Showing papers by "Jean Costentin published in 1996"
TL;DR: Nociceptin was found to increase the number of head dips in the hole-board test, indicating that the peptide stimulates exploratory behaviour, and exerted its motor-stimulant actions by increasing central dopaminergic transmission.
150 citations
TL;DR: These selectively bred lines may represent potentially useful animal models to investigate behavioural, neurochemical and neuroendocrine correlates of antidepressant action and genetic factors substantially contribute to the susceptibility to helplessness in this mouse model.
46 citations
TL;DR: It is concluded that indirect dopamine agonists are effective on the behavioral despair test independently of a stimulation of locomotion and not on the stimulation of D2 but not D1 dopamine receptors.
Abstract: Both dexamphetamine and the pure dopamine reuptake inhibitor GBR 12783 elicit a stimulation of locomotion and increase swimming activity in the behavioral despair test in mice. The dopamine D 1 dopamine receptor antagonist SCH 23390 dose dependently (7.5–30 μg/kg SC) antagonized the stimulant locomotor effect of both drugs but did not prevent their antiimmobility effect on the behavioral despair test. The D 2 dopamine receptor antagonist haloperidol dose dependently (12.5–50 μg/kg IP) antagonized the effects of dexamphetamine on both locomotor activity and behavioral despair test. By contrast, haloperidol inhibited the effects of GBR 12783 in the forced swimming test but not on locomotion. It is concluded that indirect dopamine agonists are effective on the behavioral despair test independently of a stimulation of locomotor activity. Their effects on the despair test depend on the stimulation of D 2 but not D 1 dopamine receptors.
40 citations
TL;DR: It was observed that administration of modafinil in rats habituated to their environment induced a recovery of locomotor activity, mainly oppose to the decrease in locomotion (habituation) which normally occurs in control animals.
Abstract: Summary— Locomotor effects of modafinil were analysed and compared in various strains of mice and rats. A stimulation of locomotor activity was evidenced in all tested strains of mice: Swiss CD1, BALB/c, DBA2, C3H, B6CBAF1/JICO, Nude CD1 and in all tested strains of rats: Long Evans, Sprague Dawley, Wistar. In mice, from 10 mg/kg intraperitoneal, a precocious stimulant effect was observed. The drug seems to operate in its native form on the mouse brain since its intracerebroventricular administration (from 15 μg/mouse) elicited a stimulation of locomotion. In rats, the effective doses were higher (from 40 mg/kg ip); the effects of modafinil mainly oppose to the decrease in locomotion (habituation) which normally occurs in control animals. In addition, it was observed that administration of modafinil in rats habituated to their environment induced a recovery of locomotor activity.
39 citations
Journal Article•
TL;DR: Autoradiographic analysis revealed a significant decrease in the desipramine-insensitive [3H]mazindol binding to the dopamine transporter in the shell of the nucleus accumbens, which suggests that the decrease in accumbal [2- (diphenylmethoxy)ethyl]-4-(3-phenyl-2-(propenyl)-piperazine labeling did not result from a cytotoxic effect on corresponding dopamine neurons.
Abstract: Rats were treated once daily for 15 consecutive days with either cocaine or the specific dopamine uptake inhibitor 1-[2- (diphenylmethoxy)ethyl]-4-(3-phenyl-2-(propenyl)-piperazine (GBR12783) at a dose (10 mg/kg) that given acutely increases locomotor activity. Two or 14 days after the last administration, the motor stimulant responses of rats to a challenge dose (5 mg/kg) of the drug administered previously were compared with the motor stimulant responses of rats daily injected with solvent. A sensitization to the acute stimulant locomotor effect of these drugs was only observed 14 days after cessation of chronic treatments. After this withdrawal period, autoradiographic analysis revealed a significant decrease in the desipramine-insensitive [3H]mazindol binding to the dopamine transporter in the shell of the nucleus accumbens. No change was noticed in other regions with high dopamine content: core of nucleus accumbens, striatum, olfactory tubercle, substantia nigra and ventral tegmental area. Absence of concomitant decrease in [3H]dihydrotetrabenazine labeling, which indicates lack of effect on vesicular monoamine transporters, suggests that the decrease in accumbal [3H]mazindol binding did not result from a cytotoxic effect on corresponding dopamine neurons. In addition, 14 days after the last administration of GBR12783, the levels of dopamine and metabolites (dihydroxy-phenylacetic acid, homovanillic acid) and the ability of acute GBR12783 to synergize with haloperidol-induced increase in these metabolites were not modified either in the whole nucleus accumbens or in the striatum.
38 citations
TL;DR: The VMAT immunoreactivity was not altered 2 and 30 days after the reserpine injection, whereas [3H]TBZOH binding site density, measured on adjacent slices, showed a dramatic decrease at day 2 and a moderate recovery at day 30, suggesting that despite a persistent blockade of [3 H]TB ZOH binding sites, VMAT protein density was unchanged.
Abstract: We have studied the effect of a single injection of reserpine (5 mg/kg, s.c.) on the synaptic vesicle monoamine transporter (VMAT) density in the rat striatum, using two labelling procedures: radioimmunolabelling with an antibody against VMAT, and binding of the specific ligand [(3)H]dihydrotetrabenazine ([(3)H]TBZOH). In the rostral and medial striatum, the distribution of VMAT immunoreactivity displayed the highest density in the lateral subregions. In the caudal part of the striatum, VMAT immunoreactivity showed increasing density from dorsal to ventral subregions. The VMAT immunoreactivity was not altered 2 and 30 days after the reserpine injection, whereas [(3)H]TBZOH binding site density, measured on adjacent slices, showed a dramatic decrease at day 2 and a moderate recovery at day 30, suggesting that despite a persistent blockade of [(3)H]TBZOH binding sites, VMAT protein density was unchanged.
30 citations
TL;DR: The rewarding and locomotor effects of the specific dopamine uptake inhibitor GBR12783 were compared with those of cocaine and it is suggested that these two properties are, at least in part, separable anatomically or functionally.
Abstract: The rewarding and locomotor effects of the specific dopamine uptake inhibitor GBR12783 (2.5-20 mg kg-1, i.p.) were compared with those of cocaine. For both drugs, all doses produced a conditioned place preference (CPP), even the dose of 2.5 mg kg-1, which did not modify the locomotor activity. Despite an equivalent locomotor stimulation, the magnitude of CPP induced by cocaine (10 mg kg-1) was greater than that induced by the same dose of GBR12783. This confirms the involvement of dopamine uptake inhibition in reward, but underlines differences in relative efficacies in rewarding and motor effects of both drugs and suggests that these two properties are, at least in part, separable anatomically or functionally.
30 citations
TL;DR: At 20 degrees C, [3H]GBR 12783-binding dissociation was increased by high 'cytosolic' K+ while 'synaptic' concentrations of Na+, K+, Ca2+, Mg2+ and Cl- were ineffective, suggesting that an anion-binding site could also regulate the binding.
14 citations
TL;DR: The peptide, in doses up to 1 microgram, had no effect on latency of escape jumping in the hot plate test and the peptide did not modify responses (paw licking, rearing, and escape jumping) in morphine-treated mice, which support previous hypotheses that the Leu-enkephalin sequence is not present in preproencephalin A of amphibians.
13 citations
TL;DR: The results suggest that modifications in dopamine neurotransmission do not alter the in vivo quantification of D1 receptors with [3H]SCH 23390, for example, in studies that use positron emission tomography.
10 citations
TL;DR: The data suggest that a similar mechanism may underlie the locomotor sensitization to GBR12783 and the heterosensitization to [D-Trp(11)]neurotensin.
TL;DR: The level of dopamine transmission would not interfere with the in vivo quantification of striatal dopamine uptake sites assessed with either ligands, and only dexamphetamine pretreatment significantly reduced [ 3H]cocaine and [3H]mazindol binding.
TL;DR: It appears that the sensitivity of JMV 1193 to enkephalinase depends on its route of administration, as it is exposed to this peptidase after i.c.v. injection while it is not when crossing the cerebrospinal fluid-brain barrier.
TL;DR: Low K+ concentrations are likely to prevent the decrease in uptake elicited by high Na+ concentrations by restoration, via a Na+/K+ ATPase-mediated mechanism, of the membrane potential and/or a transmembrane electrochemical Na+ gradient more favourable to DA uptake.
Abstract: The specific uptake of [3H] dopamine (DA) was studied using a crude synaptosomal fraction obtained from rat striatum. In a medium containing a 10 mM NaHC03/NaH2PO4 buffer and no added K+ ions, addition of NaCl elicited an increase in DA uptake for Na+ concentrations from 10 to 60 mM, and then a decrease of uptake for Na+ concentrations up to 130 mM. These data confirm that rather low NaCl concentrations produce a maximal DA uptake. This biphasic curve of uptake resulted from significant changes in the Vmax of the DA uptake. Except for 10 mM Na+, this curve was not significantly modified when 9 mM NaHCO3/NaH2PO4 were replaced by 9 mM NaCl. This result indicates that the Cl− dependence of the DA uptake is mainly secondary to the Na+ dependence. Addition of KCl up to 3 mM did not modify the ascending part of the NaCl-dependent uptake curve. In contrast, the reduction in uptake produced by high Na+ concentrations was prevented in a concentration-dependent manner by KCl; this effect resulted from a decrease in the Km and an increase in the Vmax for the uptake.