bluuebunny/crossref_metadata_2025_split huggingface dataset:
Differential roles of corticotropin‐releasing factor receptor subtypes 1 and 2 in opiate withdrawal and in relapse to opiate dependence
Authors: Lu Lin , Liu Dehong , Ceng Xiabo , Ma Lan 
Published: July 2009

AbstractThe possible effects on the morphine withdrawal signs of the nonspecific corticotropin‐releasing factor (CRF) receptor antagonist α‐helical CRF, the selective CRF receptor subtype 1 antagonist CP‐154,526 and the selective CRF receptor subtype 2 antagonist antisauvagine‐30 (AS‐30) were investigated in rats. The most withdrawal signs, including jumping, teeth chatter, writhing, shakes, lacrimation, piloerection, irritability and diarrhoea, were attenuated by pretreatment with α‐helical CRF (10 µg i.c.v.) and CP‐154,526 (30 mg/kg i.p.). However, no morphine withdrawal signs except for diarrhea were significantly affected by pretreatment with AS‐30 (10 µg, i.c.v.). To investigate the possible role of different CRFR antagonists (α‐helical CRF, CP‐154,526 and AS‐30) in relapse to opiate dependence, the 28‐day extinction of morphine‐conditioned place preference (CPP) was used. The morphine‐CPP disappeared following a 28‐day extinction and then was reactivated by a single injection of 10 mg/kg morphine. Pretreatment with α‐helical CRF (10 µg, i.c.v.) and CP‐154,526 (30 mg/kg, i.p.) could significantly block this reactivation of morphine‐CPP. In contrast, pretreatment with AS‐30 (1 or 10 µg i.c.v.) did not affect this reactivation of morphine‐CPP. The present study demonstrated that activation of the CRF receptor is involved in morphine withdrawal signs and relapse to morphine dependence, and that the role of CRF receptor subtypes 1 and 2 in withdrawal and reactivation of morphine dependence is not identical. CRF receptor subtype 1, but not subtype 2, is largely responsible for the action of the CRF system on opiate dependence. These results suggest that the CRF receptor antagonists, particularly the CRF receptor subtype 1 antagonist, might be of some value in the treatment and prevention of drug dependence.
Interactions between imidazoline binding sites and dopamine levels in the rat nucleus accumbens
Authors: Barrot Michel , Rettori Marie‐Claire , Guardiola‐Lemaître Béatrice , Jarry Christian , Le Moal Michel , Piazza Pier Vincenzo 
Published: July 2009

AbstractImidazoline binding sites are present in the striatal complex and in the extended amygdala and have been implicated in mood disorders. In this report we analysed the influence of these sites on the functional activity of the mesolimbic dopaminergic transmission, one of the major brain systems involved in the regulation of motivation and reward. We studied the effects of two imidazoline ligands, S23229 and S23230 (respectively S(+) and R(–) enantiomers of the S22687 or (5‐[2‐methyl phenoxy methyl] 1,3‐oxazolin‐2‐yl) amine), on extracellular dopamine in the nucleus accumbens using microdialysis in freely moving rats. We compared these imidazoline ligands to cocaine, a dopamine uptake blocker known to increase extracellular dopamine concentrations. S23229 dose‐dependently increased extracellular dopamine and locomotor activity. S23230 dose‐dependently increased extracellular dopamine and produced a near‐significant dose–effect on locomotor activity. S23229 had a stronger efficacy than S23230 and increased dopamine levels in the nucleus accumbens at an extent similar to the one of cocaine. These results suggest that central imidazoline binding sites could contribute to the functional regulation of the mesolimbic dopaminergic system.
A brain slice model for in vitro analyses of astrocytic gap junction and connexin43 regulation: actions of ischemia, glutamate and elevated potassium
Authors: Nagy J. I. , Li W. E. I. 
Published: July 2009

AbstractBrain slices prepared from adult rats and maintained for up to 3 h in vitro were used to investigate the effects of pharmacological treatments on the phosphorylation state, immunolabelling characteristics and ultrastructural localization of astrocytic gap junctions and connexin43 (Cx43). Slices deprived of glucose/oxygen to mimic ischemia or those exposed to 1 mm glutamate for 1 h exhibited Cx43 dephosphorylation, epitope masking and gap junction internalization as revealed by Western blotting and Cx43 immunolocalization with various antibodies. Treatment with 15 mm K+ caused Cx43 dephosphorylation without junction internalization. The effects of glutamate and K+ were completely blocked by the N‐methyl‐d‐aspartate (NMDA) glutamate receptor antagonist 2‐amino‐5‐phosphonovalerate (APV), which acts largely on neuronal NMDA receptors, suggesting neuronal mediation of glial gap junction responses to these treatments. Astrocytes contained a dephosphorylated form of Cx43 with a typical migration profile at 41 kDa as well as novel, apparently dephosphorylated or partially phosphorylated, forms migrating at 43 kDa. These results indicate that slices prepared from adult brain can serve as a convenient model to investigate the molecular basis and receptor‐mediated mechanisms underlying astrocytic Cx43 responses that have been observed in vivo following cerebral ischemia or neural activation. These processes can be related in part to neuronal regulation of astrocytic gap junctional coupling state, which is also amenable to analysis in brain slices.
Subcellular compartmentalization of a potassium channel (Kv1.4): preferential distribution in dendrites and dendritic spines of neurons in the dorsal cochlear nucleus
Authors: Juiz José M. , Luján Rafael , Domínguez del Toro Eduardo , Fuentes V. , Ballesta Juan J. , Criado Manuel 
Published: July 2009

AbstractVoltage‐dependent ion channels have specific patterns of distribution along the neuronal plasma membrane of dendrites, cell bodies and axons, which need to be unravelled in order to understand their contribution to neuronal excitability and firing patterns. We have investigated the subcellular compartmentalization of Kv1.4, a transient, fast‐inactivating potassium channel, in fusiform cells and related interneurons of the rat dorsal cochlear nucleus. A polyclonal antibody which binds to a region near the N‐terminus domain of a Kv1.4 channel was raised in rabbits. Using a high‐resolution combination of immunocytochemical methods, Kv1.4 was localized mainly in the apical dendritic trunks and cell bodies of fusiform cells, as well as in dendrites and cell bodies of interneurons of the dorsal cochlear nucleus, likely cartwheel cells. Quantitative immunogold immunocytochemistry revealed a pronounced distal to proximal gradient in the dendrosomatic distribution of Kv1.4. In plasma membrane localizations, Kv1.4 was preferentially present in dendritic spines, either in the spine neck or in perisynaptic locations, always away from the postsynaptic density. These findings indicate that Kv1.4 is largely distributed in dendritic compartments of fusiform and cartwheel cells of the dorsal cochlear nucleus. Its preferential localization in dendritic spines, where granule cell axons make powerful excitatory synapses, suggests a role for this voltage‐dependent ion channel in the regulation of dendritic excitability and excitatory inputs.
Topographical projection from the superior colliculus to the nucleus of the brachium of the inferior colliculus in the ferret: convergence of visual and auditory information
Authors: Doubell Timothy P. , Baron Jérôme , Skaliora Irini , King Andrew J. 
Published: July 2009

AbstractThe normal maturation of the auditory space map in the deeper layers of the ferret superior colliculus (SC) depends on signals provided by the superficial visual layers, but it is unknown where or how these signals influence the developing auditory responses. Here we report that tracer injections in the superficial layers label axons with en passant and terminal boutons, both in the deeper layers of the SC and in their primary source of auditory input, the nucleus of the brachium of the inferior colliculus (nBIC). Electron microscopy confirmed that biocytin‐labelled SC axons form axodendritic synapses on nBIC neurons. Injections of biotinylated dextran amine in the nBIC resulted in anterograde labelling in the deeper layers of the SC, as well as retrogradely labelled superficial and deep SC neurons, whose distribution varied systematically with the rostrocaudal placement of the injection sites in the nBIC. Topographical order in the projection from the SC to the ipsilateral nBIC was confirmed using fluorescent microspheres. We demonstrated the existence of functional SC‐nBIC connections by making whole‐cell current‐clamp recordings from young ferret slices. Both monosynaptic and polysynaptic EPSPs were generated by electrical stimulation of either the superficial or deep SC layers. In addition to unimodal auditory units, both visual and bimodal visual–auditory units were recorded in the nBIC in vivo and their incidence was higher in juvenile ferrets than in adults. The SC‐nBIC circuit provides a potential means by which visual and other sensory or premotor signals may be delivered to the nBIC to calibrate the representation of auditory space.
Effect of feeding on Fos protein expression in sheep hypothalamus with special reference to the supraoptic and paraventricular nuclei: an immunohistochemical study
Authors: Chaillou Elodie , Baumont René , Tramu Gérard , Tillet Yves 
Published: July 2009

AbstractThe hypothalamus plays an important role in the control of food intake in different species, but there is little relevant information for ruminants like sheep. In order to study the putative role of several hypothalamic nuclei in food intake in sheep, Fos expression, a marker of cellular activity, was compared by immunohistochemistry between fed and unfed ewes. The expression of Fos protein was stimulated in the supraoptic nucleus of fed ewes, whereas it was increased in the paraventricular nucleus of unfed animals. In the latter nucleus, Fos immunoreactivity was mainly localized close to the third ventricle, an area corresponding to the parvocellular system of the nucleus, but never in the magnocellular system. In the paraventricular nucleus, the number of corticotrophin releasing factor‐immunoreactive neurons and the number of Fos/corticotrophin releasing factor double‐labelled neurons were not affected by feeding or lack of feeding. The number of Fos‐immunoreactive neurons was higher in the lateral septum, the infundibular, the ventromedial and in the dorsomedial nuclei of unfed ewes than in those of fed ewes. Our results show for the first time that the dorsomedial and ventromedial nuclei are involved in the control of feeding in sheep as in rodents. The supraoptic nucleus of sheep is activated by the same conditions as in rodents but, conversely, the paraventricular nucleus is activated in unfed sheep, whereas in rodents and primates, this nucleus is activated by satiety as well as by fasting. In sheep, unlike in rodents, corticotrophin releasing factor did not appear to be involved in short‐term regulation of food intake.
Assignment of ecto‐nucleoside triphosphate diphosphohydrolase‐1/cd39 expression to microglia and vasculature of the brain
Authors: Braun Norbert , Sévigny Jean , Robson Simon C. , Enjyoji Keiichi , Guckelberger Olaf , Hammer Klaus , Di Virgilio Francesco , Zimmermann Herbert 
Published: July 2009

AbstractExtracellular nucleotides are ubiquitous extracellular mediators that interact with and activate nucleotide type 2 (P2) receptors. These receptors initiate a wide variety of signalling pathways that appear important for functional associations between neurons and glial cells and for the regulation of blood flow, haemostatic and inflammatory reactions in the brain. Ectonucleotidases are extracellular nucleotide‐metabolizing enzymes that modulate P2 receptor‐mediated signalling by the regulated hydrolysis of these agonists. A considerable number of ectoenzyme species with partially overlapping substrate and tissue distributions have been described. Major candidates for expression in the brain are members of the ecto‐nucleoside triphosphate diphosphohydrolase (E‐NTPDase or CD39) family. The production of cd39–/–mice and specific reagents have enabled us to analyse the specific cellular distribution of NTPDase1 (CD39), the prototype member of the enzyme family, in the mouse brain. Using monospecific antibodies and enzyme histochemical staining, we have identified NTPDase1 as a major ectonucleotidase associated with both microglia and the endothelial and smooth muscle cells of the vasculature. NTPDase1 is not expressed by neurons and astrocytes. Additional unidentified ectonucleotidase functional activity is observed at lower levels throughout the brain parenchyma. NTPDase1 may regulate P2 receptor‐mediated functions of microglia as well as influence nucleotide signalling between neurons or astrocytes that are associated with multiple microglial ramifications. The expression of NTPDase1 by cerebrovascular endothelial and smooth muscle cells also suggests involvement in the regulation of blood flow and thrombogenesis.
cDNA cloning and expression of a γ‐aminobutyric acidAreceptor ε‐subunit in rat brain
Authors: Moragues Nathalie , Ciofi Philippe , Lafon Pierrette , Odessa Marie‐Françoise , Tramu Gérard , Garret Maurice 
Published: July 2009

AbstractA cDNA encoding a GABAAreceptor subunit was isolated from rat brain. The predicted protein is 70% identical to the human ε‐subunit. It was recently reported [Sinkkonenet al. (2000),J. Neurosci.,20, 3588–3595] that the rodent ε‐subunit mRNA encoded an additional sequence (≈400 residues). We provide evidence that human and rat ε‐subunit are similar in size. The distribution of cells expressing the GABAAε‐subunit was examined in the rat brain.In situhybridization histochemistry revealed that ε‐subunit mRNA is expressed by neurons located in septal and preoptic areas, as well as in various hypothalamic nuclei, including paraventricular, arcuate, dorsomedial and medial tuberal nuclei. The mRNA was also detected in major neuronal groups with broad‐range influence, such as the cholinergic (basal nucleus), dopaminergic (substantia nigra compacta), serotonergic (raphe nuclei), and noradrenergic (locus coeruleus) systems. Immunohistochemistry using an affinity‐purified antiserum directed towards the N‐terminal sequence unique to the rat ε‐subunit revealed the presence of ε‐subunit immunoreactivity over the somatodendritic domain of neurons with a distribution closely matching that of mRNA‐expressing cells. Moreover, usingin situhybridization, α3, θ and ε GABAAsubunit mRNAs were all detected with an overlapping distribution in neurons of the dorsal raphe and the locus coeruleus. Our results suggest that novel GABAAreceptors may regulate, neuroendocrine and modulatory systems in the brain.
Dopaminergic innervation of the pallidum in the normal state, in MPTP‐treated monkeys and in parkinsonian patients
Authors: Jan Caroline , François Chantal , Tandé Dominique , Yelnik Jérôme , Tremblay Léon , Agid Yves , Hirsch Etienne 
Published: July 2009

AbstractThe aim of the present study was to characterize the dopaminergic innervation of the pallidum in primates (humans and Cercopithecus aethiops). Firstly, in monkeys, biotin dextran amine was injected into dopaminergic areas, and the anterogradely labelled axons were reconstructed from serial sections and analysed in the pallidum. Secondly, in parkinsonian patients and MPTP‐treated monkeys, the dopaminergic innervation of the pallidum was studied using tyrosine hydroxylase‐positive fibre quantification. Our study revealed that dopaminergic areas A8 and A9 innervated the two pallidal segments. Individual axonal arborizations displayed a great heterogeneity. Some dopaminergic axons crossed the pallidum without branching, other axons made small terminal arborizations in a restricted region of one pallidal segment, whereas others developed dense arborizations covering extended areas in the two pallidal segments. This heterogeneous organization suggests that dopamine could directly modulate the pallidum using either a point‐to‐point or a diffuse projection pattern. A statistically significant loss of dopaminergic fibres in the internal (−43%) and external pallidum (−39.6%) of humans, and in the internal (−54.3%) and external pallidum (−59%) of monkeys was revealed in parkinsonian states. The consequences of this alteration are still unknown but it might participate in the triggering of motor symptoms observed in Parkinson's disease.
Differential regulation of trkA and p75 in noradrenergic pelvic autonomic ganglion cells after deafferentation of their cholinergic neighbours
Authors: Keast Janet R. , Kepper Mark E. 
Published: July 2009

AbstractIn rats, following lesion of lumbar or sacral preganglionic axons, many pelvic ganglion cells undergo axogenesis to form baskets of terminals around select populations of nearby ganglion cells. The aim of the current study was to address mechanisms underlying initiation of this sprouting, focusing on a possible role for nerve growth factor (NGF). Immunohistochemical localization of NGF receptors (trkA and p75) showed that virtually all noradrenergic and a minority of cholinergic pelvic neurons expressed both receptors. Terminals immunoreactive for each substance were found in pelvic viscera. In pelvic ganglia, many glial cells expressed p75 but not trkA, and very few lumbar or sacral preganglionic neurons expressed either receptor. Lumbar and/or sacral preganglionic inputs were removed from ganglion cells by cutting the hypogastric, pelvic or both nerves, and tissues analysed 8 days later. Levels of receptor expression in noradrenergic pelvic ganglion cells were estimated by calculating the proportion that were receptor‐immunopositive, and quantifying the intensity of trkA or p75 immunofluorescence. No lesion had a significant effect on trkA expression, however, a marked decrease in p75 occurred after cutting pelvic nerves, i.e. after deafferentation of neighbouring cholinergic neurons. These injuries appeared to cause little overall change in glial p75 expression. This study shows that manipulations that trigger sprouting from noradrenergic pelvic neurons cause downregulation of p75 but not trkA. Interestingly, this is occurring while some of their target organs are synthesizing high levels of NGF. This contrasts with other NGF‐sensitive cells, in which one or both receptor types are upregulated by increased exposure to the ligand. The current study is also the first to show a change in p75 expression in neurons that are neither deafferented nor axotomized.
Central forebrain Fos responses to familiar male odours are attenuated in recently mated female mice
Authors: Halem Heather A. , Cherry James A. , Baum Michael J. 
Published: July 2009

AbstractExposure of recently mated female mice to the urinary odours of an unfamiliar male blocks pregnancy (the Bruce effect). The absence of a pregnancy block in response to the stud male's familiar odours depends on an olfactory memory that is formed in the accessory olfactory bulb (AOB) in response to vomeronasal organ (VNO) inputs during mating. Sexually naive Balb/c female mice in pro‐oestrus/oestrus were either placed onto soiled bedding (‘bedding‐only’ females) from, or allowed to mate with, a Balb/c male (‘recently mated’ females). After 42 h, females were placed for 90 min onto clean bedding (controls) or onto soiled bedding from either a C57BL/6 male (unfamiliar bedding) or a Balb/c male (familiar bedding). Significant increases in Fos‐immunoreactivity (Fos‐IR, a marker of neuronal activation) occurred in the medial amygdala and the medial preoptic area (MPA) of ‘bedding only’ females exposed to either unfamiliar or familiar bedding and in ‘recently mated’ females exposed to unfamiliar bedding but not to familiar bedding. This suggests that a mating‐induced memory prevents the later activation by the familiar stud male's odours of neurons in forebrain regions that receive inputs from the VNO–AOB. ‘Bedding‐only’ females later exposed to either familiar or unfamiliar bedding had increased Fos‐IR in the Gαo protein‐expressing basal zone of the VNO whereas no such effect occurred in ‘recently mated’ females. Familiar, as well as unfamiliar, male odours augmented Fos‐IR in significantly more rostral than caudal AOB granule cells in all groups, with the effect being strongest in ‘recently mated’ females exposed to familiar male bedding. This outcome is consistent with the absence of odour‐induced Fos‐IR in forebrain regions of these females and, presumably, the absence of a pregnancy block.
Neurotrophins BDNF and NT‐3 promote axonal re‐entry into the distal host spinal cord through Schwann cell‐seeded mini‐channels
Authors: Bamber Norman I. , Li Huaying , Lu Xiaobin , Oudega Martin , Aebischer Patrick , Xu Xiao Ming 
Published: July 2009

AbstractTo promote axonal regeneration in the injured adult spinal cord, a two‐phase repair strategy was employed to (i) bridge a spinal cord hemilesion cavity with a grafted Schwann cell (SC)‐seeded mini‐channel, and (ii) promote axonal re‐entry into the distal cord by infusing two neurotrophins, BDNF and/or NT‐3, directly into the distal cord parenchyma. Here we report that infusion of two neurotrophins, delivered alone or in combination, effectively promotes axonal outgrowth from SC‐seeded mini‐channels into the distal host spinal cord. When an anterogradely transported marker, PHA‐L or BDA, was injected into the spinal cord 3 mm rostral to the graft, a large number of axons was observed to regenerate from the SC graft into the distal cord in neurotrophin‐treated groups. A subpopulation of these axons was found to grow up to 6 mm within the distal spinal cord. These axons, which were confined mainly within the grey matter, arborized and formed structures which resemble terminal boutons. In channels containing no SCs, the infusion of neurotrophins did not promote axonal ingrowth from the proximal cord stump. In cases which received SC grafts but no neurotrophin infusion, axonal re‐entry into the distal cord was limited. Thus, the present study demonstrates that regenerating axons not only cross a lesion site when a permissive cellular bridge is provided but also penetrate into the distal host spinal cord and elongate for a distance of several cord segments after the infusion of two neurotrophins. The latter event is prerequisite for establishment of appropriate connections between regenerating axons and target neurons and thus, functional recovery.