bluuebunny/crossref_metadata_2025_split huggingface dataset:
Selective increase of tumour necrosis factor‐alpha in injured and spared myelinated primary afferents after chronic constrictive injury of rat sciatic nerve
Authors: Schäfers Maria , Geis Christian , Svensson Camilla I. , Luo Z. David , Sommer Claudia 
Published: March 2003

AbstractChronic constriction of the sciatic nerve, leading to a hyperalgesic state, results in a partial lesion wherein some axons are injured and others remain intact. Here we sought to characterize reactive changes which occur in DRG cell bodies of injured and uninjured axons projecting to skin and muscle. Using immunohistochemistry combined with flurorogold and fluororuby retrograde labelling to define DRG cell bodies associated with injured and uninjured axons, we analysed the DRG immunoreactivity (IR) for tumour necrosis factor‐alpha (TNF), interleukin‐10 (IL‐10), the sensory neuron‐specific channel vanilloid receptor 1 (VR1), isolectin B4 (IB4) and calcitonin‐gene‐related peptide (CGRP) 4 days after a unilateral chronic constriction injury (CCI) of the rat sciatic nerve. TNF IR was predominantly localized in neuronal DRG cells. In DRG with an intact nerve, TNF IR was present in 45%, IL‐10 IR in 46%, VR1 IR in 44%, IB4 IR in 51% and CGRP IR in 40% of all neuronal profiles. Four days after CCI, TNF IR was increased in medium‐sized neurons, whereas IR for IL‐10, VR1 and IB4, predominantly present in small neurons, was reduced. Importantly, not only injured but also adjacent spared neurons contributed markedly to increased TNF IR. Neurons projecting to both muscle and skin displayed upregulated TNF IR after CCI. TNF in medium‐sized neurons colocalized with neurofilament and trkB, but not with IB4, trkA or RET, suggesting a selective phenotypic switch in presumably low‐threshold myelinated primary afferents. Spared myelinated fibres with intact sensory functions but upregulated TNF expression may contribute to behavioural changes observed after nerve injury.
Analysis of penetrance and expressivity during ontogenesis supports a stochastic choice of zebrafish odorant receptors from predetermined groups of receptor genes
Authors: Argo Silke , Weth Franco , Korsching Sigrun I. 
Published: March 2003

AbstractOlfactory receptor neurons select a single odourant receptor gene for expression out of a large gene family. The mechanisms of this extreme selectivity are largely unknown. We have determined in detail the developmental expression dynamics of a representative subset of the zebrafish odourant receptor repertoire, using in situ hybridization analysis. We have thus generated a dataset, which allows us to test hypotheses of odourant receptor gene regulation. The receptors chosen belong to four different groups with respect to ontogenetic onset of expression (onset groups). Statistical analysis of the data supports a model in which the final choice of an individual odourant receptor gene occurs stochastically from within a group of genes sharing a deterministically defined onset of expression. Genomic mapping revealed a pronounced correlation of onset of expression with genomic neighbourhood. During a protracted juvenile developmental period individual regulatory influences seem to modify the expression of odourant receptor genes, a notable example being a transient decrease in expressivity of two odourant receptor genes.
β‐Amyloid peptide potentiates inflammatory responses induced by lipopolysaccharide, interferon ‐γ and ‘advanced glycation endproducts’ in a murine microglia cell line
Authors: Gasic‐Milenkovic Jovana , Dukic‐Stefanovic Sladjana , Deuther‐Conrad Winnie , Gärtner Ullrich , Münch Gerald 
Published: March 2003

Summaryβ‐Amyloid (Aβ) plaques are characteristic hallmarks of Alzheimer's disease (AD). In AD, it has been suggested that activation of microglial cells might be the link between Aβ deposition and neuronal degeneration. Activated microglia are associated with senile plaques and produce free radicals and inflammatory cytokines. However, it is still not clear whether Aβ needs a prestimulated environment to exert its proinflammatory potential. Advanced glycation endproducts (AGEs), protein‐bound oxidation products of sugars, have been shown to accumulate in senile plaques and could induce a silent but chronic inflammation in the AD brain. We tested whether Aβ acts as an amplifier of a submaximal proinflammatory response initiated by exposure to chicken egg albumin‐AGE, lipopolysaccharide or interferon‐γ. Synthetic Aβ was used to produce three different samples (Aβ‐fibrilar; Aβ‐aggregated; Aβ‐AGE), which were characterized for β‐sheeted fibrils by the thioflavin‐T test and electron microscopy. As markers of microglial activation, nitric oxide, interleukin‐6, macrophage‐colony stimulation factor and tumour necrosis factor‐α production was measured. All three Aβ samples alone could not induce a detectable microglial response. The combination of Aβ preparations, however, with the coinducers provoked a strong microglial response, whereby Aβ‐AGE and fibrilar Aβ were more potent inflammatory signals than aggregated Aβ. Thus, Aβ in senile plaques can amplify microglial activation by a coexisting submaximal inflammatory stimulus. Hence, anti‐inflammatory therapeutics could either target the primary proinflammatory signal (e.g. by limiting AGE‐formation by AGE inhibitors or cross‐link breakers) or the amplifyer Aβ (e.g. by limiting Aβ production by β‐ or γ‐secretase inhibitors).
Pairing elevation of [cyclic GMP] with inhibition of PKA produces long‐term depression of glutamate release from isolated rat hippocampal presynaptic terminals
Authors: Bailey Christopher P. , Trejos Jesus A. , Schanne Francis A. X. , Stanton Patric K. 
Published: March 2003

AbstractData suggest both presynaptic and postsynaptic changes contribute to activity‐dependent long‐term synaptic plasticity. We have shown that pairing elevation of intracellular [cyclic GMP], using the type V phosphodiesterase inhibitor zaprinast, with inhibition of cyclic AMP‐dependent protein kinase (PKA), is sufficient to elicit chemical long‐term depression (CLTD) of synaptic transmission at Schaffer collateral‐CA1 and mossy fibre‐CA3 synapses in rat hippocampus. CLTD does not require synaptic activity, and selective postsynaptic drug injections do not affect it, suggesting it is presynaptically induced and expressed. To directly evaluate this hypothesis, we tested whether CLTD of transmitter release can be expressed in isolated presynaptic nerve terminals. Presynaptic nerve terminals (synaptosomes) were isolated from rat hippocampi by Percoll density gradient centrifugation. Synaptosomes were loaded with [3H]glutamate, and basal and depolarisation‐induced release of [3H]glutamate measured in control medium versus medium containing zaprinast (20 µm) plus or minus the PKA inhibitor H‐89 (10 µm). Zaprinast produced a significant decrease in basal [3H]glutamate release. However, only combining zaprinast with H‐89 significantly depressed K+‐evoked [3H]glutamate release. After a 20‐min drug washout, basal release returned to normal in all conditions, but K+‐evoked [3H]glutamate release was persistently reduced only by the combination of zaprinast plus H‐89. Long‐term reduction of [3H]glutamate release from synaptosomes was completely prevented by the PKG inhibitor KT5823 (5 µm). These data demonstrate the existence of a presynaptic, cyclic GMP‐PKG dependent cascade capable of expressing LTD of glutamate release from isolated hippocampal nerve terminals.
Pedunculopontine tegmental stimulation evokes striatal dopamine efflux by activation of acetylcholine and glutamate receptors in the midbrain and pons of the rat
Authors: Forster Gina L. , Blaha Charles D. 
Published: March 2003

AbstractThe pedunculopontine tegmental nucleus appears to influence striatal dopamine activity via cholinergic and glutamatergic afferents to dopaminergic cells of the substantia nigra pars compacta. We measured changes in striatal dopamine oxidation current (dopamine efflux) in response to electrical stimulation of the pedunculopontine tegmental nucleus using in vivo electrochemistry in urethane‐anaesthetized rats. Pedunculopontine tegmental nucleus stimulation evoked a three‐component change in striatal dopamine efflux, consisting of: (i) an initial rapid increase of 2 min duration; followed by (ii) a decrease below prestimulation levels of 9 min duration; then by (iii) a prolonged increase lasting 35 min. Intra‐nigral infusions of the ionotropic glutamate receptor antagonist kynurenate (10 µg/µL) or the nicotinic cholinergic receptor antagonist mecamylamine (5 µg/0.5 µL) selectively attenuated the rapid first component, while systemic injections of the muscarinic cholinergic antagonist scopolamine (5 mg/kg, i.p.) diminished the second and third components. In addition, intra‐pedunculopontine tegmental nucleus infusions of the M2 muscarinic antagonist methoctramine (50 µg/µL) selectively abolished the inhibitory second component, while intranigral infusions of scopolamine (200 µg/µL) selectively abolished the prolonged third component. Intra‐nigral infusions of the metabotropic glutamate receptor antagonist (+)‐α‐methyl‐4‐carboxyphenylglycine (2 µg/µL) had no effect on pedunculopontine tegmental nucleus‐elicited striatal dopamine efflux. These results suggest that the pedunculopontine tegmental nucleus utilizes nicotinic and ionotropic glutamate receptors in the substantia nigra to mediate rapid activation, M2‐like muscarinic autoreceptors in the pedunculopontine tegmental nucleus to mediate decreased activation, and muscarinic receptors in the substantia nigra (probably of the M5 subtype) to mediate prolonged activation, of the nigrostriatal dopaminergic system.
Conditional involvement of striatal serotonin3 receptors in the control of in vivo dopamine outflow in the rat striatum
Authors: Porras Grégory , De Deurwaerdère Philippe , Moison Delphine , Spampinato Umberto 
Published: March 2003

AbstractSerotonin3 (5‐HT3) receptors can affect motor control through an interaction with the nigrostriatal dopamine (DA) neurons, but the neurochemical basis for this interaction remains controversial. In this study, using in vivo microdialysis, we assessed the hypothesis that 5‐HT3 receptor‐dependent control of striatal DA release is conditioned by the degree of DA and/or 5‐HT neuron activity and the means of DA release (impulse‐dependent vs. impulse‐independent). The different DA‐releasing effects of morphine (1 and 10 mg/kg), haloperidol (0.01 mg/kg), amphetamine (1 and 2.5 mg/kg), and cocaine (10 and 20 mg/kg) were studied in the striatum of freely moving rats administered selective 5‐HT3 antagonists ondansetron (0.1 mg/kg) or MDL 72222 (0.03 mg/kg). Neither of the 5‐HT3 antagonists modified basal DA release by itself. Pretreatment with ondansetron or MDL 72222 reduced the increase in striatal DA release induced by 10 mg/kg morphine but not by 1 mg/kg morphine, haloperidol, amphetamine or cocaine. The effect of 10 mg/kg morphine was also prevented by intrastriatal ondansetron (1 µm) administration. Reverse dialysis with ondansetron also reduced the increase in DA release induced by the combination of haloperidol and the 5‐HT reuptake inhibitor citalopram (1 mg/kg). Considering the different DA and 5‐HT‐releasing properties of the drugs used, our results demonstrate that striatal 5‐HT3 receptors control selectively the depolarization‐dependent exocytosis of DA only when central DA and 5‐HT tones are increased concomitantly.
Repeated restraint stress suppresses neurogenesis and induces biphasic PSA‐NCAM expression in the adult rat dentate gyrus
Authors: Pham Kara , Nacher Juan , Hof Patrick R. , McEwen Bruce S. 
Published: March 2003

AbstractChronic restraint stress has been shown to induce structural remodelling throughout the interconnected dentate gyrus‐CA3 fields. To find out how this stressor affects the rate of adult hippocampal neurogenesis, we subjected rats to acute or chronic restraint stress and assessed the proliferation, survival and differentiation of newly born cells in the dentate gyrus. We also examined polysialylated neural cell adhesion molecule expression, a molecule normally expressed in immature neurons and important for morphological plasticity. The results show that acute restraint stress did not change either the proliferation of dentate gyrus precursor cells or the expression of polysialylated neural cell adhesion molecule, whereas 3 weeks of chronic restraint stress suppressed proliferation by 24% and increased polysialylated neural cell adhesion molecule expression by 40%. The study was extended for an additional 3 weeks to trace the survival and development of the cells born after the initial 3 weeks of restraint. Rats subjected to 6 weeks of daily restraint stress exhibited suppressed cell proliferation and attenuated survival of the recently born cells after the extended time course, resulting in a 47% reduction of granule cell neurogenesis. Furthermore, 6 weeks of chronic stress significantly reduced the total number of granule cells by 13% and the granule cell layer volume by 5%. Expression of polysialylated neural cell adhesion molecule followed a biphasic time course, displaying a significant up‐regulation after 3 weeks of daily restraint stress that was lost after 6 weeks of stress. These studies may help us understand the basis for hippocampal shrinkage and raise questions about the ultimate reversibility of the effects of chronic stress.
Differentiation and migration of astrocytes in the spinal cord following dorsal root injury in the adult rat
Authors: Kozlova Elena N. 
Published: March 2003

AbstractNerve fibre degeneration in the spinal cord is accompanied by astroglial proliferation. It is not known whether these cells proliferate in situ or are recruited from specific regions harbouring astroglial precursors. We found cells expressing nestin, characteristic of astroglial precursors, at the dorsal surface of the spinal cord on the operated side from 30 h after dorsal root injury. Nestin‐expressing cells dispersed to deeper areas of the dorsal funiculus and dorsal horn on the operated side during the first few days after injury. Injection of bromodeoxyuridine (BrdU) 2 h before the end of the experiment, at 30 h after injury, revealed numerous BrdU‐labelled, nestin‐positive cells in the dorsal superficial region. In animals surviving 20 h after BrdU injection at 28 h postlesion, cells double‐labelled with BrdU and nestin were also found in deeper areas. Labeling with BrdU 2 h before perfusion showed proliferation of microglia and radial astrocytes in the ventral and lateral funiculi on both sides of the spinal cord 30 h after injury. Nestin‐positive cells coexpressed the calcium‐binding protein Mts1, a marker for white matter astrocytes, in the dorsal funiculus, and were positive for glial fibrillary acidic protein (GFAP), but negative for Mts1 in the dorsal horn. One week after injury the level of nestin expression decreased and was undetectable after 3 months. Taken together, our data indicate that after dorsal root injury newly formed astrocytes in the degenerating white and grey matter first appear at the dorsal surface of the spinal cord from where some of them subsequently migrate ventrally, and differentiate into white‐ or grey‐matter astrocytes.
Selective stimulation of striatal dopamine receptors of the D1‐ or D2‐class causes opposite changes of fos expression in the rat cerebral cortex
Authors: Blandini Fabio , Fancellu Roberto , Orzi Francesco , Conti Giuseppe , Greco Rosaria , Tassorelli Cristina , Nappi Giuseppe 
Published: March 2003

SummaryIt has been suggested that activation of striatal neurons expressing D1 or D2 dopamine receptors elicits opposite changes in the net output of the basal ganglia circuitry and, consequently, in the functional interactions of the circuit with the cerebral cortex. In particular, it has been recently reported that striatal D1 receptors may regulate cortex function. To further address this issue, we mapped cerebral expression of Fos protein following intrastriatal stimulation of D1‐ or D2‐class receptors in freely moving animals. Using permanent cannulas implanted in the right striatum, Sprague–Dawley rats received intrastriatal microinfusions of SKF 38393 (D1 agonist) or quinpirole (D2 agonist) or saline (controls), combined with systemic administration of D1 antagonist SCH 23390 or D2 antagonist eticlopride or saline. Animals treated with SKF 38393 showed dose‐dependent, massive Fos increases in the motor, somatosensory, auditory, visual and limbic regions of the cerebral cortex, ipsilaterally to the injected striatum. Consistent Fos expression was also found in the injected striatum and, bilaterally, in the nucleus accumbens shell. These increases were effectively counteracted by systemic SCH 23390. Conversely, quinpirole did not induce significant cortical or striatal expression of Fos, which was instead observed after the systemic administration of eticlopride. Fos was not detected in any of the other basal ganglia nuclei, regardless of the dopamine agonists or antagonists used. Our results confirm that striatal D1 dopamine receptors play a central role in the modulation of cortical activity, thus providing additional information on the functional interaction between basal ganglia circuitry and cerebral cortex.
Inhibition of hippocampal Jun N‐terminal kinase enhances short‐term memory but blocks long‐term memory formation and retrieval of an inhibitory avoidance task
Authors: Bevilaqua Lia R. M. , Kerr Daniel S. , Medina Jorge H. , Izquierdo Iván , Cammarota Martín 
Published: March 2003

AbstractLearning initiates a series of plastic events the occurrence of which are required for the storage of information related to the training experience. Several lines of evidence indicate that, in the rat hippocampus, different members of the family of mitogen‐activated protein kinases (MAPK) play a key role in the onset of such plastic events. Using SP600125, the newly developed inhibitor of the MAPK c‐Jun amino‐terminal kinase (JNK), we show a direct involvement of this protein kinase in mnemonic processes. The intra‐CA1 infusion of SP600125, at a dose that in naïve animals significantly reduced the phosphorylation levels of c‐Jun without affecting the activity of ERK1/2 or p38 MAPK, enhanced short‐term memory (STM) but blocked long‐term memory (LTM) formation and retrieval of an inhibitory avoidance learning task. No action of this drug on locomotor/exploratory activity or general anxiety state could be detected. The significance of these results is discussed in the context of others describing the independence of LTM from STM.
Local energy depletion in the basal forebrain increases sleep
Authors: Kalinchuk Anna V. , Urrila Anna‐Sofia , Alanko Lauri , Heiskanen Silja , Wigren Henna‐Kaisa , Suomela Maricel , Stenberg Dag , Porkka‐Heiskanen Tarja 
Published: March 2003

AbstractSleep saves energy, but can brain energy depletion induce sleep? We used 2,4‐dinitrophenol (DNP), a molecule which prevents the synthesis of ATP, to induce local energy depletion in the basal forebrain of rats. Three‐hour DNP infusions induced elevations in extracellular concentrations of lactate, pyruvate and adenosine, as well as increases in non‐REM sleep during the following night. Sleep was not affected when DNP was administered to adjacent brain areas, although the metabolic changes were similar. The amount and the timing of the increase in non‐REM sleep, as well as in the concentrations of lactate, pyruvate and adenosine with 0.5–1.0 mm DNP infusion, were comparable to those induced by 3 h of sleep deprivation. Here we show that energy depletion in localized brain areas can generate sleep. The energy depletion model of sleep induction could be applied to in vitro research into the cellular mechanisms of prolonged wakefulness.
Response of wheat genotypes efficient in P utilisation and genotypes responsive to P fertilisation to different P banding depths and watering regimes
Authors: Valizadeh G. R. , Rengel Z. , Rate A. W. 
Published: March 2003

The capacity of wheat roots to lift water from subsoil with high moisture content into dry topsoil (hydraulic lift) and the subsequent impact on P uptake from dry topsoil are poorly understood. Two experiments were set up to test the capacity of 4 wheat genotypes differing in P efficiency to take up P from the fertiliser banded in dry topsoil (with wet subsoil). The interactions among genotypes, banding depths, and watering regimes (whole-profile or subsoil-only watering) were also characterised. The root system increased soil water content from 64 to 90 g/kg soil around the P fertiliser band by taking up water in the subsoil and releasing it into the dry topsoil during the night. Phosphorus applied as a band at 20 mg P/kg soil in dry topsoil (5 cm deep) significantly increased P uptake and shoot weight compared with a nil P control. Westonia and Gutha genotypes (efficient in P utilisation, based on dry matter produced per unit of P taken up) had higher shoot weights than Aroona and Wawht 2074 (genotypes responsive to P fertilisation, based on dry matter produced per unit of P fertiliser applied). Greater growth of wheat genotypes occurred in the treatment with P fertiliser banded at a depth of 5 cm compared with 15 cm in the whole-profile watering treatment, but no difference between banding depths was noted in the subsoil-only watering treatment. Wheat genotypes responsive to P fertilisation increased P uptake and shoot weight at the 5-cm P banding depth and the whole-profile watering treatment compared with genotypes efficient in P utilisation. Phosphorus-utilisation-efficient genotypes increased shoot growth more than other genotypes in the subsoil-only watering treatment. It can be concluded that roots of various wheat genotypes lift water from wet subsoil into the dry topsoil (hydraulic lift). Phosphorus fertiliser banded at 5-cm depth in dry topsoil increased P uptake and wheat growth due to the presence of hydraulically lifted water. Genotypes that are efficient in utilising P increased shoot weight more than genotypes responsive to P fertilisers in the subsoil-only watering treatment. In contrast, P-responsive genotypes increased shoot growth more than P-utilisation-efficient genotypes when P fertiliser was banded at 5-cm depth, and a whole-profile watering regime was imposed.
An Optical Design for an Antarctic 2 m Telescope with a Near IR Imager
Authors: Gillingham P. R. 
Published: March 2003

AbstractA study has been made of the optical performance to be expected from an Antarctic Ritchey Chrétien telescope with a 2 m diameter primary mirror imaging directly onto a detector array in the K and L infrared windows. Near diffraction limited performance is provided across a flat 30 arcmin diameter field by compensating the astigmatism and field curvature with a meniscus lens which also serves as the Dewar window. With baffling inside and Narcissus mirrors outside the Dewar, extraneous radiation can be kept to a low level.