bluuebunny/crossref_metadata_2025_split huggingface dataset:
Depressed mothers' newborns show longer habituation and fail to show face/voice preference
Authors: Hernandez‐Reif Maria , Field Tiffany , Diego Miguel , Largie Shay 
Published: November 2002

AbstractTwenty neonates of depressed and nondepressed mothers failed to show an initial visual preference for their mother's versus a female stranger's face/voice. Subsequently, infants were habituated to their mother's face and voice. Infants of depressed mothers required 1/3 more trials and almost twice as long to habituate. A posthabituation test with their mother and a different female stranger revealed a preference for the stranger's face for 9 out of the 10 newborns of the nondepressed mothers. Again, the infants of depressed mothers displayed no visual preference. These findings reveal differences in depressed mothers newborns' speed of habituation and face/voice preferences. ©2002 Michigan Association for Infant Mental Health.
The European Early Promotion Project: A new primary health care service to promote children's mental health
Authors: Puura Kaija , Davis Hilton , Papadopoulou Kalliroi , Tsiantis John , Ispanovic‐Radojkovic Veronika , Rudic Nenad , Tamminen Tuula , Turunen Merja‐Maaria , Dragonas Thalia , Paradisiotou Anna , Vizakou Semeli , Roberts Rosemarie , Cox Antony , Day Crispin 
Published: November 2002

AbstractThe number of children in Europe with significant psychologic and social problems is large and increasing. This article describes an innovative crosscultural method of working with families to promote the psychosocial well being of children and prevent the development of psychologic and social problems. A study designed to evaluate the effects of the service is also presented. Primary health care workers in five European countries have been trained to conduct promotional interviews with all prospective mothers in their area one month before and one month after birth. They have also been taught to work with mothers identified as in need of support as a parent by using a specific counselling model to try to prevent the onset of child mental health difficulties. Effects of the intervention on children's psychologic development and family adaptation are being evaluated at two years in comparison with matched groups not receiving the intervention. ©2002 Michigan Association for Infant Mental Health.
Ca2+/calmodulin‐dependent protein kinase II‐dependent long‐term potentiation in the rat suprachiasmatic nucleus and its inhibition by melatonin
Authors: Fukunaga Kohji , Horikawa Kazumasa , Shibata Shigenobu , Takeuchi Yusuke , Miyamoto Eishichi 
Published: November 2002

AbstractWe recently reported that Ca2+/calmodulin‐dependent protein (CaM) kinase II is involved in light‐induced phase delays and Per gene induction in the suprachiasmatic nucleus (SCN). To clarify the activation mechanisms of CaM kinase II by glutamate receptor stimulation in the SCN, we documented CaM kinase II activation following induction of long‐term potentiation (LTP) in the rat SCN. High‐frequency stimulation (100 Hz, 1 sec) applied to the optic nerve resulted in LTP of a postsynaptic field potential in the rat SCN. Unlike LTP in the hippocampal CA1 region, LTP onset in the SCN was slow and partly dependent on N‐methyl‐D‐aspartate receptor activation. LTP induction in the SCN was completely inhibited by treatment with a nitric oxide synthase inhibitor or with a specific CaM kinase II inhibitor. Immunoblotting analysis using phosphospecific antibodies against autophosphorylated CaM kinase II revealed that LTP induction was accompanied by an increase in autophosphorylation. After high‐frequency stimulation, we could visualize activation of CaM kinase II in vasoactive intestinal polypeptide‐positive neurons in the SCN by immunohistochemistry. Treatment with cyclosporin A, a calcineurin inhibitor, potentiated LTP induction in the rat SCN. Interestingly, treatment with melatonin totally prevented LTP induction, without changes in basal synaptic transmission. Analyses of phosphorylation of CaM kinase II, mitogen‐activated protein kinase, and cAMP‐responsive element binding protein revealed that stimulatory and inhibitory effects on CaM kinase II autophosphorylation underlie the effects of cyclosporin A and melatonin, respectively. These results suggest that CaM kinase II plays critical roles in LTP induction in the SCN and that melatonin has inhibitory effects on synaptic plasticity through CaM kinase II. © 2002 Wiley‐Liss, Inc.
Neurotensin enhances glutamate excitotoxicity in mesencephalic neurons in primary culture
Authors: Antonelli T. , Tomasini M.C. , Finetti S. , Giardino L. , Calzà L. , Fuxe K. , Soubriè P. , Tanganelli S. , Ferraro L. 
Published: November 2002

AbstractThe tridecapeptide neurotensin has been demonstrated to increase glutamate release in discrete rat brain regions, leading to the hypothesis of a possible involvement of the peptide in neurodegenerative pathologies. The role of neurotensin in modulating glutamate excitotoxicity and the possible neuroprotective action of the neurotensin receptor antagonist SR48692 were investigated in primary cultures of mesencephalic neurons by measuring [3H]dopamine uptake and tyrosine hydroxylase immunocytochemistry 24 hr after glutamate treatment. The exposure to glutamate (30 and 100 μM, 10 min) decreased [3H]dopamine uptake into mesencephalic neurons. Neurotensin (10 and 100 nM), added before glutamate (30 μM) exposure, significantly enhanced the glutamate‐induced reduction of [3H]dopamine uptake. In addition, the peptide (10 nM) also significantly enhanced the effect of 100 μM glutamate. The effects of neurotensin were counteracted by the neurotensin receptor antagonist SR48692 (100 nM) and by the protein kinase C inhibitor calphostin C. The exposure to 100 μM, but not 30 μM, glutamate significantly reduced the number of tyrosine hydroxylase‐immunoreactive cells, and neurotensin (10 nM) significantly enhanced this effect. SR48692 (100 nM) prevented the neurotensin‐induced action. These findings support the view of a possible pathophysiological role of neurotensin in mesencephalic dopamine neuronal function. Furthermore, selective neurotensin antagonists in combination with conventional drug treatments could provide a novel therapeutic approach for the treatment of neurodegenerative disorders, such as Parkinson's disease. © 2002 Wiley‐Liss, Inc.
Estrogen receptor‐α and neural circuits to the spinal cord during pregnancy
Authors: Papka R.E. , Hafemeister J. , Puder B.A. , Usip S. , Storey‐Workley M. 
Published: November 2002

AbstractEstrogen receptor immunoreactivity and mRNAs are present in spinal cord neurons in locations that are associated with sensory and autonomic innervation of female reproductive organs. The present study was undertaken to examine the expression of estrogen receptor‐α in the spinal cord during different stages of pregnancy and to determine whether estrogen receptor‐α‐expressing neurons are related to uterine afferent nerves bringing information to the spinal cord at parturition. Immunohistochemistry showed estrogen receptor‐α‐immunoreactive neurons in the dorsal one‐half of the spinal cord, i.e., dorsal horn, dorsal intermediate gray areas (dorsal commissural nucleus), and around the central canal and sacral parasympathetic autonomic nucleus of the lumbosacral spinal cord. Neurons in these areas corresponded topographically to the distribution of central processes of visceral primary afferent neurons (e.g., containing calcitonin gene‐related peptide and substance P) that innervate and activate second‐order spinal cord neurons (evidenced by their expression of Fos) at parturition. Western blots showed that estrogen receptor‐α increases in the spinal cord, with a peak at day 20 of gestation, followed by a slight decrease by 2 days postpartum. These studies show that estrogen receptor‐α is expressed by neurons in autonomic and sensory areas of the lumbosacral spinal cord that have connections with the female reproductive system and that the level of estrogen receptor‐α changes over the course of pregnancy, which may follow profiles of steroid hormones. Many of these neurons may be involved in processing information related to reproductive organ function, changes during pregnancy, and relays to other CNS centers. © 2002 Wiley‐Liss, Inc.
Chemokine regulation of macrophage recruitment into the olfactory epithelium following target ablation: Involvement of macrophage inflammatory protein‐1α and monocyte chemoattractant protein‐1
Authors: Getchell Thomas V. , Subhedar Nishikant K. , Shah Dharmen S. , Hackley Grant , Partin James V. , Sen Goutam , Getchell Marilyn L. 
Published: November 2002

AbstractTarget ablation by olfactory bulbectomy synchronizes the degenerative cell death of olfactory receptor neurons (ORNs), infiltration of macrophages, and proliferation of progenitor cells, leading to neurogenesis, ORN replacement, and regeneration of the sensory epithelium. Although macrophages participate in the degenerative and regenerative events, little is known of the molecular and cellular mechanisms associated with their recruitment during the earliest period following target ablation. Macrophage inflammatory protein‐1α (MIP‐1α) and monocyte chemoattractant protein‐1 (MCP‐1), which are members of the CC or β‐chemokine subfamily, are chemoattractants for monocytes/macrophages. Shortly after target ablation, the protein and mRNA levels for MIP‐1α and MCP‐1 were up‐regulated, showing peak expression levels from 16 hr to 3 days post‐OBX; this coincided with the pattern of infiltration of activated F4/80+ macrophages. The mRNAs for MIP‐1α and MCP‐1, as well as their cognate receptors CCR1 and CCR2, respectively, were localized in resident and infiltrating macrophages in numbers commensurate with those of F4/80‐immunopositive macrophages in adjacent tissue sections. The mRNA+ macrophages were localized within olfactory epithelial compartments that corresponded with their proposed functions associated with phagocytosis, proliferation, and infiltration. Our data support the hypothesis that MIP‐1α and MCP‐1 are chemoattractant chemokines associated with the recruitment of macrophages into the olfactory epithelium shortly after target ablation. © 2002 Wiley‐Liss, Inc.
Glial cell line‐derived neurotrophic factor released by synthetic guidance channels promotes facial nerve regeneration in the rat
Authors: Barras Florian M. , Pasche Philippe , Bouche Nicolas , Aebischer Patrick , Zurn Anne D. 
Published: November 2002

AbstractRegeneration of the human facial nerve after lesion is often limited, leading to severe functional impairments, in particular when repair is delayed for several months, when cross‐facial nerve grafts have to be performed, or in elderly patients. To improve the outcome, the potential accelerating and maturating effects of the neurotrophic factors glial cell line‐derived neurotrophic factor (GDNF) and neurotrophin‐3 (NT‐3) on nerve regeneration were assessed using an axotomy model of the rat facial nerve. One‐centimeter‐long synthetic guidance channels releasing the neurotrophic factors over several weeks were used to bridge an 8 mm nerve gap, a distance that does not allow regeneration in the absence of growth factors. Nerve cables regenerated in the presence of GDNF showed a large number of myelinated axons 6 weeks after grafting (871 ± 373, n = 5), whereas only 106 ± 86 (n = 5) myelinated axons were counted in the presence of NT‐3. Retrograde labeling with fluorogold revealed 981 ± 450 (n = 5) and 53 ± 38 (n = 5) retrogradely labeled motoneurons in the facial nucleus in the presence of GDNF and NT‐3, respectively. No regenerated axons or retrogradely labeled cells were observed in the absence of growth factors (n = 6). These results demonstrate that GDNF, as previously described for the sciatic nerve, a mixed sensory and motor nerve, is also very efficient in promoting regeneration of the facial nerve, an essentially pure motor nerve. GDNF may therefore be useful in improving facial nerve regeneration in the clinic. © 2002 Wiley‐Liss, Inc.
Induction of radioprotective peroxiredoxin‐I by ionizing irradiation
Authors: Chen Wen‐Cheng , McBride William H. , Iwamoto Keisuke S. , Barber Chad L. , Wang Chun‐Chieh , Oh Young‐Taek , Liao Yu‐Pei , Hong Ji‐Hong , de Vellis Jean , Shau Hungyi 
Published: November 2002

AbstractResults of this study indicate a radioprotective effect of peroxiredoxin‐I. Peroxiredoxin‐I is an antioxidant that scavenges hydroperoxides, whereas reactive oxygen species are the main mediators of ionizing radiation toxicity. We hypothesized that peroxiredoxin‐I might be induced by cellular exposure to radiation and act to protect them against its cytotoxic effects. Western blot and Northern blot analyses were used to assess peroxiredoxin‐I protein and mRNA expression. Rat C6 glioma cells were engineered to overexpress sense or antisense human peroxiredoxin‐I using retroviral vectors. Clonogenic cell survival was used to assess radiosensitivities of the engineered cells. Ionizing radiation induced peroxiredoxin‐I protein and mRNA expression in human HT29 colon cancer and rat C6 glioma cells in a dose‐ and time‐dependent manner over a 24 hr period. To determine the effect of peroxiredoxin‐I on radiation responses, C6 glioma cells were engineered to overexpress sense or antisense human peroxiredoxin‐I. In clonogenic assays, cells overexpressing peroxiredoxin‐I were more radioresistant. Cells transduced with antisense peroxiredoxin‐I were marginally more sensitive to radiation toxicity. Irradiation can induce peroxiredoxin‐I expression, and the increased peroxiredoxin‐I may protect cells from further radiation damage. These results suggest that protection by peroxiredoxin‐I may play an important role in the survival of glioma and colon cancer cells in patients undergoing radiation therapy. © 2002 Wiley‐Liss, Inc.
Alternative acetylcholinesterase molecular forms exhibit similar ability to induce neurite outgrowth
Authors: De Jaco A. , Augusti‐Tocco G. , Biagioni S. 
Published: November 2002

AbstractSeveral groups have reported that acetylcholinesterase (AChE), through a mechanism not involving its catalytic activity, may have a role in fiber elongation. These observations were performed on experimental systems in which acetylcholine synthesis was active. Because neurite outgrowth can be modulated by neurotransmitters, we used the N18TG2 neuroblastoma line, which is defective for neurotransmitter production, to evaluate whether AChE may modulate neurite sprouting in nonenzymatic ways. To avoid the possibility that differences between transfected and mock‐transfected clones may be due to the selection procedure, N18TG2 cells were previously subcloned, and the FB5 subclone was used for transfections. We performed transfections of FB5 cells with three distinct constructs encoding for the glycosylphosphoinositol‐anchored AChE form, the tetrameric AChE form, and a soluble monomeric AChE form truncated in its C‐terminus. A morphometric analysis of retinoic acid‐differentiated clones was also undertaken. The results revealed that higher AChE expression following transfection brings about a greater ability of the clones to grow fibers with respect to nontransfected or mock‐transfected cells irrespective of the used construct. Having observed no differences between the morphology of the transfected clones, we tested the possibility that the culture substrate can affect the capability of the clones to extend fibers. Also in this case we revealed no differences between the clones cultured on uncoated or collagen‐pretreated dishes. These data indicate that alternative AChE molecular forms that differ in their C‐teminal region exhibit similar ability to induce fiber outgrowth and suggest that the protein region responsibile for this role is located in the invariant portion of the AChE molecule. © 2002 Wiley‐Liss, Inc.
New model of glutathione deficit during development: Effect on lipid peroxidation in the rat brain
Authors: Rougemont Michaël , Do Kim Quang , Castagné Vincent 
Published: November 2002

AbstractGlutathione is a major regulator of the redox equilibrium, so its deficit weakens tissue resistance to oxidants. The nervous system is particularly susceptible to oxidative insults and is therefore very dependent on its glutathione content, especially during development, when brain metabolism and growth are maximal. In addition, various pathologies affecting the nervous system involve oxidative stress, possibly associated with a diminution of glutathione concentrations. To study the involvement of glutathione in brain redox homeostasis, we set up an experimental model of chronic glutathione deficit. Developing rats were treated daily with L‐buthionine‐(S,R)‐sulfoximine (BSO), an inhibitor of glutathione synthesis, and their brain levels of glutathione and lipid peroxidation products (TBARS) were measured. BSO induced a 40–50% glutathione deficit in the cortex, diencephalon, and pons/medulla. Despite the glutathione deficit induced by BSO, we did not observe any signs of oxidative stress. Because it is known that rats compensate for a glutathione deficit by enhancing their synthesis and tissue levels of ascorbic acid (AA), we performed the same experiment in osteogenic‐disorder Shionogi (ODS) rats, a mutant strain that cannot synthetize AA. Although BSO induced a glutathione deficit of comparable intensity in the two strains of rats, it elevated TBARS levels in the diencephalon and pons/medulla only in ODS and not in nonmutant rats. These results suggest that ODS rats, which closely mimic the human redox regulation, will allow study of the long‐term consequences of chronic glutathione deficit observed in various clinical situations. © 2002 Wiley‐Liss, Inc.
Transgenic zebrafish model of neurodegeneration
Authors: Tomasiewicz Henry G. , Flaherty Denise B. , Soria J.P. , Wood John G. 
Published: November 2002

AbstractIn Alzheimer's disease (AD), the microtubule‐associated protein, tau, is compromised in its normal association with microtubules and forms into paired helical filaments (PHF) that are the hallmark cytoskeletal pathology of the disease. Several posttranslational modifications of tau including phosphorylation have been implicated in AD pathogenesis. In addition, and importantly, mutations in the genes encoding human tau have recently been implicated in a variety of hereditary dementias, collectively termed frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP‐17). This has rekindled interest in the importance of tau in neurodegenerative diseases (cf. Vogel [1998] Science 280:1524–1525; Goedert et al. [1998] Neuron 21:955–958; D'Souza et al. [1999] PNAS 96:5598–5603). Despite significant progress in the field of tau biology and neurodegenerative diseases, several important issues remain unresolved. The early functional consequences of tau alterations in living neurons is incompletely understood, and it is not clear how tau in neurodegenerative diseases becomes redistributed from its normal concentration in neuronal axons to pathological inclusions in neuronal soma known as neurofibrillary tangles (NFT). One of the reasons for these gaps in knowledge is the relative paucity of model systems to study these processes. We have developed a transgenic model system to study the functional consequences and trafficking patterns in zebrafish neurons of human tau either mutated on sites associated with hereditary dementias or altered at select posttranslational modification sites. The overall guiding hypothesis is that the model allows dissection of a hierarchy of events relevant to potential mechanisms of neurodegenerative diseases related to critical early stages in development of disease. We showed that a FTDP‐17 mutant form of human tau expressed in zebrafish neurons produced a cytoskeletal disruption that closely resembled the NFT in human disease. This model system will prove useful in the study of other mutant taus in vertebrate neurons in vivo, and the approaches developed here will have broad usefulness in the study of functional consequences and potential genetic analyses of introducing into living vertebrate neurons other molecules involved in the pathogenesis of neurodegenerative diseases. © 2002 Wiley‐Liss, Inc.
Transcripts of damaged genes in the brain during cerebral oxidative stress
Authors: Liu Philip K. , Arora Tarun 
Published: November 2002

AbstractRecent studies using ischemia/reperfusion models of brain injury suggest that there is a period of time during which the formation of oxidative DNA lesions (ODLs) exceeds removal. This interval is a window of opportunity in which to study the effect of gene damage on gene expression in the brain, because the presence of excessive ODLs mimics a deficiency in gene repair, which has been shown to be associated with neurological disorders. Evidence from studies using similar models indicates that expression of faulty transcripts from ODL‐infested genes and non‐sense mutation in repaired genes occur before the process of cell death. Preventing the formation of ODLs and enhancing ODL repair are shown to increase the expression of intact transcripts and attenuate cell death. Understanding this mechanism could lead to the development of therapeutic techniques (physiologic, pharmacological, and/or genomic) that can enhance recovery. © 2002 Wiley‐Liss, Inc.
Neuroectodermal and microglial differentiation of bone marrow cells in the mouse spinal cord and sensory ganglia
Authors: Corti S. , Locatelli F. , Donadoni C. , Strazzer S. , Salani S. , Del Bo R. , Caccialanza M. , Bresolin N. , Scarlato G. , Comi G.P. 
Published: November 2002

AbstractThere is now evidence that bone marrow (BM) can generate cells expressing neuronal antigens in adult mouse brain. In the present study, we examined the spinal cord and dorsal root ganglia (DRG) of adult mice 3 months after BM cell transplantation from transgenic donor mice expressing the enhanced green fluorescent protein (GFP). To determine whether GFP+ cells acquire neuroectodermal phenotypes, we tested, by immunocytochemistry followed by confocal analysis, the coexpression of the astrocytic marker glial fibrillary acidic protein (GFAP) and the neuronal markers NeuN, neurofilament (NF), and class III β‐tubulin (TuJ1). Rare GFP+ cells coexpressing TuJ1, NF, and NeuN were found both in spinal cord and in sensory ganglia. These cells have small dimensions and short cytoplasmic processes, probably reflecting an immature phenotype. Double GFP and GFAP positivity was found only in spinal cord. To determine whether cell fusion with endogenous cells occurred, we investigated the nuclear content of cells coexpressing GFP and neuronal or astrocytic markers, demonstrating that these cells have only one nucleus and a DNA ploidy that it is not different from that of surrounding neurons and astrocytes. Large numbers of GFP+ cells are also positively stained for F4/80, a microglial‐recognizing antibody, and present a characteristic microglial‐like morphology both in spinal cord and, with a higher frequency, in sensory ganglia. These data support a potential role for BM‐derived stem cells in spinal cord neuroneogenesis. They also confirm that the microglial compartment within the CNS and in DRG undergoes a relatively fast turnover, with the contribution of hematopoietic stem cells. Both these findings might prove useful for the development of treatments for spinal cord neurodegenerative and acquired disorders. © 2002 Wiley‐Liss, Inc.