bluuebunny/crossref_metadata_2025_split huggingface dataset:
Attenuation of the norepinephrine transporter activity and trafficking via interactions with α‐synuclein
Authors: Wersinger Christophe , Jeannotte Alexis , Sidhu Anita 
Published: December 2006

AbstractAlpha‐synuclein (α‐Syn) has been studied in the context of Parkinson's disease, but its normative role remains elusive. We have shown that α‐Syn regulates the homeostasis of dopaminergic and serotonergic synapses, through trafficking of the dopamine and serotonin transporter, respectively. In the present study we sought to determine if α‐Syn could also modulate noradrenergic signaling, by studying its interactions with the norepinephrine transporter (NET). We co‐transfected Ltk–cells with increasing amounts of α‐Syn DNA and a constant amount of NET DNA, and observed a progressive decrease (68%) in [3H]‐NE uptake in cells co‐transfected with a ratio of 3 : 1 α‐Syn : NET DNA. TheKdof transport did not change, but increasing α‐Syn caused a decrease in theVmaxof the transporter, from 2.27 ± 0.14 to 0.89 ± 0.15 pmol/min/105 cells, with NET expression alone or 4 : 1 ratio of α‐Syn : NET transfection, respectively. Decreases in surface biotinylation and [3H]‐nisoxetine binding kinetics in intact cells revealed that NET cell surface expression was attenuated in correlation to the amount of α‐Syn co‐transfected into cells. The interaction between NET and α‐Syn occurred via the NAC domain of α‐Syn, the region directly responsible for self‐aggregation. These findings are the first to show that α‐Syn has a central role in the homeostasis of noradrenergic neurons. Together with our previous studies on dopamine and serotonin transporters, we propose that a primary physiological role of α‐Syn may be to regulate the homeostasis of monoamines in synapses, through modulatory interactions of the protein with monoaminergic transporters.
Spinal motoneuron synaptic plasticity during the course of an animal model of multiple sclerosis
Authors: Marques K. B. , Santos L. M. B. , Oliveira A. L. R. 
Published: December 2006

AbstractDuring the course of experimental autoimmune encephalomyelitis, a massive loss of motor and sensitive function occurs, which has been classically attributed to the demyelination process. In rats, the clinical signs disappear within 5 days following complete tetraplegia, indicating that demyelination might not be the only cause for the rapid evolution of the disease. The present work investigated the occurrence of experimental autoimmune encephalomyelitis‐induced changes of the synaptic covering of spinal motoneurons during exacerbation and after remission. The terminals were typed with transmission electron microscopy as C‐, F‐ and S‐type. Immunohistochemical analysis of synaptophysin, glial fibrillary acidic protein and the microglia/macrophage marker F4/80 were also used in order to draw a correlation between the synaptic changes and the glial reaction. The ultrastructural analysis showed that, during exacerbation, there was a strong retraction of both F‐ and S‐type terminals. In this sense, both the covering as well as the length of the remaining terminals suffered great reductions. However, the retracted terminals rapidly returned to apposition, although the mean length remained shorter. A certain level of sprouting may have occurred as, after remission, the number of F‐terminals was greater than in the control group. The immunohistochemical analysis showed that the peak of synaptic loss was coincident with an increased macro‐ and microglial reaction. Our results suggest that the major changes occurring in the spinal cord network during the time course of the disease may contribute significantly to the origin of the clinical signs as well as help to explain their rapid recovery.
Nicotinic receptor‐mediated enhancement of long‐term potentiation involves activation of metabotropic glutamate receptors and ryanodine‐sensitive calcium stores in the dentate gyrus
Authors: Welsby Philip , Rowan Michael , Anwyl Roger 
Published: December 2006

AbstractLittle is known about the mechanisms underlying the enhancement of long‐term potentiation (LTP) by nicotine. In the present study, the mechanisms of nicotinic enhancement of LTP were investigated in the rat dentate gyrus in vitro. Acute application of nicotine enhanced LTP induction, an action requiring activation of α7 nicotinic acetylcholine receptors (nAChRs), as it was blocked by the nAChR antagonist methyl‐lycaconitine, mimicked by the acetylcholine receptor agonist choline and absent in mutant mice null for α7 nAChR. Nicotinic enhancement of LTP was both dependent on N‐methyl‐d‐aspartate receptor activation, as no LTP was induced in the presence of nicotine and an N‐methyl‐d‐aspartate receptor antagonist, and expressed post‐synaptically, as no change in paired‐pulse ratio accompanied nicotinic enhancement of LTP. The nicotinic‐enhanced component of LTP, unlike control LTP, was dependent on activation of metabotropic glutamate receptors (mGluRs), being inhibited by the group I/II antagonist LY341495 and the mGluR5 antagonist MPEP, and also dependent on influx of Ca via L‐type Ca channels and release from ryanodine (RyR)‐sensitive intracellular stores, being prevented by nifedipine and RyR, respectively. It is suggested that nicotinic activation of the Ca‐permeable α7 nAChRs fills RyR Ca stores and release of Ca from such stores by high‐frequency stimulation via Ca‐induced Ca release and activation of mGluRs induces an additional component of LTP which summates with control LTP. Chronic application of nicotine in vivo also enhanced LTP induction in slices and was dependent on activation of mGluRs and Ca release from RyR‐sensitive intracellular stores, although acutely applied nicotine was not required for such enhanced LTP.
Postnatal switching of NMDA receptor subunits from NR2B to NR2A in rat facial motor neurons
Authors: Xing Guo‐Gang , Wang Rengang , Yang Bo , Zhang Dongxian 
Published: December 2006

AbstractThe subunit composition ofN‐methyl‐d‐aspartate (NMDA) receptors affects their function under normal and pathological conditions. Functional NMDA receptors are expressed in lower motor neurons, but their subunit composition has not been defined. Here, we employed electrophysiology, quantitative PCR, and immunohistochemistry to investigate the subunit composition of NMDA receptors in postnatal motor neurons of the Wistar rat facial nucleus (FN). Whole‐cell patch clamp recordings of acutely dissociated motor neurons from postnatal days 3 and 4 (P3–P4) showed that ifenprodil, a specific antagonist of the NMDA receptor 2B (NR2B) subunit, inhibited 91.62% ± 2.02% of NMDA‐induced current, whereas NVP‐AAM007, a specific antagonist of the NMDA receptor 2A (NR2A) subunit, inhibited much less of the current (16.69% ± 3.28%). Starting from P5, the inhibitory effects of ifenprodil and NVP‐AAM007 gradually decreased and increased, respectively, such that the effect of NVP‐AAM007 exceeded that of ifenprodil by P10. At P14, most of the NMDA‐induced current was inhibited by NVP‐AAM007 (84.59% ± 3.35%). Consistent with this, NR2B mRNA and protein were expressed highly at P3 and then gradually decreased by more than 75% by P14 in FN motor neurons, while NR1 was expressed stably over the same ages. However, NR2A mRNA and protein showed relatively constant levels between P3–P10 and decreased to 45% and 75% of the P3 level, respectively, by P14. Thus, analysis of functional NMDA receptors is critical to revealing subunit switching, which may be an important step in postnatal development of FN motor neurons.
Context‐dependent prefrontal cortex regulation of cocaine self‐administration and reinstatement behaviors in rats
Authors: Di Pietro Nina C. , Black Yolanda D. , Kantak Kathleen M. 
Published: December 2006

AbstractEvidence of stimulus attribute‐specificity within the prefrontal cortex (PFC) suggests that different prefrontal subregions may contribute to cocaine addiction in functionally distinct ways. Thus, the present study examined the effects of lidocaine‐induced inactivation of two distinct PFC subregions, the prelimbic (PL) or dorsal agranular insular (AId) cortices, on drug‐seeking and drug‐taking behaviors under cocaine maintenance and reinstatement testing conditions in rats trained to self‐administer 1 mg/kg cocaine under a second‐order schedule of drug delivery. Throughout maintenance and reinstatement phases, rats were exposed to conditioned light cues and contextual odor or sound cues. Results showed that PL inactivation during maintenance test sessions significantly reduced drug‐seeking and drug‐taking behaviors, and disrupted patterns of responding in rats exposed to light–sound, but not light–odor, cues. Moreover, lidocaine‐induced inactivation of the PL significantly attenuated drug‐seeking behavior during cue‐induced and cocaine prime‐induced reinstatement in rats exposed to light–sound cues only. In contrast, AId inactivation significantly attenuated cue‐induced reinstatement of drug‐seeking behavior in rats exposed to light–odor cues only. Drug‐seeking and drug‐taking behaviors in these rats were not disrupted during maintenance and cocaine prime‐induced reinstatement testing regardless of the type of contextual cues used. Together, these data suggest that PL and AId subregions play separate yet overlapping roles in regulating cocaine addiction in rats in ways that are dependent on the presence or absence of cocaine and on the types of contextual cues present in the cocaine self‐administration environment.
Activation of class I metabotropic glutamate receptors limits dendritic growth of Purkinje cells in organotypic slice cultures
Authors: Sirzen‐Zelenskaya Alexandra , Zeyse Judith , Kapfhammer Josef P. 
Published: December 2006

AbstractThe development of the dendritic tree of a neuron is a complex process which is thought to be regulated strongly by signals from afferent fibers. We showed previously that the blockade of glutamatergic excitatory neurotransmission has little effect on Purkinje cell dendritic development. We have now studied the effects of glutamate receptor agonists on the development of Purkinje cell dendrites in mouse organotypic slice cultures. The activation of N‐methyl‐d‐aspartate receptors had no major effect on Purkinje cell dendrites and the activation of (RS)‐alpha‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazole proprionic acid receptors was strongly excitotoxic so that no analysis of its effects on dendritic development was possible. The activation of metabotropic glutamate receptors led to a very strong inhibition of dendritic growth, resulting in Purkinje cells with very small stubby dendrites. This effect was specific for the activation of class I metabotropic glutamate receptors and could not be reduced by blocking synaptic transmission in the cultures, indicating that it was mediated by receptors present on Purkinje cells. Pharmacological experiments suggest that the signaling pathway involved does not require activation of phospholipase C or protein kinase C. The inhibition of dendritic growth by activation of class I metabotropic glutamate receptor could be a useful negative feedback mechanism for limiting the size of the dendritic tree of Purkinje cells after the establishment of a sufficient number of parallel fiber contacts. This developmental mechanism could protect Purkinje cells from excitotoxic death through excessive release of glutamate from an overload of parallel fiber contacts.
Axonal retraction and regeneration induced byN,N‐diethyldithiocarbamate (DEDTC) in the central nervous system
Authors: Junyent Fèlix , Utrera Juana , Auladell Carme 
Published: December 2006

AbstractDithiocarbamates (DTCs), such as disulfiram, have been used in aversion therapy for alcoholism even though an inherent toxicity is induced, which is related mainly to peripheral neuropathy and is associated with behavioural and neurological complications. At anatomical and histopathological levels, DTCs affect structural elements in nervous tissue, such as axonal degeneration and alterations in the cytoskeletal proteins of astrocytes. Therefore, given the axonal effects of DTCs and to gain further insight into axonal growth and axonal pathfinding in the central nervous system (CNS), here we established anin vivoexperimental model of mouse development. Daily intraperitoneal injections ofN,N‐diethyldithiocarbamate (DEDTC), the first metabolite of disulfiram, were given from postnatal day 2 (P2) until P15. From P16 until P30, animals were not treated. Treatment induced considerable physiological alterations, such as growth delay, throughout postnatal development. Moreover, by immunohistochemistry techniques, we observed important alterations in the cytoskeletal glial protein at early stages of postnatal development. At later stages (P15), the immunoreactivity pattern detected by an antibody against axonal neurofilaments (anti‐NF‐H) showed alteration in the axonal distribution pattern followed by drastic axonal loss at P22, data that were corroborated using an anti‐MBP (myelin basic protein) antibody. Using an antibody against the beta amyloid precursor protein (APP), we detected axonal injury. Furthermore, given that we observed axonal re‐growth in adulthood in thein vivomodel presented, we propose that this model would be a good system in which to identify new strategies for inducing regenerative growth in neural diseases in which axonal regeneration is blocked.
Functional dentate gyrus neurogenesis in a rapid kindling seizure model
Authors: Smith Paul D. , McLean Karen J. , Murphy Michael A. , Turnley Ann M. , Cook Mark J. 
Published: December 2006

AbstractNeurogenesis in the adult mammalian hippocampus resulting in long‐term persistence of new neurons with features of capacity for functional activation is recognized. Many stimuli are capable of increasing the rate of neurogenesis, including seizure activity. Whether these insults result in an increased number of new functionally active neurons over and above the baseline rate of neurogenesis is not known. The rapid electrical amygdala kindling (REAK) model of seizures isolates the effects of seizures alone in the absence of neuronal death and the resulting seizures induce expression of c‐Fos in the vast majority of dentate gyrus (DG) granule cells. C57BL/6 mice were exposed to REAK then injected with bromodeoxyuridine (BrDU) to label dividing cells, then re‐exposed to REAK after a delay period to allow detection of functional activation in new neurons by measurement c‐Fos expression in response to seizures. Adult subgranular zone cells migrated into the DG granule cell layer (GCL), assumed a neuronal phenotype and demonstrated seizure‐dependent responsiveness. Larger absolute numbers of new neurons demonstrating seizure‐dependent activation were found in the GCL of previously kindled mice. Seizures are capable of increasing the number of new neurons with the capacity for functional activation laid down in the postseizure period and incorporated into seizure‐activated circuitry.
Effects of personal familiarity on early neuromagnetic correlates of face perception
Authors: Kloth Nadine , Dobel Christian , Schweinberger Stefan R. , Zwitserlood Pienie , Bölte Jens , Junghöfer Markus 
Published: December 2006

AbstractThis study investigated effects of familiarity and orientation on face processing by means of magnetoencephalography. Participants were presented with photographs of personally familiar, famous and unfamiliar faces in both upright and inverted orientation. They had to decide whether faces were familiar by means of manual yes/no responses. Independent of orientation, we observed a clear modulation of the M170 by familiarity, with personally familiar faces evoking larger amplitudes than unknown faces. The M170 was also sensitive to orientation, with larger amplitudes for inverted than upright faces. Moreover, the M170 exhibited larger amplitudes over the right than over the left hemisphere, but this asymmetry was present for upright faces only. The present data suggest that at least for personally familiar faces, neural correlates of identification start no later than ∼ 170 ms, and underline a special role of the right hemisphere for faces in their typical upright orientation.
Cholinergic modulation in the olfactory bulb influences spontaneous olfactory discrimination in adult rats
Authors: Mandairon Nathalie , Ferretti Casara Jean , Stack Conor M. , Rubin Daniel B. , Cleland Thomas A. , Linster Christiane 
Published: December 2006

AbstractCholinergic neuromodulation in the olfactory bulb has been hypothesized to regulate mitral cell molecular receptive ranges and the behavioral discrimination of similar odorants. We tested the effects of cholinergic modulation in the olfactory bulb of cannulated rats by bilaterally infusing cholinergic agents into the olfactory bulbs and measuring the rats' performances on separate spontaneous and motivated odor‐discrimination tasks. Specifically, 6 µL/bulb infusions of vehicle (0.9% saline), the muscarinic antagonist scopolamine (7.6 mm and 38 mm), the nicotinic antagonist mecamylamine hydrochloride (3.8 mm and 19 mm), a combination of both antagonists, or the acetylcholinesterase inhibitor neostigmine (8.7 mm) were made 20 min prior to testing on an olfactory cross‐habituation task or a rewarded, forced‐choice odor‐discrimination task. Spontaneous discrimination between chemically related odorants was abolished when nicotinic receptors were blocked in the olfactory bulb, and enhanced when the efficacy of cholinergic inputs was increased with neostigmine. Blocking muscarinic receptors reduced but did not abolish odor discrimination. Interestingly, no behavioral effects of modulating either nicotinic or muscarinic receptors were observed when rats were trained on a reward‐motivated odor‐discrimination task. Computational modeling of glomerular circuitry demonstrates that known nicotinic cholinergic effects on bulbar neurons suffice to explain these results.
Dynamics and identification of soil microbial populations actively assimilating carbon from 13C‐labelled wheat residue as estimated by DNA‐ and RNA‐SIP techniques
Authors: Bernard Laetitia , Mougel Christophe , Maron Pierre‐Alain , Nowak Virginie , Lévêque Jean , Henault Catherine , Haichar Feth el Zahar , Berge Odile , Marol Christine , Balesdent Jérome , Gibiat Frédéric , Lemanceau Philippe , Ranjard Lionel 
Published: December 2006

SummaryThis work is the first report on the use of DNA‐, RNA‐SIP approaches to elucidate the dynamics and the diversity of bacterial populations actively assimilating C derived from plant residues labelled at more than 90% 13C. Wheat‐residues, were incorporated and incubated into soil microcosms for 28 days. At the end of the incubation time, no more than 55% of the total CO2 released was 13C‐labelled, suggesting the occurrence of an important priming effect process. After 7 days, more than 30% of the whole DNA extracted were labelled, allowing an efficient separation of labelled from unlabelled DNA using density gradient centrifugation. The genetic structure of bacterial community, assessed by Automated Ribosomal Intergenic Spacer Analysis technique, was deduced from the 13C‐ and 12C‐fractions of control and enriched conditions, over the time course of the experiment. Dynamics showed that wheat residues directly induced a rapid and durable stimulation of fresh organic matter (FOM) degrading populations (13C), while specific soil organic matter (SOM) degrading populations (12C) seemed to be indirectly stimulated only at the early time point (t7d). After 14 days of incubations, 16S rRNA clone libraries were elaborated on 12C‐ and 13C‐RNA extracted from enriched microcosms, as well as 12C‐RNA extracted from control condition. Stimulation of the β‐ and γ‐subgroups of proteobacteria, where numerous populations were previously described as r‐strategists or copiotrophic organisms, was recorded in the 13C‐fraction. In the mean time, several phyla like Actinobacteria, Cyanobacteria, Candidate, Gemmatimonadetes and Planctomycetes were only present in 12C fractions. Surprisingly, several sequences affiliated to species characterized as oligotrophic organisms were retrieved in both types of fraction. Trophic relationships between soil bacteria involved in FOM and SOM degradation were discussed on the basis of different hypotheses of Fontaine and colleagues (2003) concerning the mechanisms of the priming effect induction.
Fire persistence traits of plants along a productivity and disturbance gradient in mediterranean shrublands of south‐east Australia
Authors: Pausas Juli G. , Bradstock Ross A. 
Published: December 2006

ABSTRACTAim To understand changes in fire persistence traits of plants along a latitudinal gradient, considering the interactions between productivity, community (fuel) structure and fire regime.Location A gradient in the south of Australia (latitude 33–37° S; longitude 140–143° E), including: Little Desert National Park (VIC), Big Desert Wilderness Park (VIC), Murray‐Sunset National Park (VIC), Danggali Conservation Park (SA) and Tarawi Nature Reserve (NSW).Methods We selected four areas along a latitudinal gradient for which information on fire history and vegetation was available. Then, we tested to what extent the four selected areas have different climate and different fire regimes. Plant cover values of different life forms provided an indication of the plant community structure and flammability, and the proportion of species with different fire persistence traits (resprouting, seedbank persistence) informed us on the trait selection.Results Precipitation decreases and temperature increases from south to north. Thus the selected sites represent a gradient from high productivity (low aridity) in the south to low productivity (high aridity) in the north. Fire statistics suggest that fire frequency parallels productivity. There is a tendency for life form dominance and community structure to shift in such a way that fuel connectivity is reduced towards the north. Resprouting species increase and obligate seeders decrease along the fire–productivity gradient.Main conclusions Changes in plant traits are difficult to understand without simultaneous consideration of both the disturbance and the productivity gradients. In our study area, fire regime and productivity interact in such a way that decreases in productivity imply changes in fuel structure that produce a reduction in fire frequency. Resprouting species are better represented at the high fire–productivity part of the gradient, while obligate seeders are better represented at the opposite end of the gradient. The results also emphasize the importance of considering not only climate changes but also changes in fuel structure to predict future fire regimes.
Unintended Consequences: Does Aid Promote Arms Races?*
Authors: Collier Paul , Hoeffler Anke 
Published: December 2006

AbstractUsing global data for the period 1960–99, we model military expenditure. Neighbours’ military spending and development aid are important determinants of military expenditure. An implication of the model is that there are regional arms races which are fuelled by aid. Potentially, aid is encouraging a ‘regional public bad’. There may, however, be an offsetting public good effect if military spending deters rebellions. In a simultaneous equation model, we find no deterrence effect of spending on the risk of civil war. Hence, there appears to be no regional public good effect offsetting the public bad arising from a neighbourhood arms race.
Hedonic Price Models for Dynamic Markets*
Authors: Kristofersson Dadi , Rickertsen Kyrre 
Published: December 2006

AbstractThe price of a product depends on its characteristics and will vary in dynamic markets. The model describes a processing firm that bids in an auction for a heterogeneous and perishable input. The reduced form of this model is estimated as an expanded random parameter model that combines a nonlinear hedonic bid function and inverse input demand functions for characteristics. The model was estimated by using 289,405 transactions from the Icelandic fish auctions. Total catch and gut ratio were the main determinants of marginal prices of characteristics, while the price of cod mainly depended on size, gutting and storage.