Biologie animale et végétale :travaux pratiques

MEDE1, DENT1, VETE1, BIME1, IRCI3-B - BIOL-G-101info:eu-repo/semantics/published1

The Effects of State Legislation on Adolescent Marijuana Use

Marijuana legislation has been changing a lot over the last few years. The recent legalizations for medical and recreational use opens the doors for public health research. Historically, there is not a lot of research on marijuana due to its long history of being classified as a schedule 1 drug, which was a large block for much research. The purpose of this study is to view and compare how different states’ marijuana legislation influences adolescent marijuana usage, specifically high school students. Using mainly the CDC’s 2015 Youth Risk Behavior Surveillance Survey, and some data obtained from state’s Department of Public Health, a one-way ANOVA test was run to compare adolescent marijuana use in states with varying marijuana legislation. The study found no significant difference in adolescent marijuana use between no legalization vs limited medical legalization and non-limited medical legalization vs recreational legalization. Both non-limited medical legalization and recreational legalization were found to show a significantly higher rate of adolescent marijuana use compared to both no legalization and limited medical legalization groups. Presentation: 4:1

Endocannabinoid and serotonergic systems are needed for acetaminophen-induced analgesia.

Acetaminophen is the most used analgesic/antipyretic drug. Its unclear mechanism of action could rely on cyclooxygenase inhibition, NO synthesis blockade or reinforcement of the serotonergic system. Here we show that in thermal, mechanical and chemical pain tests, AM-251, a specific CB(1) receptor antagonist, abolished the analgesic action of acetaminophen, which was also lost in CB(1) receptor knockout mice. Moreover, acetaminophen was shown unable to bind to CB(1) receptors demonstrating an indirect involvement of these receptors in the analgesic effect of this compound. Accordingly with these results, we also demonstrated that the inhibition of FAAH, an enzyme involved in the cerebral metabolism of acetaminophen into AM404, known to reinforce the activity of the endocannabinoid system, suppressed the antinociceptive effect of acetaminophen. In addition, similarly to the interaction of acetaminophen with bulbospinal serotonergic pathways and spinal serotonin receptors, we observed that the antinociceptive activity of ACEA, a CB(1) receptor agonist, was inhibited by lesion of bulbospinal serotonergic pathways and antagonists of spinal 5-HT receptors. We therefore propose that acetaminophen-induced analgesia could involve the following sequence: (1) FAAH-dependent metabolism of acetaminophen into AM404; (2) indirect involvement of CB(1) receptors by this metabolite; (3) endocannabinoid-dependent reinforcement of the serotonergic bulbospinal pathways, and (4) involvement of spinal pain-suppressing serotonergic receptors.Comparative StudyJournal ArticleResearch Support, Non-U.S. Gov'tinfo:eu-repo/semantics/publishe

Le récepteur de la thyrotropine. Contrôle de l'expression du gène et relations structure fonction.

Journal Articleinfo:eu-repo/semantics/publishe

Lack of CB1 receptor activity impairs serotonergic negative feedback

Serotonergic and endocannabinoid systems are important substrates for the control of emotional behavior and growing evidence show an involvement in the pathophysiology of mood disorders. In the present study, the absence of the activity of the CB1 cannabinoid receptor impaired serotonergic negative feedback in mice. Thus, in vivo microdialysis experiments revealed increased basal 5-HT extracellular levels and attenuated fluoxetine-induced increase of 5-HT extracellular levels in the prefrontal cortex of CB1 knockout compared to wild-type mice. These observations could be related to the significant reduction in the 5-HT transporter binding site density detected in frontal cortex and hippocampus of CB1 knockout mice. The lack of CB1 receptor also altered some 5-HT receptors related to the 5-HT feedback. Extracellular recordings in the dorsal raphe nucleus revealed that the genetic and pharmacological blockade of CB1 receptor induced a 5-HT1A autoreceptor functional desensitization. In situ hybridization studies showed a reduction in the expression of the 5-HT2C receptor within several brain areas related to the control of the emotional responses, such as the dorsal raphe nucleus, the nucleus accumbens and the paraventricular nucleus of the hypothalamus, whereas an overexpression was observed in the CA3 area of the ventral hippocampus. These results reveal that the lack of CB1 receptor induces a facilitation of the activity of serotonergic neurons in the dorsal raphe nucleus by altering different components of the 5-HT feedback as well as an increase in 5-HT extracellular levels in the prefrontal cortex in mice.We thank Dulce Real, Marta Linares and Rocío Martín for their excellent technical support, Arnau Busquets for his help on the in situ hybridization experiments and Dr Patricia Robledo for kind advices about in vivo microdialysis procedure. This study has been supported by grants from the UE /nSixth Framework Programme (NEWMOOD, LSHM-CT-2004-503474 to RM and LL), Spanish Ministry of Education & Science (SAF 2007/60249 to OV, BES-2005-8265 fellowship to EA) and Spanish Ministry of Health (ISCIII-RD/06/0001/1001/and PNSD Conv-2006 to OV

Impact of insulin on primary arcuate neurons culture is dependent on early-postnatal nutritional status and neuronal subpopulation

<div><p>Nutrition plays a critical role in programming and shaping linear growth during early postnatal life through direct action on the development of the neuroendocrine somatotropic (GH/IGF-1) axis. IGF-1 is a key factor in modulating the programming of linear growth during this period. Notably, IGF-1 preferentially stimulates axonal growth of GHRH neurons in the arcuate nucleus of the hypothalamus (Arc), which is crucial for the proliferation of somatotroph progenitors in the pituitary, thus influencing later GH secretory capacity. However, other nutrition-related hormones may also be involved. Among them, insulin shares several structural and functional similarities with IGF-1, as well as downstream signaling effectors. We investigated the role of insulin in the control of Arc axonal growth using an <i>in vitro</i> model of arcuate explants culture and a cell-type specific approach (GHRH-eGFP mice) under both physiological conditions (normally fed pups) and those of dietary restriction (underfed pups). Our data suggest that insulin failed to directly control axonal growth of Arc neurons or influence specific IGF-1-mediated effects on GHRH neurons. Insulin may act on neuronal welfare, which appears to be dependent on neuronal sub-populations and is influenced by the nutritional status of pups in which Arc neurons develop.</p></div

Response of arcuate neurons to insulin.

<p>Relative axonal growth in 24 h in whole arcuate neuron explants in the presence of various molar concentrations of insulin (0, 10, 50, 100, 200, 500 nM, and 1μM) was measured by immunohistochemistry against neurofilaments (NF). Arcuate explants were harvested from normally fed (dark circles and plain line) (n = 3–4) or underfed pups (open triangles and dotted line) (n = 6). Illustrative images of explants are presented above the graph for control (0 nM), 100 nM and 1000 nM of insulin. Scale bar indicates 2000 μm. Data are presented as the mean ± SEM. Results were analyzed by two-way ANOVA (see text) with a Bonferroni correction for multiple comparisons. The precise molar concentrations-response effect within each group was further analyzed by one-way ANOVA with a Newman-Keuls multiple comparison test. The results of all comparisons were non-significant.</p