cell, and ciliary cell–ciliary cell apposition sites, whereas putative chemical synaptic profiles were observed at neurite–neurite and neurite–ciliary cell apposition sites. J. Comp. Neurol. 457:313–325, 2003. © 2003 Wiley‐Liss, Inc.
Pontine sources of norepinephrine in the cat cochlear nucleus
Authors: Thompson Ann M. 
Published: February 2003

AbstractIn the current study, the distribution of noradrenergic neurons in the pontine tegmentum that project to the cochlear nucleus was determined with retrograde tract tracing combined with neurotransmitter immunohistochemistry in the cat. Double‐labeled neurons were observed in all noradrenergic cell groups, in both the dorsolateral and the ventrolateral tegmentum. Half of the double‐labeled cells were located in the locus coeruleus complex. Most of these were situated in its ventral division. Most other double‐labeled cells were located in peribrachial regions, especially lateral to the brachium conjunctivum. Relatively few double‐labeled cells were observed in both the A4 and the A5 cell groups, 2% and 0.4%, respectively, of the total. Except for neurons in A5, which projected only contralaterally, the projections were bilateral, with an ipsilateral preponderance. The results indicate that neurons located in the ipsilateral dorsolateral tegmentum, namely, in the locus coeruleus complex and the peribrachial region, are the primary source of pontine noradrenergic afferents to the cochlear nucleus of the cat. J. Comp. Neurol. 457:374–383, 2003. © 2003 Wiley‐Liss, Inc.
Differential morphology of pyramidal tract‐type and intratelencephalically projecting‐type corticostriatal neurons and their intrastriatal terminals in rats
Authors: Reiner Anton , Jiao Yun , Del Mar Nobel , Laverghetta Antonio Vincent , Lei Wan Long 
Published: February 2003

AbstractTwo types of corticostriatal projection neurons have been identified: 1) one whose intrastriatal arborization arises as a collateral of a projection to the ipsilateral brainstem via the pyramidal tract (PT‐type); and 2) one that projects intratelencephalically to the cortex and striatum, in many cases bilaterally, but not extratelencephalically (IT‐type). To assess possible functional differences between these two neuron types, we characterized their laminar location in the cortex, their perikaryal size, and the morphology of their intrastriatal terminals. IT‐type neurons were retrogradely labeled by tetramethylrhodamine‐dextran amine (RDA)3k injection into the contralateral striatum, whereas their intrastriatal terminals were labeled anterogradely by biotinylated dextran amine (BDA)10k injection into the contralateral motor or primary somatosensory cortex. To label PT‐type neurons and their ipsilateral intrastriatal terminals retrogradely, BDA3k was injected into the pontine pyramidal tract. We found that IT‐type neuronal perikarya are medium‐sized (12–13 μm) and located in layer III and upper layer V, whereas PT‐type perikarya are larger (18–19 μm) and most commonly located in lower layer V. At the electron microscopic level, the intrastriatal terminals of both corticostriatal neuron types made asymmetric synaptic contact with spine heads and less frequently with dendrites. IT‐type axospinous terminals were characteristically small (0.4–0.5 μm) and regular in shape, whereas PT‐type terminals were typically large (0.8–0.9 μm) and often irregular in shape. Perforated postsynaptic densities were common for PT‐type terminals, but not IT‐type. The clear differences between these two corticostriatal neuron types in perikaryal size and laminar location in the cortex, and in the size and shape of their intrastriatal terminals, suggest that they may differ in the nature of their influence on the striatum. J. Comp. Neurol. 457:420–440, 2003. © 2003 Wiley‐Liss, Inc.
Visualization of S100B‐positive neurons and glia in the central nervous system of EGFP transgenic mice
Authors: Vives Virginie , Alonso Gérard , Solal Anne Cohen , Joubert Dominique , Legraverend Catherine 
Published: February 2003

AbstractS100B, the EF‐hand Ca++‐binding protein with gliotrophic and neurotrophic properties implicated in the pathogenesis of Alzheimer's disease, is coined as a glial marker, despite its documented presence in rodent brain neurons. We have generated a transgenic mouse whose EGFP reporter, controlled by the −1669/+3106 sequence of the murine S100B gene, allows the direct microscopic observation of most S100B‐expressing cells in the central nervous system (CNS). From embryonic day 13 onward, EGFP expression was targeted to selected neuroepithelial, glial, and neuronal cells, indicating that cell‐specific expression of S100B is regulated at the transcriptional level during development. In adult mice, the highest level of EGFP expression was found in ependymocytes; astrocytes; and spinal, medullar, pontine, and deep cerebellar S100B neurons. Our results, thus, agree with earlier reports suggesting that S100B is not a CNS glial‐specific marker. In addition, we detected EGFP and S100B in forebrain neurons previously thought not to express S100B in the mouse, including neurons of primary motor and somatosensory neocortical areas, the ventral pallidum and prerubral field. Another interesting finding was the selected EGFP targeting to neonatal S100B oligodendrocytes and adult NG2 progenitors as opposed to mature S100B oligodendrocytes. This finding suggests that, except for oligodendrocytes at the last stage of myelin maturation, the −1669/+3106 sequence of the S100B gene is a useful reagent for driving expression of transgenes in most S100B‐expressing cells of mouse brain. J. Comp. Neurol. 457:404–419, 2003. © 2003 Wiley‐Liss, Inc.
Odor‐evoked activity is spatially distributed in piriform cortex
Authors: Illig Kurt R. , Haberly Lewis B. 
Published: February 2003

AbstractMuch data on the olfactory bulb (OB) indicates that structural characteristics of odorant molecules are encoded as ordered, spatially consolidated sets of active cells. New results with “genetic tracing” (Zou et al. [2001] Nature 414:173–179) suggest that spatial order is also present in projections from the OB to the olfactory cortex. For the piriform cortex (PC), results with this technique indicate that afferents conveying input derived from single olfactory receptors (ORs) are distributed to well‐defined patches in the anterior PC (APC) but that these patches are much larger than in the OB. We have used c‐fos induction to examine how input patterning for single ORs is translated into patterns of odor‐evoked cellular activity in the PC. The laminar distribution of labeled cells and dual‐immunostaining for γ‐aminobutyric acid (GABA)ergic markers indicated that activity was detected largely in pyramidal cells. In odor‐stimulated rats, labeled cells were present throughout the posterior PC (PPC) but were concentrated in prominent rostrocaudal bands in APC. Analysis of responses to different odorants and concentrations revealed that locations and shapes of bands conveyed no apparent information regarding odor quality, rather, they appeared to correspond to subregions of the APC distinguished by cytoarchitecture and connectivity. Small‐scale variations in labeling density were observed within APC bands and throughout the PPC that could reflect the presence of a complex topographical order, but discrete patches at consistent locations as observed by genetic tracing were absent. This finding suggests that as a result of afferent overlap and intracortical processing, odor‐quality information is represented by spatially distributed sets of cells. A distributed organization may be optimal for discriminating biologically relevant odorants that activate large numbers of ORs. J. Comp. Neurol. 457:361–373, 2003. © 2003 Wiley‐Liss, Inc.
Steroid‐triggered programmed cell death of a motoneuron is autophagic and involves structural changes in mitochondria
Authors: Kinch Ginger , Hoffman Kurt L. , Rodrigues Elizabeth M. , Zee Michele C. , Weeks Janis C. 
Published: February 2003

AbstractNeuronal death occurs during normal development and disease and can be regulated by steroid hormones. In the hawkmoth, Manduca sexta, individual accessory planta retractor (APR) motoneurons undergo a segment‐specific pattern of programmed cell death (PCD) at pupation that is triggered directly and cell autonomously by the steroid hormone 20‐hydroxyecdysone (20E). APRs from abdominal segment six [APR(6)s] die by 48 hours after pupal ecdysis (PE; entry into the pupal stage), whereas APR(4)s survive until adulthood. Cell culture experiments showed previously that 20E acts directly on APRs to trigger PCD, with intrinsic segmental identity determining which APRs die. The APR(6) death pathway includes caspase activation and loss of mitochondrial function. We used transmission electron microscopy to investigate the ultrastructure of APR somata before and during PCD. APR(4)s showed normal ultrastructure at all stages examined, as did APR(6)s until approximately stage PE. During APR(6) death, there was massive accumulation of autophagic bodies and vacuoles, mitochondria became ultracondensed and aggregated into compact clusters, and ribosomes aggregated in large blocks. Nuclear ultrastructure remained normal, without chromatin condensation, until the nuclear envelope fragmented late in the death process. Light microscopic immunocytochemistry showed that dying APR(6)s were TUNEL‐positive, which is diagnostic of fragmented DNA. These observations indicate that the steroid‐induced, caspase‐dependent, cell‐autonomous PCD of APR(6)s is autophagic, not apoptotic, and support an early role for mitochondrial alterations during PCD. This system permits the study of neuronal death in response to its bona fide developmental signal, the rise in a steroid hormone. J. Comp. Neurol. 457:384–403, 2003. © 2003 Wiley‐Liss, Inc.
Laminar and cellular targets of individual thalamic reticular nucleus axons in the lateral geniculate nucleus in the prosimian primate Galago
Authors: Uhlrich Daniel J. , Manning Karen A. , Feig Sherry L. 
Published: February 2003

AbstractThe visual sector of the thalamic reticular nucleus is the source of the primary inhibitory projection to the visual thalamic relay nucleus, the dorsal lateral geniculate nucleus. The purpose of this study was to investigate laminar and cellular targets of individual thalamic reticular nucleus axons in the highly laminated lateral geniculate nucleus of the prosimian primate Galago to better understand the nature and function of this projection. Thalamic reticular axons labeled anterogradely by means of biotinylated dextran amine were examined by using light microscopic serial reconstruction and electron microscopic analysis in combination with postembedding immunohistochemical labeling for the neurotransmitter γ‐aminobutyric acid (GABA). The synaptic targets of labeled reticular terminal profiles were primarily GABA‐negative dendrites (79–84%) of thalamocortical cells, whereas up to 16% were GABA‐positive dendritic shafts or F2 terminals of interneurons. Reconstructed thalamic reticular nucleus axons were narrowly aligned along a single axis perpendicular to the geniculate laminar plane, exhibiting a high degree of visuotopic precision. Individual reticular axons targeted multiple or all geniculate laminae, with little laminar selectivity in the distribution of swellings with regard to the eye of origin or to the parvocellular, koniocellular, or magnocellular type neurons contained in the separate layers of the Galago lateral geniculate nucleus. These results suggest that cells in the visual thalamic reticular nucleus influence the lateral geniculate nucleus retinotopically, with little regard to visual functional streams. J. Comp. Neurol. 458:128–143, 2003. © 2003 Wiley‐Liss, Inc.
Dynamics of microglia in the developing rat brain
Authors: Dalmau Ishar , Vela José Miguel , González Berta , Finsen Bente , Castellano Bernardo 
Published: February 2003

AbstractEntrance of mesodermal precursors into the developing CNS is the most well‐accepted origin of microglia. However, the contribution of proliferation and death of recruited microglial precursors to the final microglial cell population remains to be elucidated. To investigate microglial proliferation and apoptosis during development, we combined proliferating cell nuclear antigen (PCNA) immunohistochemistry, in situ detection of nuclear DNA fragmentation (TUNEL), and caspase‐3 immunohistochemistry with tomato lectin histochemistry, a selective microglial marker. The study was carried out in Wistar rats from embryonic day (E) 16 to postnatal day (P) 18 in cerebral cortex, subcortical white matter, and hippocampus. Proliferating microglial cells were found at all ages in the three brain regions and represented a significant fraction of the total microglial cell population. The percentage of microglia expressing PCNA progressively increased from the embryonic period (25–51% at E16) to a maximum at P9, when the great majority of microglia expressed PCNA (92–99%) in all the brain regions analyzed. In spite of the remarkable proliferation and expansion of the microglial population with time, the density of microglia remained quite constant in most brain regions because of the considerable growth of the brain during late prenatal and early postnatal periods. In contrast, apoptosis of microglia was detected only at certain times and was restricted to some ameboid cells in white matter and primitive ramified cells in gray matter, representing a small fraction of the microglial population. Therefore, our results point to proliferation of microglial precursors in the developing brain as a physiological mechanism contributing to the acquisition of the adult microglial cell population. In contrast, microglial apoptosis occurs only locally at certain developmental stages and thus seems less crucial for the establishment of the final density of microglia. J. Comp. Neurol. 458:144–157, 2003. © 2003 Wiley‐Liss, Inc.
Retinotopic pathways providing motion‐selective information to the lobula from peripheral elementary motion‐detecting circuits
Authors: Douglass John K. , Strausfeld Nicholas J. 
Published: February 2003

AbstractRecordings from afferent channels from the medulla supplying deep neuropils of the fly's optic lobes reveal different filter properties among the three classes of afferent neurons: transmedullary cells, T2 neurons, and Y cells. Whereas transmedullary cells respond to local flicker stimuli without discriminating these from directional or oriented motion, the T2 afferent neurons show clear motion orientation selectivity, which corresponds closely with a morphological bias in the orientation of their dendrites and could also be influenced by systems of local recurrent neurons in the medulla. A Y cell having a clearly defined terminal in the lobula, but having dendrite‐like processes in the medulla and, possibly, the lobula plate, discriminates the direction of motion and its orientation. These results demonstrate unambiguously that the lobula receives information about motion and that the channels carrying it are distinct from those supplying wide‐field motion‐selective neurons in the lobula plate. Furthermore, recordings from a newly identified recurrent neuron linking the lobula back to the inner medulla demonstrate that the lobula discriminates nondirectional edge motion from flicker, thereby reflecting a property of this neuropil that is comparable with that of primary visual cortex in cats. The present findings support the proposal that elementary motion detecting circuits supply several parallel channels through the medulla, which segregate to, but are not shared by, the lobula and the lobula plate. The results are discussed in the context of other intracellular recordings from retinotopic neurons and with analogous findings from mammalian visual systems. J. Comp. Neurol. 457:326–344, 2003. © 2003 Wiley‐Liss, Inc.
Synaptic remodeling in the dorsal motor nucleus of the vagus nerve following vagal‐hypoglossal nerve anastomosis in the cat
Authors: Lan Chyn‐Tair , Hsu Jee‐Ching , Chang Chen‐Nen , Chuang Huo‐Li , Ling Eng‐Ang 
Published: February 2003

AbstractHorseradish peroxidase (HRP) retrograde tracing techniques and morphometric analyses were performed to investigate synaptic remodeling associated with neuronal and glial changes in the dorsal motor nucleus of the vagus (DMV) of cats after vagal‐hypoglossal nerve anastomosis (VHA). At 25 days postoperation (dpo), in the early target‐reinnervation stage, there were 50% fewer presynaptic boutons containing round vesicles (R) or round and large dense‐cored synaptic vesicles (R+D) contacting HRP‐labeled DMV motoneurons. The loss of R boutons was maintained throughout the remaining postoperative intervals up to 500 dpo, whereas R+D boutons were further reduced at 123 dpo but were restored at 315 dpo, so that, by 500 dpo, 71.4% of them had gained access to the DMV motoneurons. Boutons containing pleomorphic synaptic vesicles (P) were completely disconnected from the DMV motoneurons at 25 dpo and did not reappear even in the long‐term reinnervation stage. Loss and recovery of presynaptic boutons occurred in parallel with changes in astroglial ensheathment of the DMV motoneurons. It is suggested that synaptic remodeling associated with astroglial ensheathment in the DMV may be influenced by some retrogradely transported factors/signals derived from the newly acquired target organ, viz. tongue skeletal musculature. Our results further suggest that the observed changes in boutonal configurations may be attributable to modified functions of the DMV motoneurons induced by VHA. J. Comp. Neurol. 458:195–207, 2003. © 2003 Wiley‐Liss, Inc.