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Expertise: endocannabinoïdes, stress, exercice physique

135 publication(s) since Janvier 1985:

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The indicated IF have been collected by the Web of Sciences in

04/2011 | Physiology (Bethesda)   IF 6.4
Endocannabinoids and motor behavior: CB1 receptors also control running activity.
Chaouloff F, Dubreucq S, Bellocchio L, Marsicano G


There is overwhelming evidence for multiple effects of stress on excitatory transmission and synaptic plasticity in the hippocampus. These interactions between stress and hippocampal glutamatergic neurons play a role in the cognitive and emotional consequences of aversive stimuli. Stress impacts on excitatory synapses are mediated by a complex set of neurohormones and neurotransmitters, among which corticosteroid hormones secreted from the adrenal cortex play a crucial role. Most effects of corticosteroid hormones are mediated by their binding to cytosolic mineralocorticoid (MR) and glucocorticoid receptors (GR), which after translocation to the nucleus, regulate the transcription of target genes. Recent electrophysiological and live imaging experiments have however provided experimental data which reinforce the hypothesis that beside these delayed effects, corticosteroid hormones may also act rapidly through membrane receptors. The first goal of this review is to detail the tonic and intrinsic effects of corticosteroid hormones on hippocampal excitatory transmission, glutamate receptor trafficking and expression, and synaptic plasticity, paying attention to their temporality (rapid and transient effects followed by slow and persistent genomic effects). Its second goal is to dissect the extent to which acute/repeated stress influences hippocampal excitatory synapses and whether these are accounted for by corticosteroid hormones.

07/2010 | Exp Neurol   IF 4.6
CB1 receptor deficiency decreases wheel-running activity: consequences on emotional behaviours and hippocampal neurogenesis.
Dubreucq S, Koehl M, Abrous DN, Marsicano G, Chaouloff F

Chronic voluntary wheel-running activity has been reported to hypersensitise central CB1 receptors in mice. On the other hand, pharmacological findings suggest that the CB1 receptor could be involved in wheel-running behaviour and in running-induced neurogenesis in the hippocampus. We analysed wheel-running behaviour for 6 weeks and measured its consequences on hippocampal neurogenesis in CB1 knockout (CB1(-/-)) animals, compared to wild-type (CB1(+/+)) littermates. Because wheel running has been shown to affect locomotor reactivity in novel environments, memory for aversive events and depression-like behaviours, we also assessed these behaviours in control and running CB1(+/+) and CB1(-/-) mice. When compared with running CB1(+/+) mice, the distance covered weekly by CB1(-/-) mice was decreased by 30-40%, an observation accounted for by decreased time spent and maximal velocity on the wheels. Analyses of running distances with respect to the light/dark cycle revealed that mutant covered less distance throughout both the inactive and the active phases of that cycle. Locomotion in an activity cage, exploration in an open field, and immobility time in the forced swim test proved insensitive to chronic wheel running in either genotype. Wheel running, per se, did not influence the expression and extinction of cued fear memory but counteracted in a time-dependent manner the deficiency of extinction measured in CB1(-/-) mice. Hippocampal neurogenesis, assessed by doublecortin labelling of immature neurons in the dentate gyrus, was lowered by 40% in control CB1(-/-) mice, compared to control CB1(+/+) mice. Although CB1(-/-) mice ran less than their wild-type littermates, the 6-week running protocol increased neurogenesis to similar extents (37-39%) in both genotypes. This study suggests that mouse CB1 receptors control wheel running but not its neurogenic consequences in the hippocampus.

15/03/2010 | Hippocampus   IF 3.3
Emotional consequences of wheel running in mice: Which is the appropriate control?
Dubreucq S, Marsicano G, Chaouloff F


03/2010 | Nat Neurosci   IF 21.1
Bimodal control of stimulated food intake by the endocannabinoid system
Bellocchio L*, Lafenetre P*, Cannich A, Cota D, Puente N, Grandes P, Chaouloff F, Piazza PV*, Marsicano G*


12/2009 | Neuropharmacology   IF 4.4
Bidirectional regulation of novelty-induced behavioral inhibition by the endocannabinoid system.
Lafenetre P, Chaouloff F, Marsicano G

The balance between novelty seeking and safety assessment is a key feature of adaptive behavior, and alterations in this equilibrium can lead to neuropsychiatric disorders. Excessive novelty seeking is a main form of pathological impulsivity, which is among the symptoms that define attention deficit hyperactivity disorder (ADHD). There is growing evidence that the endocannabinoid system (ECS) plays an important role in the control of this balance, but little is known about the underlying neuronal mechanisms. In this study, we aimed at dissecting the neurocircuits under the control of the ECS in novelty-induced behavioral inhibition. To reach this goal, we combined pharmacological, genetic and behavioral tools. Mice were repeatedly exposed to novel palatable food or a novel object and their responses to these stimuli were analyzed over several days. The results confirmed that systemic blockade of cannabinoid type-1 (CB(1)) receptors strongly decreases palatable food intake, but its impact onto the response to novelty is less pronounced. Using conditional mutant mice lacking the CB(1) receptor either in cortical glutamatergic or in GABAergic neurons, we found that the ECS exerts opposite functions on the balance between novelty seeking and behavioral inhibition. Whereas CB(1) receptors expressed in cortical glutamatergic neurons favors novelty seeking, CB(1)-dependent control of inhibitory GABAergic neurons promotes behavioral inhibition. These data show a tightly regulated influence of the ECS on impulsive behaviors and suggest the involvement of endocannabinoid signaling in the pathophysiological modulation of ADHD and related disorders.

08/2008 | Med Sci (Paris)   IF 0.4
[New insights in stress-induced synaptic adaptations].
Groc L, Chaouloff F


Corticosterone facilitates hippocampal glutamate transmission, but the cellular pathways by which AMPA receptor (AMPAR) signaling is adjusted remain elusive. Single quantum-dot imaging in live rat hippocampal neurons revealed that corticosterone triggers, via distinct corticosteroid receptors, time-dependent increases in GluR2-AMPAR surface mobility and synaptic surface GluR2 content. Furthermore, corticosterone potentiates the increase of synaptic surface GluR2 contents by a chemical long-term potentiation stimulus, revealing the influence that corticosterone has on AMPAR trafficking.

Long-term potentiation and long-term depression (LTD) of synaptic efficacy, two major forms of synaptic plasticity, are believed to underlie learning processes and memory storage. We have recently shown that acute stress, through corticosterone release and stimulation of glucocorticoid receptors (GRs), facilitates the LTD elicited by the group 1 metabotropic glutamate receptor (mGluR) agonist (R,S)-3,5-dihydroxyphenylglycine (DHPG) in hippocampal CA1 neurons. However, it is unknown whether sustained corticosterone release, per se, is also able to facilitate DHPG-elicited LTD in control (i.e. unstressed) conditions, and if so, whether it acts on local (i.e. hippocampal) or distant GRs. Here, we show that a brief application of 100 nM corticosterone to rat hippocampal slices lowers the threshold for DHPG-elicited LTD, an effect mimicked by the local application of the GR agonist dexamethasone. These results show that high corticosterone release facilitates hippocampal CA1 mGluR-dependent LTD, and does so through local GRs.

2008 | Future Neurology   IF 0.8
Stress, corticosteroids and excitatory neurotransmission
Groc L, Chaouloff F