bluuebunny/crossref_metadata_2025 huggingface dataset:
Synaptic localization of the glutamate receptor subunit GluR2 in the rat nucleus tractus solitarii
Authors: Lachamp Philippe , Balland Bénédicte , Tell Fabien , Crest Marcel , Kessler Jean‐Pierre
Published: March 2003

The GluR2 subunit controls several key features of the alpha amino‐3‐hydroxy‐5‐methyl‐4‐isoxazole propionate (AMPA)‐type glutamate receptor including calcium permeability, rectification and gating. In the present study, electrophysiological recordings and immunocytochemistry were used to document the synaptic localization of GluR2 in the rat nucleus tractus solitarii (NTS). Synaptic responses recorded in NTS neurons exhibited linear current–voltage relationships suggestive of GluR2‐containing AMPA receptor responses. Furthermore, after antigen retrieval GluR2 immunolabelling in the NTS mainly consisted of small puncta. Double‐labelling experiments showed that these GluR2 puncta were apposed to glutamatergic synaptic terminals identified by type II vesicular glutamate transporter immunoreactivity. These results indicate that NTS glutamatergic synapses are endowed with AMPA receptors which contain the GluR2 subunit and are therefore likely to be both calcium‐impermeable and slowly desensitizing.
Group I metabotropic glutamate receptor‐mediated calcium signalling and immediate early gene expression in cultured rat striatal neurons
Authors: Mao Limin , Wang John Q.
Published: March 2003

Group I metabotropic glutamate receptors (mGluRs) are positively coupled to phospholipase C (PLC) via Gαq‐proteins and are expressed in the medium‐sized projection neurons of striatum. To characterize the group I mGluR/PLC‐sensitive modulation of intracellular Ca2+ ([Ca2+]i) signalling, primary neuronal cultures were prepared from the striatum of E19 rat embryos or neonatal day‐1 rat pups. Cytoplasmic Ca2+ signals were examined with fura‐2/AM at a signal cell level. After 17–18 days in culture, a profound Ca2+ response consisting of two phases was induced in cultured striatal neurons following bath application of the selective group I agonist, 3,5‐dihydroxyphenylglycine (DHPG). The [Ca2+]i elevation was concentration‐ and time‐dependent, and was blocked by coexposure to the group I antagonist, N‐phenyl‐7‐(hydroxyimino)cyclopropa[b]chromen‐1a‐carboxamide (PHCCC), or the PLC inhibitor, U‐73122, but not to the group II/III antagonist (RS)‐α‐methylserine‐O‐phosphate monophenyl ester (MSOPPE). A series of further pharmacological studies demonstrated that the initial spike‐like transient was dependent on intracellular Ca2+ mobilization through 1,4,5‐triphosphate‐sensitive stores, and the second long‐lasting rise was dependent on extracellular Ca2+ influx through N‐methyl‐d‐aspartate (NMDA) receptors and especially L‐type voltage‐operated Ca2+ channels. Lastly, using an immediate early gene c‐fos as a report of inducible gene expression, the resultant [Ca2+]i elevation contributes to DHPG‐stimulated c‐fos mRNA and Fos protein expression in striatal neurons as revealed by quantitative in situ hybridization and immunocytochemistry, respectively. These results demonstrate that group I mGluRs are able to affect Ca2+ homeostasis at multiple levels and trigger Ca2+‐sensitive gene transcription in striatal neurons.
Attenuation of sucrose reinforcement in dopamine D1 receptor deficient mice
Authors: El‐Ghundi Mufida , O'Dowd Brian F. , Erclik Mary , George Susan R.
Published: March 2003

Dopaminergic systems are thought to mediate the rewarding and reinforcing effects of palatable food. However, the relative contribution of different dopamine receptor subtypes is not clear. We used dopamine D1 receptor deficient mice (D^{\,‐/‐}_{1}) and their wild‐type and heterozygous littermates to study the role of the D1 receptor in palatable food reinforced behaviour using operant responding and free access paradigms. Non‐deprived mice were trained to press a lever for sucrose pellets under three schedules of reinforcement including fixed ratios (FR‐1 and FR‐4) and a progressive ratio (PR). Responding on one lever was reinforced by the delivery of a sucrose pellet or solution while responding on a second lever had no programmed consequences. Initially, D1 mutant mice took longer to learn to discriminate between the two levers and had significantly lower operant responding for sucrose pellets and solution than wild‐type and heterozygous mice under all schedules of reinforcement. Food deprivation enhanced responding on the active lever in all mice although it remained significantly lower in D^{\,‐/‐}_{1} mice than in control mice. Following extinction of sucrose reinforcement and reversal of the levers, D^{\,‐/‐}_{1} mice showed deficits in extinguishing and reversing previously learned responses. Home cage intake and preference of sucrose pellets and solutions when given under free‐choice access paradigms were similar among the groups.

These results suggest that the dopamine D1 receptor plays a role in the motivation to work for reward (palatable food) but not in reward perception and is critical in learning new but relevant information and discontinuing previously learned responses.
Connecting the dots: trafficking of neurotrophins, lectins and diverse pathogens by binding to the neurotrophin receptor p75NTR
Authors: Butowt Rafal , Von Bartheld Christopher S.
Published: March 2003

The common receptor for neurotrophins, p75, has important roles in internalization and trafficking of neurotrophins along axons. Recent studies show that an astonishing array of proteins, including lectins, pathogens and neurotoxins, bind the p75 receptor, suggesting that they can hijack and utilize this receptor for trafficking between neuronal populations within the nervous system. Such pathogens include the neurologically important rabies viruses, prion proteins, β‐amyloid and possibly tetanus toxin. These proteins may hijack existing transport machineries designed to traffick neurotrophins, thus allowing the infiltration and distribution of pathogens and toxins among vulnerable neuronal populations with devastating effects, as seen in rabies, prion encephalopathies, Alzheimer's disease and tetanic muscle spasm. The discovery of an entry and transport machinery that is potentially shared between pathogens and neurotrophins sheds light ono trafficking systems in the nervous system and may assist the design of novel therapeutic avenues that prevent or slow the progression of diverse chronic and acute neurological disorders.
Functional NMDA receptor channels generated by NMDAR2B gene transfer in rat cerebellar Purkinje cells
Authors: Kakegawa Wataru , Tsuzuki Keisuke , Iino Masae , Ozawa Seiji
Published: March 2003

The adult cerebellar Purkinje cell is an exceptional neuron in the central nervous system in that it expresses high levels of NMDAR1 (NR1) mRNA without expressing any NMDAR2 (NR2) mRNAs. It has no functional NMDA receptor (NMDAR) channels, although it receives enormous numbers of excitatory inputs. Despite the high level of NR1 mRNA expression, the presence and localization of NR1 protein in mature Purkinje cells are controversial. To examine the presence of NR1 protein and its ability to form functional NMDARs, we expressed the NR2B subunit in rat mature Purkinje neurons by Sindbis viral‐mediated gene transfer. The recombinant virus encoding both the NR2B and enhanced green fluorescent protein (GFP) genes (designated as SIN–EG–NR2B) infected Purkinje cells without infecting glial cells. GFP fluorescence was detected in the soma and throughout dendrites of Purkinje cells 18–24 h postinfection. In most of GFP‐positive cells, the expression of NR2B protein was detected by immunostaining with NR2B‐specific antibodies. In Purkinje cells infected with SIN–EG–NR2B, the iontophoretic application of NMDA induced prominent NMDAR‐mediated current responses, indicating that the exogenous NR2B was assembled with endogenous NR1 to form functional NMDARs. Furthermore, NMDAR‐mediated synaptic currents were detected at both the climbing fibre and parallel fibre synapses in infected Purkinje cells. Thus, the mature Purkinje cell produces NR1 protein that is ready to combine with NR2 to form functional NMDARs in excitatory synapses.
Protective effect of HSV‐mediated gene transfer of nerve growth factor in pyridoxine neuropathy demonstrates functional activity of trkA receptors in large sensory neurons of adult animals
Authors: Chattopadhyay Munmun , Goss James , Lacomis David , Goins William C. , Glorioso Joseph C. , Mata Marina , Fink David J.
Published: March 2003

The distinct distribution of trkA receptors on small neurons and trkC receptors on large neurons in the dorsal root ganglion correlates with the dependence of these two classes of neurons on nerve growth factor and neurotrophin‐3, respectively, for survival during development. In adult animals, the distribution of high affinity neurotrophin (trk) is complex and overlapping; neurotrophins are not required for cell survival, but may influence cell phenotype and the response to injury. In order to test the functional activity of trkA receptors in the sensory ganglia of adult animals in vivo, we examined the ability of a nerve growth factor‐expressing recombinant replication‐defective herpes simplex virus‐based vector to prevent the selective degeneration of large sensory fibres caused by intoxication with pyridoxine. Transduction of dorsal root ganglion neurons in vivo by subcutaneous inoculation of the nerve growth factor‐expressing vector prevented the development of pyridoxine‐induced neuropathy measured by electrophysiological, morphological and behavioural measures. These results demonstrate a functional activity of trkA receptors expressed on large neurons in the dorsal root ganglion in mature animals; this observation has important implications for the choice of neurotrophic factors for treatment of peripheral nerve disease.
Long‐term potentiation of glutamatergic synaptic transmission induced by activation of presynaptic P2Y receptors in the rat medial habenula nucleus
Authors: Price Gareth D. , Robertson Susan J. , Edwards Frances A.
Published: March 2003

A novel form of long‐term potentiation of glutamatergic synaptic transmission is described in the rat medial habenula nucleus. It occurs when uridine 5′‐triphosphate is bath applied at low micromolar concentrations and is prevented by Reactive Blue 2, suggesting that it is mediated by P2Y4 receptors. Uridine 5′‐diphosphate can also cause such a Reactive Blue 2‐sensitive potentiation, but at higher concentrations (200 µm), suggesting that this might also be an effect on the relatively uridine 5′‐diphosphate‐insensitive P2Y4 receptor. The potentiation is due to an increase in presynaptic release probability. It requires neither depolarization nor calcium influx postsynaptically and is thus probably non‐Hebbian. When potentiation due to low concentrations of uridine 5′‐triphosphate is inhibited in the presence of Reactive Blue 2, uridine 5′‐triphosphate causes instead a significant inhibition of glutamate release. We suggest that this inhibition may be mediated by a Reactive Blue 2‐insensitive P2Y2‐like receptor. At higher concentrations of uridine 5′‐triphosphate (200 µm), the inhibitory effect dominates such that even in the absence of Reactive Blue 2 no potentiation is seen.
Vagal modulation of nociception is mediated by adrenomedullary epinephrine in the rat
Authors: G. Khasar Sachia , G. Green Paul , Miao Frederick J.‐P. , Levine Jon D.
Published: March 2003

Vagal afferent activity modulates mechanical nociceptive threshold and inflammatory mediator‐induced hyperalgesia, effects that are mediated by the adrenal medulla. To evaluate the role of epinephrine, the major hormone released from the adrenal medulla, the β2‐adrenergic receptor antagonist ICI 118,551 was chronically administered to vagotomized rats and epinephrine to normal rats. In vagotomized rats, chronic administration of ICI 118,551 markedly attenuated vagotomy‐induced enhancement of bradykinin hyperalgesia but had no effect on nociceptive threshold. In normal rats, chronic epinephrine had the opposite effect, enhancing bradykinin hyperalgesia. Like vagotomy‐, epinephrine‐induced enhancement of hyperalgesia developed slowly, taking 14 days to reach its peak. Vagotomy induced a chronic elevation in plasma concentrations of epinephrine. We suggest that ongoing activity in vagal afferents inhibits the release of epinephrine from the adrenal medulla. Chronically elevated levels of epinephrine, occurring after vagotomy, desensitize peripheral β2‐adrenergic receptors and lead to enhancement of bradykinin hyperalgesia. The ability of prolonged elevated plasma levels of epinephrine to sensitize bradykinin receptors could contribute to chronic generalized pain syndromes.
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

Chronic 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

Olfactory 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

β‐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

Data 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

The 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

Serotonin3 (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

Chronic 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

Nerve 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

It 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

Learning 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

Sleep 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.
Vibrational and Electronic Energy Levels of Polyatomic Transient Molecules. Supplement B
Authors: Jacox Marilyn E.
Published: March 2003

A summary is presented of recently published, critically evaluated experimental vibrational and electronic energy level data for approximately 1700 neutral and ionic transient molecules and high temperature species possessing from three to sixteen atoms. Although the emphasis is on species with lifetimes too short for study using conventional sampling techniques, there has been selective extension of the compilation to include data for isolated molecules of inorganic species such as the heavy-metal oxides, which are important in a wide variety of industrial chemical systems. Radiative lifetimes and the principal rotational constants are included. Observations in the gas phase, in molecular beams, and in rare-gas and diatomic molecule matrices are evaluated, and several thousand references are cited. The types of measurement surveyed include conventional and laser-based absorption and emission techniques, laser absorption with mass analysis, and photoelectron spectroscopy.
Vibrational lifetimes of hydrogen in silicon
Authors: Lüpke G. , Tolk N. H. , Feldman L. C.
Published: March 2003

Characterization of defect and impurity reactions, dissociation, and migration in semiconductors requires a detailed understanding of the rates and pathways of vibrational energy flow, of the energy transfer channels, and of the coupling mechanisms between local modes and the phonon bath of the host material. Significant progress in reaching this goal has been accomplished in recent landmark studies exploring the excitation and dynamics of vibrational states associated with hydrogen in silicon. The lifetime of the Si–H stretch mode is found to be extremely dependent on the local solid-state structure, ranging from picoseconds for interstitial-like hydrogen, hundreds of picoseconds for hydrogen–vacancy complexes, to several nanoseconds for hydrogen bonded to Si surfaces—over three orders of magnitude variation. Such large variations in lifetime (transition probability) are extraordinarily rare in solid-state science. The level of theoretical investigation into the vibrational lifetime of the Si–H oscillator is less advanced. This state of affairs is partly because of the difficulties in explicitly treating slow relaxation processes in complex systems, and partly because, as suggested by experiment, a highly anharmonic coupling mechanism is apparently responsible for the (multiphonon) relaxation process. Even more importantly, because of the high frequency of the Si–H stretching motion, a quantum mechanical treatment of the Si–H oscillator is required. A combination of Bloch–Redfield theory and molecular dynamics simulation seems promising in describing the relaxation process of the Si–H vibrational modes. It is the aim of this review article to present a comprehensive overview of the recent accomplishments, current understandings, and future directions in this emerging field of time-resolved vibrational spectroscopy of point defects in solids.
Simulation of nonlinear dielectric properties of polyvinylidene fluoride based on the Preisach model
Authors: Tsang C. H. , Shin F. G.
Published: March 2003

The nonlinear dielectric properties of a ferroelectric material were studied based on the concepts of the Preisach model. In this work, the ferroelectric polymer polyvinylidene fluoride was chosen as an example. The electric displacement D in the material when subjected to a sinusoidal electric field of a given frequency was calculated by use of the Preisach model. Both in-phase and out-of-phase components as well as higher harmonics emerged naturally from the model calculation. D-E loops at different field amplitudes were simulated and Fourier analyzed. The Fourier coefficients obtained were compared with the experimental data [T. Furukawa, K. Nakajima, T. Koizumi, and M. Date, Jpn. J. Appl. Phys., Part 1 26, 1039 (1987)]. Essentially, almost all the broad experimental features were reproduced by the simulations. This model is able to account for finer features than the theoretical model used in the original paper.
Laser polarimetric measurement of equilibrium and fluctuating magnetic fields in a reversed field pinch (invited)
Authors: Brower D. L. , Ding W. X. , Terry S. D. , Anderson J. K. , Biewer T. M. , Chapman B. E. , Craig D. , Forest C. B. , Prager S. C. , Sarff J. S.
Published: March 2003

New developments in Faraday rotation polarimetry have provided the first measurements of current density profile and core magnetic fluctuations in the core of a high-temperature reversed field pinch. This has been achieved by a fast-polarimeter system with time response up to 1 μs and phase resolution <1 mrad. Recent experiments on Madison Symmetric Torus have directly measured radial magnetic field fluctuations in the plasma interior with amplitude 33 G, ∼1%. A broad spectrum of magnetic fluctuations is observed up to 100 kHz. Relaxation of the current density profile at the sawtooth crash occurs on the timescale of 100 μs. Reversed-field pinch behavior is determined in large part by magnetic fluctuations driven by the radial gradient in the parallel current density. Hence, measurement of magnetic fluctuations and the current density profile is essential to understand the link between the current density profile, fluctuations, and transport.
Poloidal magnetic field measurements and analysis with the DIII-D LIBEAM system (invited)
Authors: Thomas D. M.
Published: March 2003

For over 30 yrs, neutral lithium beams have been employed as a localized, noninvasive diagnostic on a variety of plasma experiments worldwide, providing a number of key physics measurements. On DIII-D the LIBEAM diagnostic has been designed to provide precise measurements of the local poloidal magnetic field in the edge region, a parameter of basic importance to understanding the stability of high performance tokamaks. We utilize the Zeeman splitting and known polarization characteristics of the collisionally excited 670.8 nm Li resonance line to interpret local magnetic field components viewed using a closely packed (ΔR∼5 mm) array of 32 view chords. A dual photoelastic modulator/linear polarizer combination serves to amplitude modulate the light in exact correspondence to its input polarization state. Subsequent narrowband spectral filtering using etalons and standard interference filters is used to isolate one of the three Zeeman components, and the polarization state of that component is recovered using a PC-based, multichannel digital lock-in detection system. Edge magnetic pitch angle profiles for a variety of shots have been reconstructed using a small number of chords and detailed analysis of the lock-in and dc signal levels. Present system performance appears to be limited by etalon performance as well as various broadening mechanisms in the beam that tend to decrease the polarization fraction in the observed component. A careful analysis of this effect and some strategies for improving the measured polarization will be presented.
A compact electron spectrometer for hot electron measurement in pulsed laser solid interaction
Authors: Chen H. , Patel P. K. , Price D. F. , Young B. K. , Springer P. T. , Berry R. , Booth R. , Bruns C. , Nelson D.
Published: March 2003

Ultraintense laser-matter interactions provide a unique source of temporally short, broad spectrum electrons, which may be utilized in many varied applications. One such, which we are pursuing, is as part of a diagnostic to trace magnetic field lines in a magnetically confined fusion device. An essential aspect of this scheme is to have a detailed characterization of the electron angular and energy distribution. To this effect we designed and constructed a compact electron spectrometer that uses permanent magnets for electron energy dispersion and over 100 scintillating fibers coupled to a 1024×1024 pixel charge coupled device as the detection system. This spectrometer has electron energy coverage from 10 keV to 60 MeV. We tested the spectrometer on a high intensity (1017–1021 W/cm2) short pulse (<100 fs) laser, JanUSP, at Lawrence Livermore National Laboratory using various solid targets. The details of the spectrometer and the experimental results will be reported.
New wide bandwidth in-vessel magnetic measurement system for RFX
Authors: Bolzonella T. , Pomaro N. , Serianni G. , Marcuzzi D.
Published: March 2003

A new system of internal magnetic coils is being implemented in the Reversed Field eXperiment Reversed Field Pinch (RFP). The global layout of the system has to take into account the peculiar characteristics of RFP plasmas and the integration with other internal and external measurements. The design of probes measuring fluctuations of different magnetic field components is described stressing how the requirements of thermal and electrical insulations are met. In particular, due to the large number of signals needed and to the limited space available inside the vessel, original solutions to minimize probe and cable dimensions were adopted. Thermal and electrical tests on prototypes were performed allowing, in addition, the validation of a numerical model for the study of the signal bandwidth.
Overview of diagnostics system for the TPE-RX reversed-field pinch
Authors: Yagi Y. , Koguchi H. , Sekine S. , Sakakita H. , Hirano Y. , Shimada T. , Canton A. , Innocente P.
Published: March 2003

An overview of the present diagnostics system for a reversed-field pinch machine, the toroidal pinch experiment RX [TPE-RX, R/a=1.72/0.45 m, Ip<1 MA (designed)], is presented. The diagnostic system of TPE-RX consists of measurement systems for (1) equilibrium configuration, (2) perturbing modes, and (3) global confinement properties. A concise explanation is given for these diagnostics systems. The mode-measurement system, in particular, is equipped with high toroidal resolution (up to the mode number of 32), which is necessary for the reversed-field pinch configuration. We have magnetic, thermal, and spectroscopic measurement systems for the toroidal distribution of the perturbing modes, which are useful for revealing the mode-locking structure.
Proposal for halo current diagnostic system for JET
Authors: Pomaro N. , Bolzonella T. , Fiorentin P. , Grando L. , Peruzzo S. , Riccardo V. , Sonato P.
Published: March 2003

One of the critical issues for the International Thermonuclear Experimental Reactor is a deep understanding of the origin, distribution, and scaling of halo currents flowing through plasma and vacuum vessel during vertical displacement events. The Joint European Torus (JET) can play a key role in this study, provided that new and more detailed information becomes available. This fact motivated the design of a set of sensors specifically aimed at improving the diagnostic capability of halo currents at JET. This new system is described in the article. It consists mostly of Rogowski coils and of a small number of toroidal field pickup coils. The former will measure directly the current flowing through the tiles of the first wall. The latter will allow the estimation of the total poloidal halo. The system is a compromise between the maximization of the spatial resolution in both toroidal and poloidal direction and the JET capability of adding new in-vessel probes, compatibly with existing feedthroughs needed to bring the signals outside the vessel. The main issues of the system are briefly reported, then the modifications of the in-vessel components, necessary to house the probes, are described together with the technological solutions adopted to improve the measurement quality. Finally, results of the electromechanical analyses performed to assess the reliability of the modified tiles are presented, too.
Density interferometer using the fast Alfven wave
Authors: Watson George , Heidbrink W. W.
Published: March 2003

Utilizing the dependence of the fast Alfven wave upon density, the mass density evolution of a plasma can be tracked via interferometry. In previous measurements on the DIII-D tokamak [H. Ikezi et al., Phys. Plasmas 3, 2306 (1996)], fast waves (∼60 MHz, ∼5 W) were launched from an antenna at the outer midplane. Detection was hampered by the poor sensitivity of the receiving antennas that were mounted behind protective graphite tiles on the inner wall. New antennas were installed where the graphite tiles were converted to be part of the receiving antenna, increasing reception by at least one order of magnitude. Density evolution measurements with these new antennas (∼100 MHz, 20 mW) were made for the first several hundred milliseconds until tracking was lost. The plasma shape and an evanescent layer are the main factors for this loss. Changes in wave propagation (as determined by the ray tracing code CURRAY) are less important. When tracking was successful, the density evolution observed from the new antennas show reasonable agreement with existing diagnostics. In addition, by placing receiving antennas on the same wall as the launching antenna and launching a frequency near the ion–ion hybrid frequency, it may be possible to make an ion species mix ratio measurement using the same diagnostic.
Velocity fluctuations and time dependent E×B flows in the JET boundary region
Authors: Gonçalves B. , Hidalgo C. , Pedrosa M. A. , Silva C. , Erents K. , Mathews G.
Published: March 2003

Fluctuations in the phase velocity of fluctuations have been computed from floating potential fluctuations in the JET plasma boundary region. Experimental results reinforce the idea that, in some conditions, fluctuations in the phase velocity are linked with fluctuations in radial–poloidal electric fields opening the possibility to investigate turbulent transport in the plasma core region from measurements of density fluctuations. These results indicate that time dependent radial electric fields and E×B shearing rates might be computed in the plasma core from measurement of density fluctuations.
Calorimeter probe for the DIII-D divertor
Authors: Watkins J. G. , Lasnier C. J. , Whyte D. G. , Stangeby P. C. , Ulrickson M. A.
Published: March 2003

Heat flux measurements of the DIII-D divertor plate have been obtained with 6 mm spatial resolution using a calorimeter probe. These measurements complement the infrared camera system normally used for heat flux measurements on DIII-D but at higher-spatial resolution. The calorimeter probe is inserted into the tokamak from below to a position which is flush with the lower divertor plate tiles using the divertor materials experimental station (DiMES). The DiMES mechanism allows for retraction of the probe behind a gate valve and removal from the tokamak for modification or calibration. A 6 mm diameter insulated graphite cylinder for collecting energy is mounted within a standard DiMES sample. A 0.8 mm diameter thermocouple, installed 4 mm below the surface, provides a measurement of the temperature during and after the plasma exposure. The 80 ms time constant for the measurement is fast enough to determine heat flux changes during the 5 s plasma discharge and heat flux profiles have been obtained using both fixed strike points and slow strike point sweeps across the calorimeter. Special electronics and isolation is necessary as the sample is in direct electrical contact with the plasma. The calorimeter observes approximately 100 °C temperature rise over one tokamak discharge. The thermocouple signals are typically less than 1 mV and must be amplified near the vacuum feedthrough, passed through a low-pass filter to eliminate magnetic pickup, isolated, and sent to the data acquisition system approximately 8 m away. Initial measurements are included.