bluuebunny/crossref_metadata_2025_split huggingface dataset:
Mapping of c‐fos gene expression in the brain during morphine dependence and precipitated withdrawal, and phenotypic identification of the striatal neurons involved
Authors: Georges François , Stinus Luis , Le Moine Catherine 
Published: March 2003

AbstractThe c‐fos gene is expressed in the central nervous system in response to various neuronal stimuli. Using in situ hybridization, we examined the effects of chronic morphine treatment and withdrawal on c‐fos mRNA in the rat brain, and particularly within identified striatal neurons. Morphine dependence was induced by subcutaneous implantation of two pellets of morphine for 6 days and withdrawal was precipitated by administration of naltrexone. Placebo animals and morphine‐dependent rats showed a very weak c‐fos mRNA expression in all the structures studied. Our study emphasized the spatial variations in c‐fos mRNA expression, and also revealed a peak expression of c‐fos mRNA at 1 h after naltrexone‐precipitated withdrawal in the projection areas of dopaminergic neurons, noradrenergic neurons and in several regions expressing opiate receptors. Interestingly, morphine withdrawal induces c‐fos mRNA expression in the two efferent populations of the striatum (i.e. striatonigral and striatopallidal neurons) both in the caudate putamen and nucleus accumbens. Moreover, the proportions of activated neurons during morphine withdrawal are different in the caudate putamen (mostly in striatopallidal neurons) and in the shell and core parts of the nucleus accumbens (mostly in striatonigral neurons). The activation of striatopallidal neurons suggests a predominant dopaminergic regulation on c‐fos gene expression in the striatum during withdrawal. On the contrary, c‐fos induction in striatonigral neurons during withdrawal seems to involve a more complex regulation like opioid–dopamine interactions via the µ opioid receptor and the D1 dopamine receptor coexpressed on this neuronal population or the implication of other neurotransmitter systems.
Differential neuronal expression and projections of melanin‐concentrating hormone (MCH) and MCH‐gene‐overprinted‐polypeptide (MGOP) in the rat brain
Authors: Toumaniantz Gilles , Ferreira Patricia C. , Allaeys Isabelle , Bittencourt Jackson C. , Nahon Jean‐Louis 
Published: March 2003

AbstractThe rat melanin‐concentrating hormone (MCH) gene may produce, through alternative splicing, either the precursor of MCH and neuropeptide EI, two neuropeptides coexpressed in the zona incerta (ZI) and lateral hypothalamus (LHA), or a putative protein we named previously MCH‐gene‐overprinted‐polypeptide (MGOP). First, we investigated the distribution and relative expression of MCH and MGOP mRNA in the rat brain by Northern blotting, RT‐PCR and in situ hybridization. MGOP gene transcripts were detected mainly in the hypothalamus only by RT‐PCR. Second, different antisera were raised toward the C‐terminus of MGOP and used to identify the translational products. In the rat brain, no MGOP‐processed peptide could be detected based on RP‐HPLC coupled to specific RIA. A polypeptide of 14 kDa was found in the secretory pathway of transfected monkey COS7 cells expressing recombinant MGOP. In the rat hypothalamus, a specific protein of 12 kDa was identified by Western blot analysis. Finally, distribution of MGOP‐immunoreactivity (IR) was investigated in the rat brain. Colocalization studies demonstrated that 98% of the MGOP‐expressing perikarya in ZI/LHA also synthesized MCH. In addition, numerous, strongly stained MGOP‐containing neurons were encountered in the hypothalamic periventricular nucleus. Perikarya labelled with MGOP antiserum were also found scattered in the cortex, caudate putamen, amygdala and lateral septal nucleus. MCH was not detected in these MGOP‐containing neurons. Strikingly, dense staining of terminals was observed with MGOP antiserum but not with MCH antibodies in the suprachiasmatic, ventromedial and arcuate nuclei, and also in the external layer of the median eminence. These results demonstrated that MGOP and MCH‐IR overlapped in LHA/ZI but displayed a differential distribution in other areas. Based on this cerebral distribution, MGOP may act as a new secreted protein in regulating many neuroendocrine functions, such as nursing, feeding and growth control in associated behavioural components.
Muscarinic and PACAP receptor interactions at pontine level in the rat: significance for REM sleep regulation
Authors: Ahnaou A. , Laporte A. M. , Ballet S. , Escourrou P. , Hamon M. , Adrien J. , Bourgin P. 
Published: March 2003

AbstractCholinergic and PACAPergic systems within the oral pontine reticular nucleus (PnO) play a critical role in REM sleep generation in rats. In this present work, we have investigated whether REM sleep enhancement induced by carbachol (a cholinergic agonist) or PACAP, depends on an interaction between muscarinic and PACAP receptors. This hypothesis was tested by recording sleep–wake cycles in freely moving rats injected into the PnO with PACAP in combination with the muscarinic receptor antagonist atropine, or with carbachol in combination with the PACAP receptor antagonist PACAP6‐27. When administered alone, PACAP (3 pmol) or carbachol (110 pmol) induced an enhancement of REM sleep during 8 h (+61%, n = 8; +70%, n = 5), which was totally prevented by infusion of atropine (290 pmol) for PACAP, or of PACAP6‐27 (3 pmol) for carbachol. Quantitative autoradiographic studies indicated that (i) PACAP (10−9−10−7 m) induced in the PnO an increase (+35%) of the specific binding of the muscarinic antagonist [3H]quinuclidinyl benzylate, which could be completely prevented by PACAP6‐27 (IC50 = 8 × 10−8 m) and (ii) both carbachol and PACAP enhanced [35S]GTP‐γ‐S binding in a concentration‐dependent manner in the PnO. The maximal increase due to carbachol was significantly higher in the presence (+126%) than in the absence (+102%) of PACAP (0.1 µm). These data showed that interactions between muscarinic and PACAP receptors do exist within the PnO and play a role in the local mechanisms of REM sleep control in the rat.
Differential induction of NF‐κB activity and neural cell death by antidepressants in vitro
Authors: Post Anke , Crochemore Christophe , Uhr Manfred , Holsboer Florian , Behl Christian 
Published: March 2003

AbstractTricyclic antidepressants and selective serotonin reuptake inhibitors are here shown to induce cell death in a neural cell line. The exposure to these drugs led to increased generation of reactive oxygen species and a concomitant reduction of intracellular glutathione levels. Furthermore, these antidepressants induced DNA fragmentation and increased the transcriptional and DNA‐binding activity of NF‐κB. In contrast, treatment with type A and B monoamine oxidase inhibitors did not induce changes in NF‐κB activity and did not exert a detrimental influence on cell viability. These results indicate that some antidepressant drugs may cause both oxidative stress and changes in cellular antioxidative capacity, resulting in altered NF‐κB activity and, ultimately, cell death.
Nerve growth factor expression in parasympathetic neurons: regulation by sympathetic innervation
Authors: Hasan Wohaib , Smith Peter G. 
Published: March 2003

AbstractInteractions between sympathetic and parasympathetic nerves are important in regulating visceral target function. Sympathetic nerves are closely apposed to, and form functional synapses with, parasympathetic axons in many effector organs. The molecular mechanisms responsible for these structural and functional interactions are unknown. We explored the possibility that Nerve Growth Factor (NGF) synthesis by parasympathetic neurons provides a mechanism by which sympathetic–parasympathetic interactions are established. Parasympathetic pterygopalatine ganglia NGF‐gene expression was examined by in situ hybridization and protein content assessed by immunohistochemistry. Under control conditions, NGF mRNA was present in ≈ 60% and NGF protein was in 40% of pterygopalatine parasympathetic neurons. Peripheral parasympathetic axons identified by vesicular acetylcholine transporter‐immunoreactivity also displayed NGF immunoreactivity. To determine if sympathetic innervation regulates parasympathetic NGF expression, the ipsilateral superior cervical ganglion was excised. Thirty days postsympathectomy, the numbers of NGF mRNA‐positive neurons were decreased to 38% and NGF immunoreactive neurons to 15%. This reduction was due to a loss of sympathetic nerve impulse activity, as similar reductions were achieved when superior cervical ganglia were deprived of preganglionic afferent input for 40 days. These findings provide evidence that normally NGF is synthesized by parasympathetic neurons and transported anterogradely to fibre terminals, where it may be available to sympathetic axons. Parasympathetic NGF expression, in turn, is augmented by impulse activity within (and presumably transmitter release from) sympathetic axons. It is suggested that parasympathetic NGF synthesis and its modulation by sympathetic innervation provides a molecular basis for establishment and maintenance of autonomic axo‐axonal synaptic interactions.
Activation of ionotropic glutamate receptors reduces the production of transforming growth factor‐ß2 by developing neurons
Authors: Dobbertin Alexandre , Gervais Annie , Glowinski Jacques , Mallat Michel 
Published: March 2003

AbstractNeuronal cultures derived from developing rat cerebral cortex were used to investigate the influence of glutamate receptors on the neuronal production of transforming growth factor‐ß2 (TGFß2), a multifunctional cytokine that modulates neuronal and glial growth. Long‐term exposure (48 h) of cortical neurons to selective antagonists of N‐methyl‐d‐aspartate (NMDA) and α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid (AMPA)/kainate receptors markedly increased TGFß2 levels in the culture medium. Conversely, treatment with NMDA or kainate reduced TGFß2 to levels below those in untreated cultures. The effect of kainate did not require NMDA receptor activity. Neuronal depolarization with K+ also reduced TGFß2 levels by opening voltage‐gated L‐type Ca2+ channels. Semi‐quantitative RT–PCR measurements of neuronal TGFß2 mRNA showed that NMDA or AMPA/kainate receptor stimulation reduced TGFß2 mRNA levels. These results demonstrate that tonic activation of glutamate‐gated cation channels downregulates neuronal expression of the TGFß2 gene and provide evidence for a novel mechanism whereby excitatory amino acids could influence the development of glial and neuronal lineages.
The effect of riluzole treatment in rats on the survival of injured adult and grafted embryonic motoneurons
Authors: Nógrádi Antal , Vrbová Gerta 
Published: March 2003

AbstractThe effect of riluzole on the survival of injured motoneurons was studied. The L4 ventral root was avulsed and reimplanted into the spinal cord. Immediately after the operation, 4 animals were treated with riluzole for 3 weeks while another 4 animals received no treatment after the operation. Three months later the fluorescent dyes, Fast Blue and Diamidino Yellow, were applied to the cut ventral ramus of the L4 spinal nerve, for retrograde labelling of neurons. Three days later, the spinal cords were processed to reveal the retrograde‐labelled cells. In untreated animals, there were 20 ± 2.1 labelled neurons (± SEM), while in animals treated with riluzole there were 723 ± 26. Thus, treatment with riluzole dramatically enhanced the survival of injured motoneurons. In another series of experiments, after avulsion of the L4 ventral root and its reinsertion, embryonic spinal cord pieces were grafted into the host cord. Five animals received riluzole treatment and 4 were left untreated. In the untreated animals, 125 ± 5.1 retrograde‐labelled cells of both graft and host origin were detected. In rats treated with riluzole, 645 ± 35.7 retrograde‐labelled cells were seen and almost all of these were of host origin. Thus, treatment with riluzole enhanced the survival of injured host motoneurons, and by doing so, (i) reduced the ability of grafted neurons to extend their axons into the reimplanted L4 ventral root, and (ii) reduced the survival of the grafted cells.
Enhancement of hippocampal LTP, reference memory and sensorimotor gating in mutant mice lacking a telencephalon‐specific cell adhesion molecule
Authors: Nakamura Kazuhiro , Manabe Toshiya , Watanabe Masahiko , Mamiya Takayoshi , Ichikawa Ryoichi , Kiyama Yuji , Sanbo Makoto , Yagi Takeshi , Inoue Yoshiro , Nabeshima Toshitaka , Mori Hisashi , Mishina Masayoshi 
Published: March 2003

AbstractTelencephalin (TLCN) is a cell adhesion molecule selectively expressed in the telencephalon of the mammalian brain. The mutant mice lacking TLCN had no detectable abnormalities in their neural development and synaptic structures. Ablation of TLCN increased the hippocampal long‐term potentiation and its saturation level. The TLCN mutation selectively enhanced the performance of the radial maze and water‐finding tasks, learning tasks with appetitive reinforcers, but not the contextual fear conditioning and Morris water maze tasks with aversive stimuli for conditioning. Furthermore, the TLCN mutant mice showed an increase of prepulse inhibition of the acoustic startle response. These results suggest that TLCN is a determinant of the dynamic range of synaptic plasticity and plays roles in reward‐motivated learning and memory and sensorimotor gating.
Modulation of spinal excitability during observation of hand actions in humans
Authors: Baldissera Fausto , Cavallari Paolo , Craighero Laila , Fadiga Luciano 
Published: March 2003

AbstractThere is growing evidence that observation of actions performed by other individuals activates observer's cortical motor areas. This matching of observed actions on the observer's motor repertoire could be at the basis of action recognition. Here we investigated if action observation, in addition to cortical motor areas, involves also low level motor structures mimicking the observed actions as if they were performed by the observer. Spinal cord excitability was tested by eliciting the H‐reflex in a finger flexor muscle (flexor digitorum superficialis) in humans looking at goal‐directed hand actions presented on a TV screen. We found that, in the absence of any detectable muscle activity, there was in the observers a significant modulation of the monosynaptic reflex size, specifically related to the different phases of the observed movement. The recorded H‐reflex rapidly increased in size during hand opening, it was depressed during hand closing and quickly recovered during object lifting. This modulation pattern is, however, opposite to that occurring when the recorded muscles are actually executing the observed action [Lemon et al. (1995) J. Neurosci., 15, 6145–56]. Considering that, when investigated at cortical level the modulation pattern of corticospinal excitability replicates the observed movements [Fadiga et al. (1995) J. Neurophysiol., 73, 2608–2611], this spinal ‘inverted mirror’ behaviour might be finalised to prevent the overt replica of the seen action.
The central aromatic amino acid DOPA decarboxylase inhibitor, NSD‐1015, does not inhibit l‐DOPA‐induced circling in unilateral 6‐OHDA‐lesioned‐rats
Authors: Treseder Sarah A. , Rose Sarah , Jenner Peter 
Published: March 2003

AbstractThe centrally acting aromatic amino acid dopa decarboxylase (AADC) inhibitor, 3‐hydroxybenzyl hydrazine (NSD‐1015), is widely used to study the neurotransmitter‐like actions of l‐DOPA. However, the effects of NSD‐1015 on l‐DOPA‐induced motor activity are unclear as both increases and decreases have been reported. We now investigate the effects of NSD‐1015 on l‐DOPA‐induced contralateral circling behaviour in 6‐OHDA‐lesioned rats and on striatal levels of l‐DOPA, 3‐O‐methyl‐DOPA (3‐OMD), dopamine, dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) using microdialysis techniques. NSD‐1015 (50–200 mg/kg i.p.) inhibited AADC activity both in the liver and striatum of normal rats. Administration of NSD‐1015 (50–200 mg/kg i.p.), delayed the onset of circling produced by administration of l‐DOPA (25 mg/kg i.p.) and carbidopa (12.5 mg/kg i.p.), suggesting blockade of central AADC activity. However, the duration of the l‐DOPA‐induced circling was prolonged and overall no inhibition of circling behaviour occurred. l‐DOPA (25 mg/kg i.p.) plus carbidopa (12.5 mg/kg i.p.) increased extracellular levels of l‐DOPA, 3‐OMD, dopamine, DOPAC and HVA in the 6‐OHDA‐lesioned striatum. Pretreatment of rats with the central AADC inhibitor, NSD‐1015 (100 mg/kg i.p.), potentiated the increase in dialysate levels of l‐DOPA and 3‐OMD. However, it did not reduce striatal dopamine levels in the 6‐OHDA‐lesioned hemisphere, which were elevated following l‐DOPA administration. The increases in DOPAC and HVA levels were abolished by NSD‐1015 pretreatment. These results suggest that, while NSD‐1015 blocks central AADC activity, it also acts as a monoamine oxidase inhibitor so maintaining striatal dopamine concentration by reducing dopamine metabolism. NSD‐1015, therefore, may not be an appropriate tool for the study of brain AADC activity and for assessing the neuromodulatory role of l‐DOPA.
Stage‐dependent changes in the modulation of spinal nociceptive neuronal activity during the course of inflammation
Authors: Danziger Nicolas , Weil‐Fugazza Jeanne , Le Bars Daniel , Bouhassira Didier 
Published: March 2003

AbstractSpinal and supraspinal controls can tonically or phasically modulate the output of spinal nociceptive neurons. Alterations of these modulatory systems have been described during the acute stage of inflammation. In the present study in the rat, tonic descending controls were assessed during acute (24–48 h) and chronic (3–4 weeks) stages of monoarthritis of the ankle. The electrophysiological properties of spinal convergent neurons with ankle input were compared before and after spinalization. In a parallel series of experiments, spinal convergent neurons were recorded from the normal side in order to assess the propriospinal and supraspinal inhibitory controls triggered by nociceptive stimulation of the inflamed ankle. Tonic descending inhibition of convergent neurons with input from the inflamed ankle was enhanced during the acute stage and then decreased during the chronic stage of monoarthritis. Contralateral‐induced inhibitions exhibited a similar temporal evolution. Time‐dependent changes in the spinal transmission of nociceptive signals were shown by removing descending modulation in animals with monoarthritis; sensitization of spinal neurons with input from the inflamed ankle was demonstrated during the acute stage of monoarthritis, whereas a crossed transmission between inflamed and normal sides was observed during the chronic stage of the disease. These results show that dynamic and stage‐dependent modifications of descending controls tend to dampen the central changes associated with inflammation.
Taste laterality in the split brain
Authors: Aglioti S. M. , Tassinari G. , Fabri M. , Del Pesce M. , Quattrini A. , Manzoni T. , Berlucchi G. 
Published: March 2003

AbstractTwo patients with corpus callosum resection, one complete and the other sparing the genu and the rostrum, were tested for discrimination of three basic taste stimuli (sour, bitter, salty) applied to the right or left sides of the tongue. Responses were made by pointing with either hand to written words or images of visual objects corresponding to the stimuli, a language‐based discrimination. In both patients, response accuracy was significantly above chance for both hemitongues but there was a significant advantage for the left side. Reaction time was shorter for left stimuli than for right stimuli but the difference was not significant. Eight normal controls matched for age with the patients performed equally well with right and left hemitongue stimuli and so did a third callosotomy patient with sparing of the posterior callosum, including the splenium. Tactile and visual tests showed that the left hemisphere was responsible for language‐based responses in the first two patients. The results confirm and extend previous findings in another callosotomy patient, indicating that: (i) taste information from either side of the tongue can reach the left hemisphere in the absence of the corpus callosum; (ii) the ipsilateral input from the tongue to the left hemisphere is more potent functionally than the contralateral input and (iii) in the normal brain, the corpus callosum, specifically its posterior part including the splenium, appears to equalize the effects of the ipsilateral and contralateral gustatory inputs on the left hemisphere. Taken together with evidence about lateralized taste deficits following unilateral cortical lesions, the results also suggest that the gustatory pathways from tongue to cortex are bilaterally‐distributed with an ipsilateral predominance that may be subject to individual variations.
Altered striatal amino acid neurotransmitter release monitored using microdialysis in R6/1 Huntington transgenic mice
Authors: NicNiocaill B. , Haraldsson B. , Hansson O. , O'connor W. T. , Brundin P. 
Published: March 2003

AbstractHuntington's disease is an autosomal dominant disease which presents with striatal and cortical degeneration causing involuntary movements, dementia and emotional changes. We employed 16‐week‐old transgenic Huntington mice (R6/1 line developed by Bates and coworkers) that express exon 1 of the mutant human Huntington gene with 115 CAG triplet repeats. At this age, R6/1 mice do not exhibit an overt neurological phenotype nor any striatal neuronal loss. Using microdialysis, we monitored basal and intrastriatal N‐methyl d‐aspartate (NMDA, 100 µm, 15 min)‐ and KCl (100 mm, 15 min)‐induced increases in local aspartate, glutamate and GABA release in halothane‐anaesthetized transgenic mice and wild‐type controls. Basal striatal dialysate glutamate levels were reduced by 42% in R6/1 mice whilst aspartate and GABA levels did not differ from those observed in control mice. Intrastriatal NMDA was associated with significantly greater aspartate (at 15 min) and GABA (at 30 min) levels in the R6/1 mice compared to controls, whilst glutamate release rapidly increased to the same extent in both groups. Intrastriatal KCl was associated with enhanced increases (30 min) in local aspartate and glutamate release in the R6/1 mice above those observed in controls whilst the rapid increase (15 min) in GABA release was similar in both groups. The results provide compelling evidence for specific alterations in both basal, as well as NMDA‐ and KCl‐induced, release of striatal amino acid neurotransmitters in this transgenic model of Huntington's disease, even in the absence of manifest neurodegeneration.
Neuromagnetic evidence for early semantic access in word recognition
Authors: Pulvermüller Friedemann , Assadollahi Ramin , Elbert Thomas 
Published: March 2003

AbstractMagnetic brain responses recorded in the human magnetoencephalogram (MEG) distinguished between words with different semantics but carefully matched for frequency and length. Multiple recordings from a single subject showed that 100 ms following stimulus onset, significantly stronger neuromagnetic responses were elicited by words with strong multimodal semantic associations than by other word material. At this early processing step, there was a highly significant correlation (0.80) between the magnitude of brain responses to individual words recorded over parieto‐occipital areas and their semantic association strengths. Subsequent to this early difference related to word meaning, additional differences in MEG responses emerged for words from different grammatical categories. Together, these results suggest that word meaning can be reflected by early neuromagnetic brain responses and before the grammatical information about the word is encoded.