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D Hervé

Publications and source records attributed to D Hervé.

At least 19 recordsLinked to original sources
PubMed2006

[Role and regulation of dopamine D1 receptors in the striatum: implications for the genesis of dyskinesia in Parkinson's disease].

L-dopa treatment of Parkinson's disease is complicated in the long term by the appearance of dyskinesia. Hypersensitivity of D1 dopamine receptor has been suggested to play a role in these delayed adverse effects. Hypersensitivity of dopamine D1 receptor in Parkinson's disease can be accounted for by increased levels of Galphaolf, the stimulatory G protein which couples D1 receptor to adenylyl cyclase in the striatum. We here discuss the possible role of D1 receptor signal transduction in the genesis of L-dopa-induced dyskinesia in the light of Galphaolf regulation.

Antiparkinson Agents↗
PubMed2005

Longitudinal thalamic diffusion changes after middle cerebral artery infarcts.

BACKGROUND: Cerebral infarcts are responsible for functional alterations and microscopic tissue damage at distance from the ischaemic area. Such remote effects have been involved in stroke recovery. Thalamic hypometabolism is related to motor recovery in middle cerebral artery (MCA) infarcts but little is known concerning the tissue changes underlying these metabolic changes. Diffusion tensor imaging (DTI) is highly sensitive to microstructural tissue alterations and can be used to quantify in vivo the longitudinal microscopic tissue changes occurring in the thalamus after MCA infarcts in humans. METHODS: Nine patients underwent DTI after an isolated MCA infarct. Mean diffusivity (MD), fractional anisotropy (FA), and thalamic region volume were measured from the first week to the sixth month after stroke onset in these patients and in 10 age matched controls. RESULTS: MD significantly increased in the ipsilateral thalamus between the first and the sixth month (0.766 x 10(-3) mm(2)/s first month; 0.792 x 10(-3) mm(2)/s third month; 0.806 x 10(-3) mm(2)/s sixth month). No significant modification of FA was detected. In six patients, the ipsilateral/contralateral index of MD was higher than the upper limit of the 95% CI calculated in 10 age matched controls. An early decrease of MD preceded the increase of ipsilateral thalamic diffusion in one patient at the first week and in two other patients at the first month. CONCLUSION: After MCA infarcts, an increase in diffusion is observed with DTI in the ipsilateral thalamus later than 1 month after the stroke onset. This is presumably because of the progressive loss of neurons and/or glial cells. In some patients, this increase is preceded by a transient decrease in diffusion possibly related to an early swelling of these cells or to microglial activation. Further studies in larger series are needed to assess the clinical correlates of these findings.

Adult↗
PubMed2002

Quality of dredged material in the river Seine basin (France). II. Micropollutants.

Dredging rivers is needed to ensure safe navigable waters, rivers and waterways. To anticipate the management of dredged materials in the case of the river Seine basin, the quality of the sediments in the river is checked every 3 years before dredging operations. The river Seine Basin is heavily submitted to pollution pressure from nearby industrial activities and urban expansion of Paris and its region. Here, the micropollutant content of the sediment sampled in 1996, 1999 and 2000 before dredging is discussed compared to regulatory standards. The results indicate that most of the sediment samples from the river Seine basin are lightly to moderately contaminated with organic and inorganic micropollutants (heavy metals, PAH, PCB), which makes the management after dredging easier. This pollution is strongly correlated with the organic matter content and to the fine fraction (<50 microm) of the sediment. These results can lead to other management options than the ones already used in the river Seine basin: (1) dumping of lightly to moderately polluted sediments in quarries; and (2) physical treatment (sieving, hydrocycloning) of contaminated sediments issued from 'hot spots'.

Conservation of Natural Resources↗
PubMed2002

Quality of dredged material in the River Seine basin (France). I. Physico-chemical properties.

In rivers, sediments are frequently accumulating persistent chemicals, especially for those that are more contaminated as a consequence of pressure related to environmental pollution and human activity. The Seine river basin (France) is heavily polluted from nearby industrial activities, and the urban expansion of Paris and its suburbs within the Ile de France region and the sediments present in the Seine river basin are contaminated. To ensure safe, navigable waters, rivers and waterways must be dredged. In this paper, the quality of the sediment dredged in 1996, 1999 and 2000 is discussed. Physico-chemical characteristics of the sediment itself and of the pore-water are presented. Seine basin sediments show very diverse compositions depending on the sampling site. Nevertheless, a geographic distribution study illustrated that the Paris impact is far from being the only explanation to this diversity, the quality of this sediment is also of great concern. The sediment once dredged is transported via barges to a wet disposal site, where the dredged material is mixed with Seine water in order to be pumped into the receiving site. This sort of dumping might be responsible for the potential release of contaminants to the overlying water from the significantly contaminated sediments.

Environmental Monitoring↗
PubMed2001

Galpha(olf) levels are regulated by receptor usage and control dopamine and adenosine action in the striatum.

In the striatum, dopamine D(1) and adenosine A(2A) receptors stimulate the production of cAMP, which is involved in neuromodulation and long-lasting changes in gene expression and synaptic function. Positive coupling of receptors to adenylyl cyclase can be mediated through the ubiquitous GTP-binding protein Galpha(S) subunit or through the olfactory isoform, Galpha(olf), which predominates in the striatum. In this study, using double in situ hybridization, we show that virtually all striatal efferent neurons, identified by the expression of preproenkephalin A, substance P, or D(1) receptor mRNA, contained high amounts of Galpha(olf) mRNA and undetectable levels of Galpha(s) mRNA. In contrast, the large cholinergic interneurons contained both Galpha(olf) and Galpha(s) transcripts. To assess the functional relationship between dopamine or adenosine receptors and G-proteins, we examined G-protein levels in the striatum of D(1) and A(2A) receptor knock-out mice. A selective increase in Galpha(olf) protein was observed in these animals, without change in mRNA levels. Conversely, Galpha(olf) levels were decreased in animals lacking a functional dopamine transporter. These results indicate that Galpha(olf) protein levels are regulated through D(1) and A(2A) receptor usage. To determine the functional consequences of changes in Galpha(olf) levels, we used heterozygous Galpha(olf) knock-out mice, which possess half of the normal Galpha(olf) levels. In these animals, the locomotor effects of amphetamine and caffeine, two psychostimulant drugs that affect dopamine and adenosine signaling, respectively, were markedly reduced. Together, these results identify Galpha(olf) as a critical and regulated component of both dopamine and adenosine signaling.

Adenosine↗
PubMed2001

Galpha(olf) is necessary for coupling D1 and A2a receptors to adenylyl cyclase in the striatum.

In the brain, dopamine and adenosine stimulate cyclic AMP (cAMP) production through D1 and A2a receptors, respectively. Using mutant mice deficient in the olfactory isoform of the stimulatory GTP-binding protein alpha subunit, Galpha(olf), we demonstrate here the obligatory role of this protein in the adenylyl cyclase responses to dopamine and adenosine in the caudate putamen. Responses to dopamine were also dramatically decreased in the nucleus accumbens but remained unaffected in the prefrontal cortex. Moreover, in the caudate putamen of mice heterozygous for the mutation, the amounts of Galpha(olf) were half of the normal levels, and the efficacy of dopamine- and CGS 21680 A(2) agonist-stimulated cAMP production was decreased. Together, these results identify Galpha(olf) as a critical parameter in the responses to dopamine and adenosine in the basal ganglia.

Adenosine↗
PubMed2001

QTL analysis of photosynthesis and water status traits in sunflower (Helianthus annuus L.) under greenhouse conditions.

The identification of QTL for several physiological traits in sunflower is described. Traits related to photosynthesis (leaf chlorophyll concentration, net photosynthesis and internal CO(2) concentration) and water status (stomatal conductance, transpiration, predawn leaf water potential, and relative water content) were evaluated in a population of recombinant inbred lines under greenhouse conditions. Narrow-sense heritabilities were low to average. Using an AFLP linkage map, 19 QTL were detected explaining 8.8-62.9% of the phenotypic variance for each trait. Among these, two major QTL for net photosynthesis were identified on linkage group IX. One QTL co-location was found on linkage group VIII for stomatal movements and water status. Coincident locations for QTL regulating photosynthesis, transpiration and leaf water potential were described on linkage group XIV. These results lead to the first description of the organization of genomic regions related to yield in sunflower.

Carbon Dioxide↗
PubMed1998

[Bilateral intracranial subdural hematoma following lumbar puncture: report of a case].

A chronic, bilateral, intra-cranial subdural hematoma was diagnosed in a 28 year old man. A standard diagnostic spinal tap had been performed 6 weeks before. There was no other etiologic factor. Intra-cranial subdural hematoma is a rare complication of either diagnostic, therapeutic, or accidental lumbar puncture. Extensive literature review disclosed the description of 49 other cases, including only 3 cases following a standard diagnostic lumbar puncture. Outcome was fatal in 9 of them. The possibility of an intra-cranial subdural hematoma has to be considered in case of prolonged or unusual headache following a lumbar puncture, even with a headache-free period, knowing the emergency of the surgical therapeutic procedure. The most likely mechanism is subdural venous bleeding induced by the chronic intracranial hypotension due to the persisting lumbar meningeal wound.

Adult↗
PubMed1995

Tyrosine phosphorylation of NMDA receptor in rat striatum: effects of 6-OH-dopamine lesions.

N-Methyl-D-aspartate (NMDA) glutamate receptor properties are subject to a fine tuning by several regulatory mechanisms including phosphorylation of the receptor subunits. Here we show that two of these subunits, NR2B and NR2A, are phosphorylated on tyrosine residues in vivo, in rat striatum, where NR2B is by far the most prominent tyrosine phosphorylated protein. Two weeks after unilateral lesioning of nigrostriatal dopaminergic neurones with 6-hydroxydopamine, tyrosine phosphorylation of NR2B was increased by approximately 20% in the ipsilateral striatum. The total amount of NR2B protein was unaltered. Thus, increased tyrosine phosphorylation of NR2B may account for some of the consequences of dopamine deprivation on corticostriatal transmission and may play a role in some forms of synaptic plasticity.

Animals↗
PubMed1995

Molecular analysis of the multiple Golf alpha subunit mRNAs in the rat brain.

The alpha subunit of GTP-binding protein Golf (G alpha olf), identified in the olfactory epithelium, in which it is supposed to mediate odorant-generated adenylyl cyclase activations, is much more expressed in the striatum than G alpha s, the classical stimulatory G protein alpha subunit (Hervé et al., J Neurosci., 13 (1993) 2237-2248). Four species of G alpha olf messenger RNA (mRNA) were observed by Northern blot in the rat striatum. Analysis of striatal G alpha olf cDNA clones demonstrated that despite extensive variations in their 5' and 3' untranslated regions, these four G alpha olf mRNAs encode the same G alpha olf polypeptide. One of the four mRNA species, which was selectively observed in the striatum, is generated by a novel promoter whose activity was barely detectable in the olfactory epithelium. Surprisingly, this promoter generates an unexpectedly high proportion of transcripts in which the first intron is unspliced. The retention of intron was found to abolish the translation of G alpha olf mRNA in the reticulocyte lysate system, suggesting that it could be involved in the down regulation of G alpha olf expression in the striatum. Furthermore, a new polyadenylation site with a non canonical sequence, AATACA, was found to be responsible of the two shortest forms of G alpha olf mRNA. In conclusion, we have shown that the G alpha olf proteins present in the striatum and the olfactory epithelium are identical and that multiple variations in the untranslated parts of the mRNAs could affect G alpha olf expression.

Animals↗
PubMed1994

Blockade of prefronto-cortical alpha 1-adrenergic receptors prevents locomotor hyperactivity induced by subcortical D-amphetamine injection.

The stimulation of cortical dopaminergic D1 receptors can counteract the increased locomotor activity evoked by D-amphetamine application in the nucleus accumbens (Vezina et al., Eur. J. Neurosci., 3, 1001-1007, 1991). Moreover, an alpha 1 antagonist, prazosin, prevents the locomotor hyperactivity induced by electrolytic lesions of the ventral tegmental area (Trovero et al., Neuroscience, 47, 69-76, 1992). Attempts were thus made to see whether blockade of alpha 1-adrenergic receptors in the rat prefrontal cortex could reduce nucleus accumbens D-amphetamine-evoked locomotor activity. Rats implanted chronically and bilaterally with cannulae into the medial prefrontal cortex and the nucleus accumbens were used for this purpose and locomotor activity was monitored in circular corridors. Preliminary experiments indicated that intraperitoneal injection of prazosin (0.06 mg/kg) reduces the locomotor hyperactivity induced by the peripheral administration of D-amphetamine (0.75 mg/kg). This effect of prazosin was not observed when locomotor hyperactivity was obtained by an intraperitoneal injection of scopolamine (0.8 mg/kg). Bilateral nucleus accumbens injections of D-amphetamine (4.0 nmol/side) markedly increased locomotor activity, as estimated in a 30 min period. Prior (20 min) bilateral injections of either prazosin or WB-4101 (0.16 pmol) into the medial prefrontal cortex abolished the nucleus accumbens D-amphetamine-evoked response. The recovery of the nucleus accumbens D-amphetamine-evoked response was closely dependent on the amount of prazosin used, very prolonged inhibitory effects of the drug being seen with a high amount (> 4 days with 160 pmol). In contrast, whatever the amount of WB-4101 used (0.16-160 pmol), recovery occurred within 3 days.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-1 Receptor Antagonists↗
PubMed1994

Injections of 6-hydroxydopamine into the ventral tegmental area destroy mesolimbic dopamine neurons but spare the locomotor activating effects of nicotine in the rat.

The locomotor response to nicotine was assessed four weeks following destruction of mesolimbic dopamine (DA) neurons in rats by infusion of 6-hydroxydopamine into the ventral tegmental area. Resulting depletions of nucleus accumbens (N.Acc.) DA of up to 100% of control concentrations did not block the acute locomotor response to nicotine (0.4 mg/kg, base, s.c.). Such depletions also did not prevent the progressive enhancement of nicotine's locomotor effects when injections were repeated daily for nine days. These results suggest that mesolimbic DA is not necessary for the elicitation of locomotor activation by nicotine.

Animals↗
PubMed1993

G(olf) and Gs in rat basal ganglia: possible involvement of G(olf) in the coupling of dopamine D1 receptor with adenylyl cyclase.

Using specific antibodies and cDNA probes, we have investigated, in rat basal ganglia, the distribution and the regulation of the expression of the alpha subunits of Gs and G(olf), two GTP-binding proteins (G-proteins) that stimulate adenylyl cyclase. We confirmed that G(olf) alpha is highly expressed in caudate-putamen, nucleus accumbens, and olfactory tubercle, whereas Gs alpha is less abundant in these areas than in the other brain regions. Intrastriatal injections of quinolinic acid decreased dramatically the levels of G(olf) alpha protein in the striatum and the substantia nigra, and those of G(olf) alpha mRNA in the striatum. Retrograde lesions of striatonigral neurons with volkensin reduced markedly the levels of D1 dopamine (DA) binding sites, as well as those of G(olf) alpha protein and mRNA in the striatum, without altering D2 binding sites. In contrast, both types of lesions increased the levels of Gs alpha protein in the striatum and substantia nigra. Immunocytochemistry showed the presence of G(olf) alpha protein in striatal medium-sized neurons and in several other neuronal populations. These results demonstrate that striatonigral neurons contain high levels of G(olf) alpha and little, if any, Gs alpha, suggesting that the coupling of D1 receptor to adenylyl cyclase is provided by G(olf) alpha. The levels of G(olf) alpha were five- to sixfold higher in the striatum than in the substantia nigra, indicating a preferential localization of G(olf) alpha in the somatodendritic region of striatonigral neurons and providing a basis for the low efficiency of D1 receptor coupling in the substantia nigra. Six weeks after 6-hydroxydopamine lesions of DA neurons, an increase in G(olf) alpha (+53%) and Gs alpha (+64%) proteins was observed in the striatum. This increase in G(olf) alpha levels may account for the DA-activated adenylyl cyclase supersensitivity, without change in D1 receptors density, that follows destruction of DA neurons. Fine regulation of the levels of G(olf) alpha in physiological or pathological situations may be a critical parameter for the efficiency of DA neurotransmission.

Adenylyl Cyclases↗
PubMed1992

Stimulation of protein-tyrosine phosphorylation in rat striatum after lesion of dopamine neurons or chronic neuroleptic treatment.

Even though the short-term actions of dopamine on postsynaptic receptors are well-characterized, the molecular bases for long-term trophic interactions between dopamine neurons and their targets remain unclear. Since protein-tyrosine phosphorylation plays a key role in the action of trophic factors, we have investigated its possible involvement in the interactions between dopamine neurons and their striatal targets. Lesioning rat nigrostriatal dopamine neurons by using 6-hydroxydopamine increased the phosphorylation on tyrosine of several proteins, including a major 180-kDa protein (pp180) in the ipsilateral striatum. Protein-tyrosine kinase activity was also increased in the striatum ipsilateral to the lesion, whereas no change in phosphotyrosine phosphatase activity was detected. The stimulation of pp180 phosphorylation was observed 1, 2, and 8 weeks after 6-hydroxydopamine lesion, was selective for the destruction of dopamine neurons, and was mimicked by chronic blockade of dopamine receptors with neuroleptics. Additional lesion experiments and subcellular fractionation showed that pp180 is located in neuronal postsynaptic densities, suggesting that pp180 is a postsynaptic component of corticostriatal synapses. Our results indicate that lesion of specific afferent fibers can activate tyrosine phosphorylation in central neurons and suggest that tyrosine phosphorylation is involved in the long-term consequences of dopamine deficiency and may play a role in synaptic plasticity.

Animals↗
PubMed1992

Contribution of an alpha 1-adrenergic receptor subtype to the expression of the "ventral tegmental area syndrome".

Bilateral electrolytic lesions of the rat ventral tegmental area, a mesencephalic structure containing the cell bodies of ascending dopaminergic neurons, induce a behavioural syndrome characterized by a permanent locomotor hyperactivity. Acute intraperitoneal injections of prazosin, an alpha 1-adrenergic receptor antagonist, at a dose (0.5 mg/kg) which does not affect locomotor activities of control animals, abolished locomotor hyperactivities of lesioned rats. Antagonists of other monoaminergic receptors (propranolol, ritanserin, yohimbine), and also another antagonist of alpha 1-adrenergic receptors, 2-(2',6'-dimenthoxyphenoxyethyl)-aminomethyl-1,4-benzodioxan (WB4101) were ineffective. Comparisons of autoradiograms of brain slices incubated in the presence of 1 nM [3H]prazosin or 10 nM [3H]WB4101 indicated clear topographical differences. [3H]Prazosin labelling is present in the septum and in layer III of the cerebral cortex but absent in the striatum. [3H]WB 4101 labelling is diffuse in the superficial layers of the cerebral cortex and present in the striatum. In addition, intraperitoneal injection of WB4101 displaces, only weakly, [3H]prazosin binding in layer III of the cerebral cortex (-18%) while it decreases by 50% [3H]prazosin binding in the more superficial cortical layers. These observations strongly suggest that the binding site labelled by [3H]prazosin is different from alpha 1A- and alpha 1B-adrenergic receptor subtypes labelled by [3H]WB4101. Finally, it is proposed that the prazosin-induced blockade of the locomotor hyperactivity exhibited by ventral tegmental area lesioned animals is linked to the previously demonstrated regulatory role of noradrenergic neurons on cortical dopamine transmission.

Adrenergic alpha-Antagonists↗