Leptin Prevents Lipopolysaccharide-Induced Depressive-Like Behaviors in Mice: Involvement of Dopamine Receptors

Depression is a chronic and recurrent disorder, associated with high morbidity and risk of suicide. Leptin was firstly described as an anti-obesity hormone, but several actions of leptin in CNS have been reported. In fact, leptin regulates dopaminergic neurotransmission in mesolimbic areas and has antidepressant-like properties in stress-based models. In the present study, we investigated, for the first time, putative antidepressant-like effects of leptin in an animal model of depressive-like behaviors induced by lipopolysaccharide (LPS), and the potential involvement of dopamine receptors as mediators of those behavioral effects. Mice were injected leptin (1.5 mg/kg, IP) or imipramine prior to LPS administration. To evaluate the involvement of dopamine receptors, different experimental groups were pretreated with either the dopaminergic antagonist SCH23390, for D1 receptors or raclopride, for D2/D3 receptors, prior to leptin injection. Twenty-four hours post-LPS, mice were submitted to the forced swimming and sucrose preference tests. In addition, IL-1β levels were determined in the prefrontal cortex (PFC), hippocampus and striatum. BDNF levels were measured in the hippocampus. Our results showed that leptin, similarly to imipramine, prevented the core behavioral alterations induced by LPS (despair-like behavior and anhedonia), without altering locomotion. In neurochemical analysis, leptin restored LPS-induced changes in IL-1β levels in the PFC and striatum, and increased BDNF levels in the hippocampus. The blockade of dopamine D1 and D2/D3 receptors inhibited leptin's antidepressant-like effects, whilst only the blockade of D1-like receptors blunted leptin-induced increments in prefrontal IL-1β levels. Our results indicate that leptin has antidepressant-like effects in an inflammatory model of depression with the contribution, at least partial, of dopamine receptors

Apport du laboratoire de toxicologie clinique

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Du bon usage du laboratoire de toxicologie: II. Utilité clinique et interprétation des résultats.

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Survival despite Intravenous self-injection of a potentially fatal dose of aniline hydrochloride

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Du bon usage du laboratoire de toxicologie: I. Aspects techniques

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Prophylactic diclofenac infusions in major orthopedic surgery: effects on analgesia and acute phase proteins

The influence of diclofenac, given by continuous i.v. infusion starting preoperatively, on postoperative pain and inflammation was assessed in a double‐blind, randomized, placebo‐controlled study in 40 patients scheduled for major orthopedic surgery. Starting 30 min before induction the patients received either diclofenac (0.35 mg.kg‐1 bolus followed by a constant‐rate infusion of 90 μ.min‐1) or placebo for 24 h. The pain intensity (VAS) and the amount of rescue narcotic (piritramide on demand) were significantly lower in the diclofenac group from 4 and 6 h postsurgery, respectively, till end of infusion. Acute phase proteins used as inflammation markers (C‐reactive protein, α1‐chymotrypsin, α1‐acid glycoprotein, haptoglobin and coeruloplasmin) showed similar variations in both groups for 24 h. The diclofenac treatment had no influence on hematological and coagulation profiles, nor on muscle and liver enzymes in comparison with placebo. Both patients and observer rated the diclofenac treatment as significantly superior to the placebo treatment. © 1992 Acta Anaesthesiologica Scandinavica FondenSCOPUS: ar.jinfo:eu-repo/semantics/publishe

Amoxycillin metabolism studied by combination of HPLC and spectrophotometry on urinary samples

A method is presented to determine the antibiotic amoxycillin and its inactive penicilloic acid metabolite in urine by the combination of two techniques.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Trichloroethylene abuse :an unreported source of ketoacidosis

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Cobas Mira S endpoint enzymatic assay for plasma formate.

In methanol intoxication, increased levels of the metabolite formate are associated with metabolic acidosis and an increased risk for ocular and neurological dysfunction. A simple method for plasma formate measurement by adaptation of a manual enzymatic assay to a Cobas Mira S analyzer is presented. Six microliters of sample is incubated for 5 min with buffer containing nicotinamide-adenine dinucleotide. Fifteen microliters of a suspension of formate dehydrogenase is then added. Absorbance at 340 nm is measured every 25 s. The NADH produced when formate is oxidized is stoichiometric to the amount of formate. The method is sensitive, reproducible, and specific and has a broad measurement range. The frozen reagents are stable for at least six months, so the described method can be applied to irregular and semi-urgent requests. A recent case is reported.Evaluation StudiesJournal ArticleSCOPUS: ar.jinfo:eu-repo/semantics/publishe

Hemodynamic and respiratory effects of epidural liposomal morphine given at induction of anesthesia

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