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Patent
Toulouse University Hospital Center and Aix - Marseille University | Date: 2011-05-25

The present invention relates to a compound which is an agonist of the oxytocin receptor o for use in the treatment of a feeding disorder with early-onset. In a particular embodiment, the agonist of the oxytocin receptor is the oxytocin or an active fragment thereof.


Patent
French Institute of Health, Medical Research, Aix - Marseille University and Toulouse University Hospital Center | Date: 2014-08-29

The present invention relates to a compound which is an agonist of the oxytocin receptor o for use in the treatment of a feeding disorder with early-onset. In a particular embodiment, the agonist of the oxytocin receptor is the oxytocin or an active fragment thereof.


Chollet F.,Toulouse University Hospital Center
Dialogues in Clinical Neuroscience | Year: 2013

Brain plasticity is an intrinsic characteristic of the nervous system that allows continuous remodeling of brain functions in pathophysiological conditions. Although normal aging is associated with morphological modifications and decline of cerebral functions, brain plasticityis at least partially preserved in elderly individuals. A growing body of evidence supports the notion that cognitive enrichment and aerobic training induce a dynamic reorganization of higher cerebral functions, thereby helping to maintain operational skills in the elderly and reducing the incidence of dementia. The stroke model clearly shows that spontaneous brain plasticity exists after a lesion, even in old patients, and that it can be modulated through external factors like rehabilitation and drugs. Whether drugs can be used with the aim of modulating the effects of physical training or cognitive stimulation in healthy aged people has not been addressed until now. The risk:benefit ratio will be the key question with regard to the ethical aspect of this challenge. We review in this article the main aspects of human brain plasticityas shown in patients with stroke, the drug modulation of brain plasticity and its consequenceson recovery, and finally we address the question of the influence of aging on brain plasticity. © 2013 LLS SAS. Source


BACKGROUND: The accumulation of beta amyloid (Aβ) peptides, a hallmark of Alzheimer's disease (AD) is related to mechanisms leading to neurodegeneration. Among its pleiotropic cellular effects, Aβ accumulation has been associated with a deregulation of sphingolipid metabolism. Sphingosine 1-phosphate (S1P) derived from sphingosine is emerging as a critical lipid mediator regulating various biological activities including cell proliferation, survival, migration, inflammation, or angiogenesis. S1P tissue level is low and kept under control through equilibrium between its synthesis mostly governed by sphingosine kinase-1 (SphK1) and its degradation by sphingosine 1-phosphate lyase (SPL). We have previously reported that Aβ peptides were able to decrease the activity of SphK1 in cell culture models, an effect that could be blocked by the prosurvival IGF-1/IGF-1R signaling.RESULTS: Herein, we report for the first time the expression of both SphK1 and SPL by immunohistochemistry in frontal and entorhinal cortices from 56 human AD brains. Immunohistochemical analysis revealed a decreased expression of SphK1 and an increased expression of SPL both correlated to amyloid deposits in the entorhinal cortex. Otherwise, analysis of brain tissue extracts showed a decrease of SphK1 expression in AD brains whereas SPL expression was increased. The content of IGF-1R, an activator of SphK1, was found decreased in AD brains as well as S1P1, the major receptor for S1P.CONCLUSIONS: Collectively, these results highlight the importance of S1P in AD suggesting the existence of a global deregulation of S1P signaling in this disease from its synthesis by SphK1 and degradation by SPL to its signaling by the S1P1 receptor. Source


Minville V.,Toulouse University Hospital Center
British journal of anaesthesia | Year: 2011

The aim of this study was to assess any interaction between ondansetron and paracetamol on a model of post-fracture pain in mice. In protocol A, after fracture of the tibia, mice were assigned to four groups: paracetamol 30 mg kg 1, paracetamol 50 mg kg 1, paracetamol 100 mg kg 1, or a saline vehicle i.p. In protocol B, after fracture of the tibia, mice were randomized to receive either paracetamol (100 mg kg 1) plus saline (vehicle), paracetamol (100 mg kg 1) plus ondansetron (1 mg kg 1), paracetamol (100 mg kg 1) plus ondansetron (2 mg kg 1), saline plus ondansetron (2 mg kg 1), or saline plus saline i.p. Three tests were used to assess pain behaviour: von Frey filament application, hot-plate test, and a subjective pain scale. Rescue analgesia with morphine was administered as necessary. In protocol A, paracetamol (100 mg kg 1)-treated animals had less mechanical nociception, thermal nociception, and a lower subjective pain scale rating, when compared with those receiving paracetamol at 30 or 50 mg kg 1 or saline [ED paracetamol=46.3 (6.34) mg kg 1]. No difference was found between paracetamol (30 mg kg 1) and saline-treated animals. In protocol B, the mechanical withdrawal threshold, the thermal withdrawal latency, and the subjective pain scale were lower after injection of paracetamol (100 mg kg 1)+saline, paracetamol (100 mg kg 1)+ondansetron (1 mg kg 1), and paracetamol (100 mg kg 1)+ondansetron (2 mg kg 1), whereas in mice receiving saline+ondansetron (2 mg kg 1) or saline+saline, there was no difference. We found that paracetamol 100 mg kg 1 blocked the development of hyperalgesia and allodynia after fracture pain and ondansetron did not modify the antinociceptive effect of paracetamol in this model. Source

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