bluuebunny/crossref_metadata_2025_split huggingface dataset:
Reciprocal regulation of estrogen and NGF receptors by their ligands in PC12 cells
Authors: Sohrabji Farida , Greene Lloyd A. , Miranda Rajesh C. , Toran‐Allerand C. Dominique 
Published: January 2005

AbstractRecent work has shown that estrogen receptor mRNA and protein co‐localize with neurotrophin receptor systems in the developing basal forebrain. In the present study we examined the potential for reciprocal regulation of estrogen and neurotrophin receptor systems by their ligands in a prototypical neurotrophin target, the PC12 cell. using in situ hybridization histochemistry, RT‐PCR and a modified nuclear exchange assay, we found both estrogen receptor mRNA and estrogen binding in PC12 cells. Moreover, while estrogen binding was relatively low in naive PC12 cells, long‐term exposure to NGF enhanced estrogen binding in these cells by sixfold. Furthermore, concurrent exposure to estrogen and NGF receptor mRNAs deifferentially regulated the expression of the two NGF receptor mRNAs. The expression of trkA mRNA was up‐regulated, while p75NGFR mRNA was down‐regulated transiently. The present data indicate that NGF may increase neuronal sensitivity to estrogen, and that estrogen, by differentially regulating p75NGFR and trkA mRNA, may alter the ratio fo the two NGF receptors, and, conseuqnetly, neurotrophin responsivity. In view of the widespread co‐localization of estrogen and neurotrophin receptor systems in the developing CNS, the reciprocal regulation of these receptor systems by NGF and estrogen may have important implications for processes governing neural maturation and the maintenance of neural funciton. 1994 John Wiley & Sons, Inc.
Response of thoracic interneurons to tactile stimulation in the cockroach, Periplaneta americana
Authors: Ritzmann Roy E. , Pollack Alan J. 
Published: January 2005

AbstractReceåfindings indicate that cockroaches escape in response to tactile stimulation as well as they do in response to the classic wind puff stimulus. The thoracic interneurons that receive inputs from ventral giant interneurons also respond to tactile stimulation and therefore, represent a potential site of convergence between wind and tactile stimulation as well as other sensory modalities. In this article, we characterize the tactile response of these interneurons, which are referred to as type‐A thoracic interneurons (TIAs). In response to tactile stimulation of the body cuticle, TIAs typically respond with a short latency biphasic depolarization which often passes threshold for action potentials. The biphasic response is not typical of responses to wind stimulation nor of tactile stimulation of the antennae. It is also not seen in tactile responses of thoracic interneurons that are not part of the TIA group. The responses of individual TIAs to stimulation of various body locations were mapped. The left‐right directional properties of TIAs are consistent with their responses to wind puffs from various different directions. Cells that respond equally well to wind from the left and right side also respond equally well to tactile stimuli on the left and right side of the animal's body. In contrast, cells that are biased to wind on one side are also biased to tactile stimulation on the same side. In general, tactile responses directed at body cuticle are phasic rather than tonic, occurring both when the tactile stimulator is depressed and released. The response reflects stimulus strength and follows repeated stimulation quite well. However, the first phase of the biphasic response is more robust during high‐frequency stimulation than the second phase. TIAs also respond to antennal stimulation. However, here the response characteristics are complicated by the fact that movement of either antenna evokes descending activity in both left and right thoracic connectives. The data suggest that the TIAs make up a multimodal site of sensory convergence that is capable of generating an oriental escape turn in response to any one of several sensory cues. 1994 John Wiley & Sons, Inc.
Neuronal responses to purinoceptor agonists in the leech central nervous system
Authors: Backus Kurt H. , Braum Susanne , Lohner Frank , Deitmer Joachim W. 
Published: January 2005

AbstractExracellular nucleotides like ATP and its derivatives are possible chemical messengers in vertebrate nervous systems. In invertebrate nervous systems, however, little is known about their role in neurotransmission. We have studied the reponse of identified neurones of the leech Hirudo medicinalis to the purinoceptor agonist ATP, ADP, AMP, and adenosine using conventional intracellular microelectrodes and whole‐cell patch‐clamp recording. Bath application of the agoinsts depolarized the different neurons, but not neuropil glial cells. The most effective responses (up to 10 mV) were observed with ATP (100 μM) or ADP (100 μM) in the noxious and touch cells. In most neurons the nonhydrolyzable ATP derivative ATP‐γ‐S (5 μM) induced larger depolarizations that 100 μM ATP, indicating that most of the potency of ATP is lost presumably due to its degradation by ectonucleotidases. In medial noxios cells, ATP (100 μM) induced an inward current of 1.7 ± 1.1 nA at a holding potential of −60 mV. The ATP‐induced current‐voltage relationship showed an inward rectification and a reversal potential close to 0 m V. In a Na+‐free extracellular solution, the ATP‐induced inward current decreased and in a Na+‐ and Ca2+‐free saline only a small residual current persisted. The possible P2 purinoceptor antagonist suramin did not antagonize the ATP‐induced current, but itself evoked an inward current and a conductance increase. We conclude that ATP activates nonselective cation channels in medial noxious cells of the leech with the order of potency of purinoceptor agonists ATP ≥ ADP > AMP. The results suggest that these cells express purinoceptors of the P2 type. 1994 John Wiley & Sons, Inc.
The role of neurotrophins in the developing nervous system
Authors: Davies Alun M. 
Published: January 2005

AbstractNeurotrophins were originally identified by their ability to promote the survival of developing neurons. However, recent work on these proteins indicates that they may also influence the proliferation and differentiation of neuron progenitor cells and regular several differentiated traits of neurons throughout life. Moreover, the effects of neurotrophins on survival have turned out to be more complex than originally thought. Some neurons switch their survival requirements from one set of neurotrophins to another during development, and several neurotrophins may be involved in regulating the survival of a population of neurons at any one time. Much of our understanding of the developmental physiology of neurotrophins has come from studying neurons of the peripheral nervous system. Because these neurons and their progenitors are segregated into anatomically discrete sites, it has been possible to obtain these cell for in vitro experimental studies from the earliest stage of their development. The recent generation of mice having null mutations in the neurotrophin and neurotrophin receptor genes has opened up an unparalleled opportunity to assess the physiological relevance of the wealth of data obtained from these in vitro studies. Here I provide a chronological account of the effects of members of the NGF family of neurotrophins on cells of the neural lineage with special reference to the peripheral nervous system. 1994 John Wiley & Sons, Inc.
Neurotrophin signal transduction by the Trk receptor
Authors: Kaplan David R. , Stephens Robert M. 
Published: January 2005

AbstractThe initial event in the neuronal differentiation of PC12 cells is the binding of the neurotrophin nerve growth factor (NGF) to the Trk receptor. This interaction stimulates the intrinsic tyrosine kinase activity of TRk, initiating a signalling cascade involving the phosphorylation of intracellular proteins on tyrosine, serine, and threonine residues. These signals are then in turn propagated to other messengers, ultimately leading to differentiation, neurotrophin‐dependent survival and the loss of proliferative capacity. To transmit NGF signals, NGF‐activated Trk rapidly associated with the cytoplasmic proteins, SHC, PI‐3 kinase, and PLC‐γ1. These proteins are involved in stimulating the formation of various second messenger molecules and activating the Ras signal transduction pathway. Studies with Trk mutants indicate that the acivation of the Ras pathway is necessary for complete differentiation of PC12‐derived cells and for the maintenance of the differentiated phenotype. Trk also induces the tyrosine phosphorylation of SNT, a specific target of neurotrophic factor activity in neuronal cells. This review will discuss the potential roles of Trk and the proteins of the Trk signalling pathways in NGF function, and summarize our attempts to understand the mechanisms used by Trk to generate dthe many phenotypic responses of PC12 cells to NGF. 1994 John Wiley & Sons, Inc.
Ciliary neurotrophic factor
Authors: Sendtner M. , Carrol P. , Holtmann B. , Hughes R. A. , Thoenen H. 
Published: January 2005

AbstractCiliary neurotrophic factor (CNTF) was first identified and partially purified from embryonic chick eye tissues. Subsequently, it was shown that CNTF is also present in large amounts in sciatic nerves of adult rats and rabbits, which led to its final purification and cloning. CNTF is not secreted by the classical secretory pathway involving the endoplasmatic reticulum and Golgi complex, but can be detected in high quantities within the cytoplasm of myelinating Schwann cells and astrocytes using immunohistochemistry. CNTF supports survival and / or differentiation of a variety of neuronal cell types including sensory, sympathetic and motoneurons. Also, nonneuroanl cells, such as oligodendrocytes, microglial cells, liver cells, and skeletal muscle cells, respond to exogenously administered CNTF, both in vitro and in vivo. During development, expression of CNTF is very low, if indeed it is expressed at all, and the phenotype of mice lacking endogenous CNTF, suggesting that CNTF after inactivation of the CNTF gene by homologous recombination suggests that CNTF does not play a crucial role for responsive cells during embryonic development. However, motoneurons are lost postnatally in mice lacking endogenous CNTF, suggesting that CNTF acts physiologically on the maintenance of these cells. The ability of exogenous CNTF to protect against motoneuron loss following lesion or in other animal models indicates that CNTF might be useful in the treatment of human motoneuron disorders, provided appropriate means of administration can be found. 1994 John Wiley & Sons, Inc.
The growth of PC‐12 neurites is biased towards the anode of an applied electrical field
Authors: Cork R. J. , McGinnis M. E. , Tsai J. , Robinson K. R. 
Published: January 2005

AbstractWe have exposed cultures of PC12 cells to uniform DC electric fields following the addition of NGF. The success of these experiments relied upon the design of new chambers enabling fields to be applied to mammalian cell cultures. After 48 h of field application, the distribution of neurite outgrowths was biased towards the anode. More neurites faced the anode than would be expected if growth was uniform. The magnitude of this bias was strongly correlated with field strenght, with a threshold value of about 1 mV/mm. At field strengths above 30 mV/mm, the neurites growing towards the cathode were shorter than those growing towards the anode or perpendicular to the field. This response was not correlated with field strenght. This report confirms that mammalian neurons respond to electrical fields and supports the notion that neurites are influenced by endogenous electrical fields during development. As far as we are aware, this is the only report the documents a response towards the anode. 1994 John Wiley & Sons, Inc.
GABAA receptor subunit polypeptides increase in parallel but exhibit distinct distributions in the developing rat cerebellum
Authors: Nadler Laurie S. , Guirguis Eman R. , Siegel Ruth E. 
Published: January 2005

AbstractThe GABAA receptor, a multisubunit ligand‐gated ion channel, plays a central role in cell–cell communication in the developing and adult nervous system. Although the developmental expression of mRNAs encoding many subunit isoforms has been extensively characterized throughout the central nervous system, little is known concerning the relationship between subunit mRNA and polypeptide expression. To address this issue, we examined the developmental expression of the α1, β2/3, and γ2 subunit polypeptides, subunits that are thought to coassemble in many brain regions. Western blot analysis using subunit‐specific antibodies revealed that the levels of these polypeptides in both the cerebral cortex and cerebellum increased severalfold during the second postnatal week. Whereas polypeptide expression in the cerebellum paralleled that of the corresponding subunit mRNAs, increase in β2/3 and γ2 polypeptide expression in the cerebral cortex occurred in the absence of detectable changes in the mRNA levels. To determine whether the increases in subunit polypeptide expression in the cerebellum were accompanied by changes in distribution, immunohistochemistry was performed. These studies demonstrated that the subunits exhibited different but partially overlapping distributions that remained constant throughout postnatal development. Our findings suggest that although GABAA receptor subunit polypeptide expression may be regulated primarily at the level of the mRNA, additional regulatory mechanisms may play role. Furthermore, the observation that subunit distribution remains constant in the cell bodies of cerebellar Purkinje neurons, which express the α1, β2, β3, and γ2 subunit mRNAs exclusively, suggests that GABAA receptor subunit composition in this cell population does not change during postnatal maturation. 1994 John Wiley & Sons, Inc.
Long‐term survival followed by degradation of neurofilament proteins in severed Mauthner axons of goldfish
Authors: Moehlenbruck Jeffrey W. , Cummings Jennifer A. , Bittner George D. 
Published: January 2005

AbstractThe morphology and protein composition of intact and severed Mauthner axons (M‐axons) from goldfish were examined on electron micrographs, sodium dodecyl sulfate gels, and immunoblots. Neurofilaments were the most common cytoskeletal element on electron micrographs, and neurofilament proteins (NFPs) were the most intensely silver‐stained bands in M‐axoplasm microdissected from control M‐axons. NFPs at about 235, 145, 123, 105, 80, and 60 kD in M‐axoplasm were identified with four monoclonal and three polyclonal antibodies. Similar immunoblots of samples of the M‐axon myelin sheath (M‐sheath) showed no reactivity to antibodies against NFPs. For up to 62 days following spinal cord severance in goldfish maintained at 15°C, the ultrastructure, protein banding pattern, and anti‐NFP immunoreactivity of severed distal segments of M‐axons did not change compared with control M‐axons. At 62 to 81 days after severance, novel bands appeared in many silver‐stained gels and anti‐NFP immunoblots of distal M‐axons. NFP bands completely disappeared from distal M‐axon segments of some M‐axons as early as 72 days after severance. However, NFP bands persisted in some distal segments for up to 81 days after severance. The degradation of NFPs occurred equally along the entire length of a distal M‐axon segment, that is, there was no indication of a proximal‐to‐distal or distal‐to‐proximal sequence of NFP degradation in distal segments of severed M‐axons. These biochemical data were consistent with morphological data that showed little change in the diameter or ultra‐structure of severed M‐axons held at 15°C for about 2 months followed by a rapid collapse of the entire distal segment at 72 to 85 days postseverance. 1994 John Wiley & Sons, Inc.
Differential estrogen accumulation among populations of projection neurons in the higher vocal center of male canaries
Authors: Johnson Frank , Bottjer Sarah W. 
Published: January 2005

AbstractThe higher vocal center (HVC) of adult male canries undergoes a seasonal change in volume that corresponds to seasonal modifications of vocal behavior: HVC is large when birds produce stereotyped song (spring) and is small when birds produce plastic song and add new song syllables into their vocal repertoires (fall). We reported previously that systemic exposure to testosterone (T) produces an increase in the volume of HVC similar to that observed with long‐day photoperiods. T‐induced growth of HVC occured regardless of wheter the borders of HVC were defined by Nissl‐staining, the distribution of androgen‐concentrating cells, or the distribution of projection neurons [separate neuronal populations within HVC project to the robust nucleus of the archistriatum (RA) and to Area X of the avian striatum (X)]. In the present study we used steroid autoradiography to determine whether T can influence the distribution of HVC cells that bind estrogen, and we combined estrogen autoradiography with retrograde labeling to determine whether HVC neurons that project to RA versus X differ in their ability to accumulate estrogen. Results showed that T increased the volume of Nissl‐defined HVC and although HVC contained a low density of estrogen‐concentrating cells, T increased the spatial distribution of these cells to match the Nissl borders of HVC. We also identified a region containing a high density of estrogenconcentrating cells located medial to HVC [we call this region paraHVC (pHVC)], and T also increased the volume of pHVC. pHVC also contained numerous X‐projecting neurons, but few if any RA‐projecting neurons. Double‐labeling analysis revealed the RA‐projecting neurons did not accumulate estrogen, a small percentage of X‐projecting neurons in HVC accumulated estrogen, and the majority of X‐projecting neurons in pHVC showed heavy accumulation of estrogen. The data reported here and in our previous article suggest distinct roles for gonadal steroids within the HVC‐pHVC complex: estrogens are concentrated by neurons that project to a striatal region that influences vocal production during song learning (X), whereas androgens are concentrated primarily by neurons that project to a motor region that is involved in vocal production during both song learning and the recitation of already‐learned song (RA). © 1995 John Wiley & Sons, Inc.
Embryonic fibronectins are up‐regulated following peripheral nerve injury in rats
Authors: Mathews Greta A. , Ffrench‐Constant Charles 
Published: January 2005

AbstractFibronectin mRNAs that include the alternatively spliced exons EIIIA, EIIIB, and V are prevalent during embryogenesis, and EIIIA and EIIIB reappear during wound healing. Using ribonuclease protection analyses, we found an up‐regulation of V120 (containing the α4β1 integrin binding site), as well as EIIIA, and EIIIB in fibronectin mRNAs in the crush‐injured adult rat sciatic nerve. In situ hybridization using splice variant‐specific probes revealed that cells within endoneurial tubes of the injured nerve synthesize these embryonic forms of fibronectin. Our results suggest that embryonic fibronectins synthesized within the nerve contribute to the permissiveness of the peripheral nervous system to axon regrowth and a mechanism by which alternative splicing of the V region in fibronectin mRNA could enhance nervous system regeneration. © 1995 John Wiley & Sons, Inc.
Suppression of programmed neuronal death by a thapsigargin‐induced Ca2+ influx
Authors: Lampe Patricia A. , Cornbrooks Ellen B. , Juhasz Anna , Johnson Eugene M. , Franklin James L. 
Published: January 2005

AbstractRat sympathetic neurons undergo programmed cell death (PCD) in vitro and in vivo when they are deprived of nerve growth factor (NGF). Chronic depolarization of these neurons in cell culture with elevated concentrations of extracellular potassium ([K+]o) prevents this death. The effect of prolonged depolarization on neuronal survival is thought to be mediated by a rise of intracellular calcium concentration ([Ca2+]i) caused by Ca2+ influx through voltage‐gated channels. In this report we investigate the effects of chronic treatment of rat sympathetic neurons with thapsigargin, an inhibitor of intracellular Ca2+ sequestration. In medium containing a normal concentration of extracellular Ca2+ ([Ca2+]o), thapsigargin caused a sustained rise of intracellular Ca2+ concentration and partially blocked death of NGF‐deprived cells. Elevating [Ca2+]o in the presence of thapsigargin further increased [Ca2+]i, suggesting that the sustained rise of [Ca2+]i was caused by a thapsigargin‐induced Ca2+ influx. This treatment potentiated the effect of thapsigargin on survival. The dihydropyridine Ca2+ channel antagonist, nifedipine, blocked both a sustained elevation of [Ca2+]i and enhanced survival caused by depolarization with elevated [K+]o, suggesting that these effects are mediated by Ca2+ influx through L‐type channels. Nifedipine did not block the sustained rise of [Ca2+]i or enhanced survival caused by thapsigargin treatment, indicating that these effects were not mediated by influx of Ca2+ through L‐type channels. These results provide additional evidence that increased [Ca2+]i can suppress neuronal PCD and identify a novel method for chronically raising neuronal [Ca2+]i for investigation of this and other Ca2+‐dependent phenomena. © 1995 John Wiley & Sons, Inc.
The Ca2+ influx induced by β‐amyloid peptide 25–35 in cultured hippocampal neurons results from network excitation
Authors: Brorson James R. , Bindokas Vytautas P. , Iwama Toshi , Marcuccilli Charles J. , Chisholm Jane C. , Miller Richard J. 
Published: January 2005

AbstractAlthough a neurotoxic role has been postulated for the β‐amyloid protein (βAP), which accumulates in brain tissues in Alzheimer's disease, a precise mechanism underlying this toxicity has not been identified. The peptide fragment consisting of amino acid residues 25 through 35 (βAP25‐35), in particular, has been reported to be toxic in cultured neurons. We report that βAP25‐35, applied to rat hippocampal neurons in culture, caused reversible and repeatable increases in the intracellular Ca2+ concentration ([Ca2+]i), as measured by fura 2 fluorimetry. Furthermore, βAP25‐35 induced bursts of excitatory potentials and action potential firing in individual neurons studied with whole cell current clamp recordings. The βAP25‐35–induced [Ca2+]i elevations and electrical activity were enhanced by removal of extracellular Mg2+, and they could be blocked by tetrodotoxin, by non‐N‐methyl‐D‐aspartate (NMDA) and NMDA glutamate receptor antagonists, and by the L‐type Ca2+ channel antagonist nimodipine. Similar responses of bursts of action potentials and [Ca2+]i increases were evoked by βAP1‐40. Responses to βAP25‐35 were not prevented by pretreatment with pertussis toxin. Excitatory responses and [Ca2+]i elevations were not observed in cerebellar neuron cultures in which inhibitory synapses predominate. Although the effects of βAP25‐35 depended on the activation of glutamatergic synapses, there was no enhancement of kainate‐ or NMDA‐induced currents by βAP25‐35 in voltage‐clamp studies. We conclude that βAP25‐35 enhances excitatory activity in glutamatergic synaptic networks, causing excitatory potentials and Ca2+ influx. This property may explain the toxicity of βAP25–35. © 1995 John Wiley & Sons, Inc.