Neurocentre Magendie

Les publications







IF du Neurocentre
IF1234567891011121314151617181920253035404550
Nombre2211221181021041411232403513392028131813000
%131817151522440112123121132000


700 publications

* equal contribution
Les IF indiqués ont été collectés par le Web of Sciences en Juin 2016



Abstract:
Cortical cells obtained from rat embryos (ED14 to ED20) were implanted in various regions of rat brain and the presence of tyrosine hydroxylase (TH)-, neuropeptide Y (NPY)- and Met-enkephalin (ENK)-immunoreactive neurons within the grafts were tested using an immunohistochemical approach. TH-like immunoreactive (TH-LI) neurons were present within the implants obtained from ED14, but not ED18 or ED20, embryos up to 10 months post-implantation and their presence was not dependent on the age of the host (adult or neonate) at the time of implantation. Furthermore, the density of such cells varied with the site of implantation, being the highest in the dorsomedial corner of the striatum. This distorted development seems to affect also other cell populations, such as NPY-LI neurons which could be observed within the implants in a density much higher than that found in the normal cortex and which presented generally a rather immature morphology. It has been described that the rat cortex contains TH-LI neurons only during a limited period of development. The survival of such neurons within intracerebral grafts of cortical tissue indicates that their disappearance during normal cortical development is dependent upon environmental cues. The survival of TH-LI cells in grafts implanted to neonatal hosts suggests that these cues are not some humoral factors appearing postnatally. On the other hand, the present observations are compatible with several other hypothesis concerning the nature of such cues: humoral factors present during the late embryonic period, signals dependent on neuronal connectivities (input and/or outputs) established during embryonic or postnatal life.(ABSTRACT TRUNCATED AT 250 WORDS)





1988 | Exp Brain Res   IF 2.1
Intrastriatal dopaminergic grafts restore inhibitory control over striatal cholinergic neurons.
Herman JP, Lupp A, Abrous N, Le Moal M, Hertting G, Jackisch R

Abstract:
The aim of the study was to examine the influence of intrastriatal dopaminergic grafts on the functioning of striatal cholinergic neurons using an in vitro superfusion method. Rats bearing unilateral 6-hydroxydopamine lesion of the nigrostriatal dopaminergic system received a cell suspension obtained from ED 14 rat embryonic mesencephali which was injected into the denervated striatum. Lesioned animals displayed an ipsilateral rotation in response to amphetamine (5 mg/kg i.p.). This rotational response disappeared following grafting and there was even a significant contralateral rotation in response to the drug. Apomorphine (0.1 mg/kg s.c.) induced a contralateral rotation following the lesion. This latter response was attenuated in the grafted group. Three months after grafting 350 microns thick slices were prepared from striata from the control and experimental sides of lesioned and graft-bearing animals. The slices were preincubated either with 3H-dopamine (10(-7) M) or 3H-choline (10(-7) M) and then superfused with an oxygenated Krebs-Ringer solution. Stimulation with electrical pulses following preincubation with 3H-dopamine elicited a marked increase of tritium outflow from control slices. Stimulation-evoked overflow was of similar magnitude from slices from striata containing the graft, while it was much reduced in slices from lesioned striata. Amphetamine markedly potentiated the effect of electrical stimulation in slices obtained from control and graft-containing striata. Nomifensine (a dopamine uptake blocker) led to a significant decrease of the overflow of 3H-acetylcholine evoked by electrical stimulation from control striatal slices. This inhibition was antagonized by domperidone, a D2 dopamine receptor blocker, a finding which indicates that the action of nomifensine was indeed due to a potentiation of the action of endogenous dopamine released by the electrical stimulation. A similar, although somewhat attenuated, action of nomifensine and domperidone was observed for striatal slices containing the graft. Amphetamine inhibited the stimulation evoked overflow of 3H-acetylcholine in a dose-dependent manner from striatal slices obtained both from the intact and experimental sides of graft-bearing animals, while it had no action on slices from denervated striata. Finally, the dose-response curve for the inhibition of 3H-acetylcholine release by apomorphine was significantly shifted to the left for slices from the lesioned striata as compared with control slices. This leftward shift was totally abolished in the slices from the graft-containing striatum.(ABSTRACT TRUNCATED AT 400 WORDS)





Abstract:
Lateral hypothalamus (LH) stimulation in cats which do not spontaneously attack rats, produces an attack pattern which may be divided into 3 main stages: the first, defined as exploratory time (ET), begins with an environmental search and culminates in orienting towards the prey; in the second, defined as attack time (AT), the cat stalks the rat; the last is the biting stage in which the cat seizes and kills the prey by biting its head and neck. The effects of ventral tegmental area (VTA) stimulation on the latency of the whole sequence and on the different stages of the attack pattern were studied. VTA activation resulted in a significant decrease of biting latency, due to the reduction of exploratory time. Moreover, a significant period of prey fixation, seldom present during LH stimulation alone, was observed after VTA-LH co-stimulation. Sulpiride injection caused the disappearance of VTA effects on the predatory pattern. The results indicate that VTA activation induces a decrease in behaviour related to exploration of the environment, and an increase in the focusing of attention on the prey, which seems an important component in the regulation of the predatory pattern. Pharmacological evidence indicates that the VTA effect is mediated by the mesolimbic-mesocortical dopaminergic (DA) system.





31/10/1987 | Boll Soc Ital Biol Sper
[Device for the automatic recording of the latency of the mouth-opening reflex in the cat].
Cucinella F, Piazza PV, Amato G



10/1987 | Neuroendocrinology   IF 2.6
Bradykinin parallels thyrotropin-releasing hormone actions on prolactin release from rat anterior pituitary cells.
Drouhault R, Abrous N, David JP, Dufy B

Abstract:
Bradykinin (BK), a nonapeptide, originally discovered in blood, is also present in neurons and fibers of the hypothalamus. We tested the putative releasing factor properties of BK on prolactin (PRL) release from anterior pituitary cells in vitro. BK stimulated the release of PRL in a dose-dependent manner, the threshold concentration being in the range. 0.1-1.0 nM. The release of PRL induced by BK at 1 nM concentration was about 2-fold, delayed and sustained over many minutes. Higher concentrations of BK stimulated PRL release in two phases. The shape of the BK-induced PRL release was superficially similar to that induced by thyrotropin-releasing hormone (TRH). 10 nM BK and 10 nM TRH induced about a 4-fold increase in PRL release within 5 min, followed by a gradual recovery to basal secretion. These results indicate that this peptide can act directly at the anterior pituitary gland to release PRL. Phorbol ester also promoted PRL release over the range of 1-10 nM, but the time course of the release was somewhat different.





Abstract:
The influence of A10 region neurons of the ventral tegmental area (VTA) on the defence reaction evoked by stimulation of the ventromedial hypothalamic nucleus (VMH) was studied in the cat. The latency of the hissing in the defence reaction increased when the VTA was stimulated both ipsi- and contralaterally. A sulpiride (50mg/kg i.p.) injection totally abolished the VTA-provoked increase of the hissing latency without affecting the basal response.





05/1987 | Proc Natl Acad Sci U S A   IF 9.6
Intracellular human gamma-interferon triggers an antiviral state in transformed murine L cells.
Sanceau J, Sondermeyer P, Beranger F, Falcoff R, Vaquero C

Abstract:
Interaction of human gamma-interferon (IFN-gamma) with a cell-surface receptor is known to be essential for the cell to become resistant to viral infection. Here we demonstrate that IFN-gamma, when present inside the cell, is also capable of inducing a permanent antiviral state. Mouse cells transformed with a truncated human cDNA encoding a mature IFN-gamma protein lacking the signal peptide accumulate high levels of intracellular human IFN-gamma. Not only do these cells acquire a permanent resistance to viral infection, they also exhibit all the biochemical characteristics normally observed after exposure to exogenous IFN. The observed loss of species specificity normally associated with IFN-gamma suggests that this restriction is strictly dependent on the interaction of the molecule with the cell-surface receptor.





1987 | Ann N Y Acad Sci   IF 2.7
Behavioral effects of intraaccumbens transplants in rats with lesions of the mesocorticolimbic dopamine system.
Choulli K, Herman JP, Abrous N, Le Moal M



04/1986 | j interferon res
Regulation of human gamma-interferon and beta-interferon gene expression in PHA-activated lymphocytes.
Vaquero C, Sanceau J, Weissenbach J, Beranger F, Falcoff R

Abstract:
Two interferon (IFN) messengers were synthesized in phytohemagglutinin (PHA)-activated lymphocytes: IFN-gamma mRNA and a messenger hybridizing with the IFN-beta 2 probe. They were induced rapidly and declined at a stage when overall RNA was still efficiently transcribed. The IFN-beta 2 mRNA (15S) present in the lymphocytes was slightly different from its fibroblastic counterpart (14S). The kinetics of the accumulation and decay of both lymphocyte IFN messengers differed when assessed by hybridization with the two IFN probes, IFN-gamma mRNA was not detected before mitogenic activation and accumulated for up to 15 h postactivation, while IFN-beta 2 mRNA accumulated even in the absence of PHA activation for up to 5 h, even though the activation raised the IFN-beta 2 mRNA level at 5 h. The disappearance of IFN messengers was prevented when cycloheximide was added 5 h after PHA activation, when the transcription of both messengers had already been turned on, suggesting the presence of the repressor mechanism proposed for IFN-beta 1 and IFN-beta 2 mRNAs in fibroblasts. In the absence of PHA activation, cycloheximide did not induce IFN-beta 2 mRNA transcription as it did in fibroblasts and moreover prevented the accumulation of the messenger observed in the control cells. In contrast to IFN-beta 2 mRNA, cycloheximide treatment of lymphocytes produced a slight accumulation of IFN-gamma mRNA. This accumulation was already detectable 6 h posttreatment and its level remained unchanged for up to 24 h. Addition of actinomycin D, 5 h after PHA activation, did not impair the shut off and accelerated the decay of IFN messengers.





28/03/1986 | Biochem Biophys Res Commun
Expression of extracellular and intracellular human IFN-gamma in mouse L cells transformed with the human IFN-gamma cDNA gene.
Sanceau J, Lewis JA, Sondermeyer P, Beranger F, Falcoff R, Vaquero C

Abstract:
Cotransformation with a plasmid containing a thymidine kinase gene (pTK2) and a plasmid encoding human IFN-gamma (pTG11) has been used to establish murine L cell lines expressing human IFN-gamma. The HuIFN-gamma gene was present in 30% of the tk+ cell lines and some of these secreted low levels of IFN into the culture medium. Two of the clones obtained after transformation were selected for detailed analysis. Clone 1-12 constitutively secreted very low levels of HuIFN-gamma in the culture medium. This antiviral activity was characterized by its species specificity and antigenicity as authentic human IFN-gamma In contrast, clone 3-47 produced a HuIFN-gamma activity which could only be detected intracellularly. This clone was resistant to infection both by Vesicular stomatitis (VSV) and Mengo viruses and contained increased levels of enzymes known to be induced by interferon. Our results suggest that clone 3-47 produces a non-secreted HuIFN-gamma like molecule which is able to trigger an antiviral state in the murine cell independent of the interaction with a specific IFN-gamma surface receptor.