How can I buy cocaine online in Vina del Mar

__________________________

📍 Verified store!

📍 Guarantees! Quality! Reviews!

__________________________

▼▼ ▼▼ ▼▼ ▼▼ ▼▼ ▼▼ ▼▼

▲▲ ▲▲ ▲▲ ▲▲ ▲▲ ▲▲ ▲▲

How can I buy cocaine online in Vina del Mar

Either your web browser doesn't support Javascript or it is currently turned off. In the latter case, please turn on Javascript support in your web browser and reload this page. Refer to the copyright information in the article for licensing details. Free full text in Europe PMC. Agonism of the glucagon-like peptide 1 GLP-1 receptor GLP-1R has been effective at treating aspects of addictive behavior for a number of abused substances, including cocaine. However, the molecular mechanisms and brain circuits underlying the therapeutic effects of GLP-1R signaling on cocaine actions remain elusive. Recent evidence has revealed that endogenous signaling at the GLP-1R within the forebrain lateral septum LS acts to reduce cocaine-induced locomotion and cocaine conditioned place preference, both considered dopamine DA -associated behaviors. Interestingly, acute administration of Ex-4 reduces septal expression of the retrograde messenger 2-arachidonylglycerol 2-AG , as well as a product of its presynaptic degradation, arachidonic acid AA. Cocaine addiction is a highly prevalent disorder characterized by continued drug use in spite of negative consequences. Despite the harmful effects of cocaine, the development of pharmacotherapies to treat cocaine addiction has been slow. This is because modulators of addictive behavior are limited and we lack a comprehensive understanding of their mechanisms. Starting with the discovery that glucagon-like peptide 1 GLP-1 regulates amphetamine-induced locomotion, 1 GLP-1 receptor GLP-1R agonism has been shown to reduce the rewarding properties of cocaine and other drugs of abuse in rodents. GLP-1 is both a hormone produced by L cells of the intestine and a neuropeptide produced by the nucleus of the tractus solitarius. The neurotransmitter dopamine DA underlies the rewarding properties of drugs of abuse, as well as natural rewards. One such node is found within the forebrain lateral septum LS. Recently, Harasta et al. This phenomenon is associated with increased DAT surface expression and function mediated by a reduction in endocannabinoid and arachidonic acid AA levels in the LS. These findings reveal a novel mechanism of GLP-1R action in brain and provide a more comprehensive understanding of how emerging GLP-1R-targeted therapies affect signaling in the brain. All the experiments were performed during the light cycle. For immunohistochemical characterization of GLP-1R localization, bacterial artificial chromosome transgenic mice containing a fluorescent reporter expressed in GLP-1R-expressing cells were generated as described in Supplementary Information. The suppliers for all chemicals not otherwise identified can be found in the Supplementary Information. The sections were immunostained and imaged as described in the Supplementary Information. The procedure for c-fos IHC is as previously described. Microdialysis was performed as described previously 4 with few modifications. The dialysis probe was positioned in LS, anteroposterior: 0. The first two min samples were discarded to obtain stable basal values. Hereafter, two min fractions were collected to establish baseline DA levels. Subsequently, the mice were injected with Ex-4 or vehicle, and three min fractions were collected. All the fractions were assayed immediately after collection using high-performance liquid chromatography with electrochemical detection. Total protein was taken, and the samples were processed for protein concentration using a Bio-Rad Philadelphia, PA, USA protein assay and spectrometry at nm. Equivalent volumes of the sample were added to 3 ml of scintillation fluid Ecoscint H, National Diagnostics, Atlanta, GA, USA and radioactive counts were measured by scintillation counter. The mice were injected with Ex-4 or vehicle intraperitoneally 30 min before being killed. The mice were rapidly decapitated and the brains were obtained and blocked to obtain DS and LS punches. The samples were homogenized in methanol and centrifuged; water was added to the supernatant for a final ratio of methanol:water. The pellets were resuspended and processed for protein concentration using a Bio-Rad protein assay and spectrometry at nm. Krebs—Henseleit buffer was used m m NaCl, 4. The cell viability was measured using Trypan blue staining. Immunoprecipitations were performed using 1 mg total protein. The data were examined with Student's t -test for comparisons of only two data sets and one-way or two-way analysis of variance for comparisons of multiple groups, followed by Tukey's- or Bonferroni-corrected comparisons. Optical density of bands was determined using Image J software. The statistical analysis was performed with GraphPad Prism software, version 5. The methods for Supplementary Figures can be found in the Supplementary Information. To this end, we generated a transgenic mouse expressing a bacterial artificial chromosome for the protein mApple under the control of the promoter for the GLP-1R. The mApple signal was amplified by immunostaining Figures 1a, c, d and f and DAT was labeled in parallel Figures 1b, c, e and f. Within the caudal LS Figures 1d—f , there is similar evidence for this anatomical overlap. The DA terminals are labeled as two strips extending dorsomedially to ventrolaterally in the LSi. The GLP-1R-expressing cells are also found in the caudal LSi, but the cell bodies additionally extend further into the more medial laterodorsal tegmental area. Dotted lines delineate region boundaries. Dotted box includes the LS. Extracellular concentrations of DA are expressed as the percentage of basal levels in two fractions collected before the intervention; significant analysis of variance. We next tested whether a therapeutically relevant administration that is, systemic administration of Ex-4 was capable of altering neuronal activity in the LS. We first evaluated the effect of Ex-4 on the activation of septal neurons by measuring c-fos expression. Ex-4 administration intraperitoneally 30 min before killing decreased basal c-fos gene expression by in situ hybridization relative to vehicle-treated mice Figures 1h and i. This result indicates that systemic administration of Ex-4 alters neuronal activity in the LS. The psychogenic and addictive properties of cocaine are mediated, at least in part, through the blockade of DAT-mediated DA reuptake and an increase in extracellular DA. We determined the effect of systemic Ex-4 on local cocaine-induced changes in DA homeostasis in vivo within the LS, as measured by microdialysis in freely moving mice. Systemic pretreatment with Ex-4 intraperitoneally 90 min prior impaired the cocaine's ability to significantly increase extracellular DA. Ex-4 or vehicle was perfused through the microdialysis probe concurrently with cocaine Supplementary Figure 2B. The local administration of Ex-4 impaired the ability of cocaine to increase extracellular DA levels. These studies were performed in slices in which only the local circuits are intact; therefore, we can assume that our observations were the result of local GLP-1R stimulation and not the result of feed-forward circuit-level changes. The slices were treated with 1 n m GLP-1 for 20 min. Indeed, 2-AG hydrolysis via monoacylglycerol lipase is the primary mechanism for free AA generation in the central nervous system. To this end, mice were injected with Ex-4 intraperitoneally 30 min prior to sacrifice, and the LS was punched and analyzed by mass spectrometry for 2-AG and free AA levels. Significant analysis of variance followed by post hoc tests. The PC12 cells contain vesicles capable of neurotransmitter release. Notably, psychostimulants are known to induce oxidative stress, 55 , 56 , 57 whereas GLP-1R signaling, which reduces AA levels, is known to reduce it. These results show that in the presence of AA, there is a significant reduction in DAT function under both oxidizing and non-oxidizing conditions. Notably, a greater loss of function was observed under oxidizing conditions, which also affects DAT's apparent affinity for DA Figure 3f. DAT plasma membrane trafficking is a key regulator of DA transport capacity. Our results indicate that in hDAT cells, AA, under both oxidative and non-oxidative conditions, decreases significantly and to the same extent plasma membrane DAT Figures 4a and b as determined by biotinylation. These data also point to additional mechanisms promoted in terms of DAT function by oxidative stress. Lipid rafts are regions highly enriched in phospholipids containing AA, and DAT localization to lipid rafts has been associated with regulation of DAT function and trafficking. In the presence of salicylamine, there were no significant changes in Vmax Figure 5g or Km Figure 5h when cells were treated with AA under non-oxidative or oxidative conditions with respect to the control condition. Importantly, our findings demonstrate that DAT is a target of AA oxidative products, and that this interaction has profound functional implications. Synthetic isoketals form adducts with human dopamine transporter hDAT and decrease its function. No significant differences were observed between the groups. The statistical analysis was performed with analysis of variance. AA, arachidonic acid; Veh, vehicle. Since the discovery that the LS is a potent site of electrical self-stimulation in both rodents and humans, 20 , 71 it has historically received relatively little attention as a reward center. Recent studies, however, suggest that it integrates output from traditional reward areas including the VTA and lateral hypothalamus. GLP-1Rs are highly expressed in the LS and their signaling has been shown to attenuate the locomotor response to the psychostimulant d -amphetamine, 1 to reduce cocaine CPP, 14 , 16 and to block self-administration for cocaine in rodents. Cocaine, by targeting the DAT, increases extracellular DA levels, which leads to cocaine's behavioral actions. DAT expression level is an important factor in determining the effects of cocaine, likely through effects on basal DA tone. For example, extended access to cocaine, which results in escalating cocaine intake, causes lower expression of striatal DAT and reduced DA clearance in rats. However, it is clear to us that other mechanisms in addition to DAT occupancy participate in the behavioral actions of cocaine. These kinds of mechanisms have been defined for other drugs of abuse, such as morphine, and may be contributing in parallel to altered cocaine reward. This increase translates into an increase in transport capacity, and is paralleled by reduced ability of cocaine to increase extracellular DA levels. Our data suggest that increasing the amount of DAT expressed at the cell surface may reduce the extent to which cocaine is effective at increasing extracellular DA within the LS. These data offer an additional mechanism for GLP-1R signaling regulation of the reinforcing and rewarding properties of cocaine without precluding the possibility that GLP-1R signaling may also affect DA release and firing properties of VTA neurons. Here we find that stimulating the GLP-1R through administration of Ex-4 in a therapeutically relevant manner systemic administration reduces septal 2-AG levels. Indeed, 2-AG diffuses across synapses. Of note, AA is known to facilitate a pro-inflammatory state in the brain; 86 GLP-1 analogs, on the other hand, possess both anti-inflammatory and neuroprotective effects. On the basis of our findings, GLP-1R signaling may oppose the effects of psychostimulants by affecting levels of AA as well as oxidative stress. We believe that the increase in DAT surface expression promoted by GLP-1R signaling represents a mechanism by which this neuropeptide controls both cocaine-induced increase in LS DA as well as cocaine actions. The treatment of hDAT cells with AA under conditions favoring lipid peroxidation significantly decreased DAT surface expression and transport capacity; the latter effect was also demonstrated with synthetic isoketals. These results are consistent with the known ability of isoketals to impair the function of plasma membrane proteins. However, this reduction was smaller than that obtained under conditions favoring lipid peroxidation or in the presence of isoketals. These results provide a mechanism for the results reported by Chen et al. However, we hypothesize that covalent interactions of AA metabolites with specific lysine residues on the DAT support these actions. This decrease is important as cocaine has been shown to increase 2-AG tone in the brain. These brain regions include the nucleus accumbens and VTA, which have been identified as targets of Ex-4 actions on brain reward. Our study points to septal GLP-1R as a potential novel target for the treatment of drug abuse. SP has an active research contract with Lundbeck Pharmaceuticals; however, the work presented in the manuscript was supported entirely by the grants named above and Vanderbilt University. The remaining authors declare no conflict of interest. Sci Rep , 14 1 , 18 Oct Cited by: 0 articles PMID: Int J Mol Sci , 25 5 , 05 Mar Front Psychiatry , , 29 Aug Jerlhag E. Front Pharmacol , , 30 Mar Exp Clin Psychopharmacol , 31 3 , 08 Dec This data has been provided by curated databases and other sources that have cited the article. To arrive at the top five similar articles we use a word-weighted algorithm to compare words from the Title and Abstract of each citation. Neurochem Int , , 25 May Physiol Behav , , 11 Jun Neuropsychopharmacology , 40 8 , 11 Feb Life Sci , 73 6 , 01 Jun Cited by: 31 articles PMID: Europe PMC requires Javascript to function effectively. Search life-sciences literature 44,, articles, preprints and more Search Advanced search. This website requires cookies, and the limited processing of your personal data in order to function. By using the site you are agreeing to this as outlined in our privacy notice and cookie policy. Reddy IA 1 ,. Pino JA 2, 8 ,. Weikop P 3 ,. Osses N 2 ,. Bering T 3 ,. Valle C 4 ,. Bluett RJ 1, 7 ,. Erreger K 5 ,. Wortwein G 3 ,. Reyes JG 2 ,. Graham D 6 ,. Stanwood GD 6 ,. Hackett TA 1 ,. Patel S 7 ,. Fink-Jensen A 3 ,. Torres GE 8 ,. Galli A 1, 5. Affiliations 1. Authors Valle C 4. Authors Erreger K 5 Galli A 1, 5. Share this article Share with email Share with twitter Share with linkedin Share with facebook. Abstract Agonism of the glucagon-like peptide 1 GLP-1 receptor GLP-1R has been effective at treating aspects of addictive behavior for a number of abused substances, including cocaine. Free full text. Transl Psychiatry. Published online May PMID: Author information Article notes Copyright and License information Disclaimer. E-mail: ude. This work is licensed under a Creative Commons Attribution 4. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. This article has been cited by other articles in PMC. Go to:. Supplementary Information. Drugs and materials The suppliers for all chemicals not otherwise identified can be found in the Supplementary Information. In vivo microdialysis in mice Microdialysis was performed as described previously 4 with few modifications. Immunoprecipitations Immunoprecipitations were performed using 1 mg total protein. Open in a separate window. Figure 1. Systemic administration of a GLP-1R agonist reduces cocaine-induced DA elevation and c-fos expression in the LS We next tested whether a therapeutically relevant administration that is, systemic administration of Ex-4 was capable of altering neuronal activity in the LS. Figure 2. Figure 3. Figure 4. Figure 5. Supplementary Information Click here for additional data file. Exendin-4 decreases amphetamine-induced locomotor activity. Physiol Behav ; : — Moving beyond energy homeostasis: new roles for glucagon-like peptide-1 in food and drug reward. Neurochem Int ; 73 : 49— Septal glucagon-like peptide 1 receptor expression determines suppression of cocaine-induced behavior. Neuropsychopharmacology ; 40 : — The glucagon-like peptide 1 GLP-1 receptor agonist exendin-4 reduces cocaine self-administration in mice. Gastroenterology ; : — GLP-1 neurons in the nucleus of the solitary tract project directly to the ventral tegmental area and nucleus accumbens to control for food intake. Endocrinology ; : — The incretin system: glucagon-like peptide-1 receptor agonists and dipeptidyl peptidase-4 inhibitors in type 2 diabetes. Lancet ; : — A randomized, controlled trial of 3. N Engl J Med ; : 11— Entry of exendin-4 into brain is rapid but may be limited at high doses. Distribution of pre-pro-glucagon and glucagon-like peptide-1 receptor messenger RNAs in the rat central nervous system. J Comp Neurol ; : — The glucagon-like peptide 1 GLP-1 analogue, exendin-4, decreases the rewarding value of food: a new role for mesolimbic GLP-1 receptors. J Neurosci ; 32 : — Gut peptide GLP-1 and its analogue, exendin-4, decrease alcohol intake and reward. PLoS One ; 8 : e The glucagon-like peptide 1 analogue exendin-4 attenuates the nicotine-induced locomotor stimulation, accumbal dopamine release, conditioned place preference as well as the expression of locomotor sensitization in mice. The glucagon-like peptide 1 analogue, exendin-4, attenuates the rewarding properties of psychostimulant drugs in mice. The glucagon-like peptide 1 analogue Exendin-4 attenuates alcohol mediated behaviors in rodents. Psychoneuroendocrinology ; 38 : — GLP-1 analog attenuates cocaine reward. Mol Psychiatry ; 18 : — The glucagon-like peptide-1 receptor as a potential treatment target in alcohol use disorder: evidence from human genetic association studies and a mouse model of alcohol dependence. Transl Psychiatry ; 5 : e How can drug addiction help us understand obesity? Nat Neurosci ; 8 : — What is the role of dopamine in reward: hedonic impact, reward learning, or incentive salience? Brain Res Brain Res Rev ; 28 : — Positive reinforcement produced by electrical stimulation of septal area and other regions of rat brain. J Comp Physiol Psychol ; 47 : — Regulation of affect by the lateral septum: implications for neuropsychiatry. Brain Res Brain Res Rev ; 46 : 71— Linking context with reward: a functional circuit from hippocampal CA3 to ventral tegmental area. Science ; : — A septal-hypothalamic pathway drives orexin neurons, which is necessary for conditioned cocaine preference. J Neurosci ; 35 : — Neuropeptide Y Y5 receptor antagonism attenuates cocaine-induced effects in mice. Psychopharmacology Berl ; : — The Mouse Brain in Stereotaxic Coordinates. J Neurosci Methods ; : 59— Insulin reveals Akt signaling as a novel regulator of norepinephrine transporter trafficking and norepinephrine homeostasis. J Neurosci ; 30 : — Genetic disruption of 2-arachidonoylglycerol synthesis reveals a key role for endocannabinoid signaling in anxiety modulation. Cell Rep ; 9 : — Ligand-induced internalization of the p75 neurotrophin receptor: a slow route to the signaling endosome. J Neurosci ; 23 : — Physical and functional interaction between the dopamine transporter and the synaptic vesicle protein synaptogyrin J Neurosci ; 29 : — The dopamine transporter: immunochemical characterization and localization in brain. J Neurosci ; 15 3 Pt 1 : — The dopamine hypothesis of the reinforcing properties of cocaine. Trends Neurosci ; 14 : — Abolished cocaine reward in mice with a cocaine-insensitive dopamine transporter. Hyperlocomotion and indifference to cocaine and amphetamine in mice lacking the dopamine transporter. Nature ; : — Impaired striatal Akt signaling disrupts dopamine homeostasis and increases feeding. PLoS One ; 6 : 1— Hypoinsulinemia regulates amphetamine-induced reverse transport of dopamine. PLoS Biol ; 5 : — Rescue of dopamine transporter function in hypoinsulinemic rats by a D2 receptor-ERK-dependent mechanism. Rapid regulation of dopamine transporter function by substrates, blockers and presynaptic receptor ligands. Eur J Pharmacol ; : — Rapid regulation of the dopamine transporter: role in stimulant addiction? Neuropharmacology ; 47 : 80— Mice expressing markedly reduced striatal dopamine transporters exhibit increased locomotor activity, dopamine uptake turnover rate, and cocaine responsiveness. Synapse ; 67 : — Cocaine reward and locomotion stimulation in mice with reduced dopamine transporter expression. BMC Neurosci ; 8 : Exendin-4 is a high potency agonist and truncated exendin- -amide an antagonist at the glucagon-like peptide 1- -amide receptor of insulin-secreting beta-cells. J Biol Chem ; : — Reduced neural response to reward following 7 days treatment with the cannabinoid CB1 antagonist rimonabant in healthy volunteers. Int J Neuropsychopharmacol ; 13 : — Insulin induces long-term depression of ventral tegmental area dopamine neurons via endocannabinoids. Nat Neurosci ; 16 : — Endocannabinoid signalling in reward and addiction. Nat Rev Neurosci ; 16 : — Brain cannabinoid CB 2 receptors modulate cocaine's actions in mice. Nat Neurosci ; 14 : — Cannabinoid CB1 receptor antagonists attenuate cocaine's rewarding effects: experiments with self-administration and brain-stimulation reward in rats. Neuropsychopharmacology ; 33 : — Endocannabinoid hydrolysis generates brain prostaglandins that promote neuroinflammation. Effects of arachidonic acid on dopamine synthesis, spontaneous release, and uptake in striatal synaptosomes from the rat. J Neurochem ; 64 : — Inhibition by arachidonic acid and other fatty acids of dopamine uptake at the human dopamine transporter. Eur J Pharmacol ; : 89— Regulation of the functional activity of the human dopamine transporter by the arachidonic acid pathway. The PC12 cell as model for neurosecretion. Acta Physiol Oxf ; : — Role of oxidative metabolites of cocaine in toxicity and addiction: oxidative stress and electron transfer. Med Hypotheses ; 64 : — Cocaine-induced oxidative stress precedes cell death in human neuronal progenitor cells. Neurochem Int ; 50 : 69— Oxidative stress in psychiatric disorders: evidence base and therapeutic implications. Int J Neuropsychopharmacol ; 11 : — Exendin-4, a glucagon-like peptide-1 receptor agonist, provides neuroprotection in mice transient focal cerebral ischemia. J Cereb Blood Flow Metab ; 31 : — Identification of extremely reactive gamma-ketoaldehydes isolevuglandins as products of the isoprostane pathway and characterization of their lysyl protein adducts. Nat Protoc ; 2 : — Isoketals: highly reactive gamma-ketoaldehydes formed from the H2-isoprostane pathway. Chem Phys Lipids ; : 85— Pyridoxamine analogues scavenge lipid-derived gamma-ketoaldehydes and protect against H2O2-mediated cytotoxicity. Biochemistry ; 45 : — Neurochem Int ; 33 : — Peroxynitrite inactivates the human dopamine transporter by modification of cysteine potential mechanism of neurotoxicity in dopamine neurons. J Neurosci ; 22 : — Hydrogen peroxide induces loss of dopamine transporter activity: a calcium-dependent oxidative mechanism. J Neurochem ; 86 : — A closer look at amphetamine-induced reverse transport and trafficking of the dopamine and norepinephrine transporters. Mol Neurobiol ; 39 : 73— Dynamic regulation of the dopamine transporter. Biochemistry ; 41 : — Dopamine transporter endocytic trafficking in striatal dopaminergic neurons: differential dependence on dynamin and the actin cytoskeleton. J Neurosci ; 33 : — Electrical self-stimulation of the brain in man. Am J Psychiatry ; : — Brain stimulation reward and dopamine terminal fields. Septal and cortical projections. Brain Res ; : — On lateral septum-like characteristics of outputs from the accumbal hedonic 'hotspot' of Pecina and Berridge with commentary on the transitional nature of basal forebrain 'boundaries'. J Comp Neurol ; : 50— Transition from moderate to excessive drug intake: change in hedonic set point. Extended access of cocaine self-administration results in tolerance to the dopamine-elevating and locomotor-stimulating effects of cocaine. J Neurochem ; : — Cocaine self-administration produces pharmacodynamic tolerance: differential effects on the potency of dopamine transporter blockers, releasers, and methylphenidate. Neuropsychopharmacology ; 37 : — Methylphenidate and cocaine self-administration produce distinct dopamine terminal alterations. Addict Biol ; 19 : — A single amphetamine infusion reverses deficits in dopamine nerve-terminal function caused by a history of cocaine self-administration. Substrates and inhibitors display different sensitivity to expression level of the dopamine transporter in heterologously expressing cells. Relationship between subjective effects of cocaine and dopamine transporter occupancy. Role for mTOR signaling and neuronal activity in morphine-induced adaptations in ventral tegmental area dopamine neurons. Neuron ; 72 : — The glucagon-like peptides: a double-edged therapeutic sword? Trends Pharmacol Sci ; 24 : — Cyclic AMP-mediated pleiotropic effects of glucagon-like peptide-1 receptor activation. Focus on 'Exendin-4 attenuates high glucose-induced cardiomyocyte apoptosis via inhibition of endoplasmic reticulum stress and activation of SERCA2a'. The role of endocannabinoid signaling in motor control. Physiology Bethesda ; 25 : — D-Amphetamine stimulates D2 dopamine receptor-mediated brain signaling involving arachidonic acid in unanesthetized rats. J Cereb Blood Flow Metab ; 26 : — Modulation of inflammation in brain: a matter of fat. Impairment of synaptic plasticity and memory formation in GLP-1 receptor KO mice: Interaction between type 2 diabetes and Alzheimer's disease. Behav Brain Res ; : — Central effects of GLP new opportunities for treatments of neurodegenerative diseases. J Endocrinol ; : T31—T New roles for insulin-like hormones in neuronal signalling and protection: new hopes for novel treatments of Alzheimer's disease? Neurobiol Aging ; 31 : — Glucagon-like peptide 1 receptor stimulation reverses key deficits in distinct rodent models of Parkinson's disease. J Neuroinflammation ; 5 : Modification of proteins by isoketal-containing oxidized phospholipids. Cocaine self-administration differentially modulates the expression of endogenous cannabinoid system-related proteins in the hippocampus of Lewis vs. Fischer rats. Int J Neuropsychopharmacol ; 16 : — J Neurosci ; 34 : — Smart citations by scite. The number of the statements may be higher than the number of citations provided by EuropePMC if one paper cites another multiple times or lower if scite has not yet processed some of the citing articles. Explore citation contexts and check if this article has been supported or disputed. The risk of depression, anxiety, and suicidal behavior in patients with obesity on glucagon like peptide-1 receptor agonist therapy. Case Report: Semaglutide-associated depression: a report of two cases. The therapeutic potential of glucagon-like peptide-1 for persons with addictions based on findings from preclinical and clinical studies. Glucagon-like peptide-1 receptors in nucleus accumbens, ventral hippocampus, and lateral septum reduce alcohol reinforcement in mice. Data Data that cites the article This data has been provided by curated databases and other sources that have cited the article. Proteins in UniProt 8. Similar Articles To arrive at the top five similar articles we use a word-weighted algorithm to compare words from the Title and Abstract of each citation. Glucagon-like peptide-1 receptor regulation of basal dopamine transporter activity is species-dependent. Substance P and cholecystokinin regulate neurochemical responses to cocaine and methamphetamine in the striatum. Funding Funders who supported this work. External link. Please review our privacy policy.

Genomic and structural basis for evolution of tropane alkaloid biosynthesis

How can I buy cocaine online in Vina del Mar

Eating attitudes and their relation with drug consumption in a university sample. Manuel Herrero, Ph. Background and Objectives: Some relations between abnormal eating behaviours and attitudes, and other psychiatric disorders have been found in different populations. This study was carried out to examine the relations between eating attitudes and substance use among university students from Spain. Methods: The EAT and a substance use questionnaire were administered to a sample of 1, male and female university students in a cross-sectional design. Results: There were significant differences in drug consumption between students that met cut-off score criteria for the 40 and item versions, and those that did not. Significant differences also emerged between extreme groups 25 vs. A clearly distinct pattern of differences appeared in male and female students. Conclusions: Outcomes are in consonance with the theories proposed by several authors to explain the etiological relation between eating disorders and substance use. High co-morbidity rates between abnormal eating behaviours and attitudes, and other psychological disorders are commonly found in the literature. Anxiety and mood disorders, personality disorders, and substance use and abuse disorders are conspicuous amongst these Regarding substance use, co-morbidity with eating disorders EDs have been reported by several authors These outcomes have also been found in general population studies which selected persons who met DSM diagnostic criteria for eating disorders , and in studies using both of these populations, plus a normal student comparison group To investigate this relation this research team previously carried out a pilot study with university students Significant correlations between abnormal eating behaviours and attitudes EAT and substance use were not found. Nevertheless, there were significant differences between extreme groups 25 vs. In the present study, the sample has been enlarged in order to check the results obtained in the pilot study. The ages ranged from 17 to 45 years old, with a mean of Instruments: Two questionnaires were used in this study. The first instrument, the EAT, contains forty items that are rated on a scale ranging from 0 never to 5 always. These items measure behaviours, feelings and thoughts associated with eating disorders. This questionnaire has been factorized by different authors 27, In this work the factor solution obtained in 30 has been used. This instrument has a short version, the EAT, 28 which is composed by twenty six items selected from the original version EAT The authors of the short version obtained three empirical factors: Dieting, Bulimia and Food Preoccupation, and Oral Control. Both versions of the test have shown adequate levels of validity and reliability 30, In this study the two versions of the EAT have been used for several reasons. From the clinical standpoint, it has been stated 36 that is more relevant the score of the subscales separately that the global score of an inventory and, as each version of the EAT has different subscales, is advisable to use both. In addition, since both versions have different factor solutions, we were interested in checking on the relative importance of each one of the subscales when the time comes to detect differences in the use of substances and, especially, if the subscale more related to bulimia Bulimia and Food Preoccupation of the EAT was the one that caused the greater differences. In our pilot study 26 we also saw that, depending on which version of the EAT was used to form the extreme groups, significant differences in different variables arose from substance consumption. Another important reason to report the results with the two versions of the questionnaire is that it allows to compare these results with other studies that use anyone of them, since science is based, to a great extent, in the accumulation and comparison of data. The second instrument has been used 29 in a wide epidemiological study in Madrid Spain , and is composed of four items that briefly trace the recency and ways of use of some of the most used drugs in the population. The first item inquires whether the student has taken or not at least one alcoholic drink in the last month. The second asks at what age the person began to consume alcohol weekly. The fourth question explores the recency of consumption of different substances: tranquilizers without medical prescription, cannabis, cocaine, heroin, amphetamines, and any other drugs not included in this list. This question is rated on the following scale: 0 never ; 1 any time in your life ; 2 any time in the last year ; and 3 any time in the last month. Procedure: Instruments were administered collectively during class hours and were completed voluntarily. Issues regarding anonymity and confidentiality were assured. Participants did not receive any type of incentive for their participation in the study. Only two of the approached people refused to participate. Statistical analysis: Pearson correlations were used to analyze the relation between EAT and consumption variables. Pearson correlations between EAT scales and subscales scores, and the different drugs were calculated, and no correlation emerged with statistical significance. Nevertheless, as in the pilot study mentioned above, it was checked whether there were significant differences in substance consumption between the groups with extreme scores in both EAT versions and their subscales, and between those formed by the cut-off scores criteria. We are going to present separately the male and female subsamples since the epidemiological data 1 clearly indicate that the prevalence of EDs is much higher in the case of women. The results for women can be seen in Tables 1 and 2 only substances with significant differences between groups are shown. As can be seen in Table 2 , the significant differences arise between extreme groups of the two versions of the EAT 40 and 26 items in the age of onset of weekly alcohol consumption women at 75 percentile start before , and in the recency of consumption of tranquilizers without medical prescription, cocaine and amphetamines this variable only in the EAT , with higher recency of consumption in women at percentile 75 the direction of all the differences that will be commented below is the same. As to subscales, it can be seen that, in general, the EAT subscales yield a smaller number of significant differences than the EAT subscales. In the former there are significant differences between extreme groups of Perceived Social Pressure and Eating Distress onset age of alcohol consumption and tranquilizers recency , and of Psychobiological Disorders cocaine. Regarding the shortened version of the EAT, there are significant differences between extreme groups of the three subscales. One significant difference tranquilizers emerges in Dieting. In the Bulimia and Food Preoccupation subscale there are five significant differences: more than cigarettes smoked in life, age of onset of weekly alcohol consumption; and consumption recency of cocaine, amphetamines, and other drugs. Finally, in Oral Control there are two significant differences between extreme groups: age of onset of weekly alcohol consumption and tranquilizers. With regard to the cut-off scores of both versions of the EAT, significant differences appear between women who meet the cut-off score criteria and those who do not. These differences arise in age of onset of alcohol consumption at least once per week; and in recency of consumption of tranquilizers and cocaine. The differences found in men are not presented in a table as there were only four differences between groups. As can be seen in these results, only in this last variable, does the group with the highest scores present a more recent consumption. In the other three, the differences are in the opposite direction. In this study, the correlations between eating attitudes and drug consumption pointed out by authors mentioned above have not been found. This outcome may be due to the fact that here a university sample was used, while the other studies used patients or, when general population was studied, individuals who met DSM diagnostic criteria for EDs were selected. Nevertheless, when EAT highest and lowest score groups were compared, significant differences emerged in a similar way as in the pilot study However, in this study, there were significant differences between extreme groups not only in the whole scores of both versions EAT and EAT and in the Bulimia and Food Preoccupation subscale, but in all the subscales. Besides, as it has been seen, significant differences appeared between women who met the cut-off score criteria and those who did not, in three consumption variables onset age of alcohol consumption, tranquilizers and cocaine recency. Moreover, these differences were almost the same as those found between extreme groups 25 vs. The number of variables with significant differences increased when the extreme groups of the Bulimia and Food Preoccupation subscale were compared. This result agrees with the findings indicated in the introduction to this study, that emphasize the association of psychoactive substance consumption with bulimic behaviours, and can be explained by the theory that alludes to the impulsivity features shared by both kinds of disorder 5,10,15,39, As to the consumption variables, those that presented a higher number of significant differences were: age of onset of weekly alcohol consumption, and the recency of consumption of cocaine, amphetamines and tranquilizers. According to some of the authors previously mentioned 5 , the higher lever of cocaine and amphetamines consumption would be explained by the developmental perspective which posits that individuals consume these substances with the aim of achieving and maintaining a shape and weight adjusted to social standards. On the other hand, the self-medication theory suggests that individuals with EDs use substances in order to cope with eating problems and the preoccupation that these cause. This could explain the higher recency in the use of tranquilizers without medical prescription, and the earlier onset of alcohol consumption, all of these in the group of women with the highest scores in the EAT. The number of significant differences found in men was clearly lower, and three out of four of these were in the opposite direction to those found in women. On the one hand, this result fits with the gender differences repeatedly found in the literature On the other hand, this result could be explained arguing that, perhaps, in men the cause of substance consumption is more social and, therefore, of a less ED-associated symptomatology. In general, the findings of this study obtained with self-report instruments in a university sample are in a similar direction to those obtained with clinical samples, and could be useful for further exploration of the causal factors common to both substance use and eating disorders, one of these being the impulsivity factor. Nevertheless, as it has been asserted 5 , assessment instruments such as semi-structured interviews could be useful for more focused empirical investigations aimed at clarifying the etiological relation between eating disorders and substance use. However, much further research will be required before this question is completely clarified, and, as other authors have recently asserted 46 , drug abuse in people with eating disorders is an area of clinical concern that should be monitored routinely. This relation is so important that it has been proposed 47 a model of treatment that focus on ways in which therapists can address co-existing eating disorders and drug problems. Regarding the limitations of the present study, we can mention that from this type of studies conclusions cannot be extracted about the causal direction of the observed relations. One cannot talk about the possible evolution of the people with this type of anomalous behaviours and attitudes substance consumption and eating either, as this study is a cross-sectional and no longitudinal one. We also have to mention that the used sample has not been obtained by a procedure of stratified random sampling, although we have to indicate that the sample 1, people is important in relation to the total studied population 3,20, American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. Text Revised. Washington, D. Pshychiatric comorbidities of female inpatients with eating disorders. Psychosom Med ; Bulik CM. Anxiety, depression, and eating disorders. Eating disorders and obesity. New York: Guilford; Levels of cigarette and alcohol use related to eating-disorder attitudes. Am J Health Behav ; 26 1 : The relationship between eating disorders and substance use Moving beyond co-prevalence research. Clin Psychol Rev ; 20 5 : Wonderlich SA. Personality and eating disorders. Eating disorders and comorbidity: Empirical, conceptual, and clinical implications. Psychopharmacol Bull ; 33 3 : Int J Eat Disord ; 28 1 : In: Flament M, Jeammet P, editors. La boulimie. Paris: Masson; Lifetime comorbidity of alcohol dependence in women with bulimia nervosa. Addict Behav ; Treatment dropout in drug-addicted women: Are eating disorders implicated? Eat Weight Disord ; 13 2 : Psychoactive substance consumption in eating disorders. Eat Behav ; 2 1 : Cigarrette smoking and its relationship to other substance use among eating disordered inpatients. Eat Weight Disord ; 6: Drug abuse in women with eating disorders. Int J Eat Disord ; 39 5 : Co-morbidity of eating disorders and substance abuse review of the literature. Int J Eat Disord ; 16 1 : Eating disorders in female substance use disorders: A preliminary research on the relationship of substances and eating behaviors. Seishin Igaku Clinical Psychiatry ; 45 2 : Eating disorders in a national sample of hospitalized female and male veterans: Detection rates and psychiatric comorbidity. Int J Eat Disord ; Wiederman MW, Pryor T. Substance use among women with eating disorders. Int J Eat Disord ; 20 2 : Comorbidity of bulimia nervosa and alcohol use disorders: Results from the National Women's Study. Int J Eat Disord ; 27 2 : Self-harm and substance use in a community sample of black and white women with binge eating disorder or bulimia nervosa. Int J Eat Disord ; 32 4 : Alcohol and drug-related negative consequences in college students with bulimia nervosa and binge eating disorder. Int J Eat Disord ; 32 2 : Purging and non purging forms of bulimia nervosa in a community sample. Int J Eat Disord ; 20 3 : Present and lifetime comorbidity of tobacco, alcohol and drug use in eating disorders: A European multicenter study. Drug Alcohol Depen ; 97 : Substance use in female adolescent with eating disorders. J Adol Health ; 31 2 : Life adjustment of women with anorexia nervosa and anorexic-like behaviour. Int J Eat Disord ; 1: The Eating Attitudes Test: An index of the symptoms of anorexia nervosa. Psychological Medicine ; 9: The Eating Attitudes Test: Psychometric features and clinical correlates. Psychol Med ; Gandarillas A, Febrel C. Psychol Assess ; 7 2 : Eisler I, Szmukler GI. Social class as a confounding variable in the Eating Attitudes Test. J Psychiat Res ; The factor structure of the Eating Attitudes Test with adolescent schoolgirls. Gross J, Rosen JC. Bulimia in adolescents: Prevalence and psychosocial correlates. Int J Eat Disord ; 7: Rosen JC, Srebnick D. Assessment of eating disorders. Advances in Psychological Assessment. New York: Plenum Press; Vol 7; p. Barcelona: Masson; Management of substance abuse and dependence. Handbook of treatment for eating disorders. New York: The Guilford Press; Adolescents in engaging in unhealthy weight control behaviors: Are they at risk for other health compromising behaviors? Am J Public Health ; The relationship of dieting severity and bulimic behaviors to alcohol and other drug use in young women. J Subst Abuse ; 4: Bulimia nervosa with and without alcoholism a comparative study in Japan. Eating attitudes in college males. Int J Eat Disord ; 7 2 : An epidemiologic study of maladaptated eating attitudes in a Canadian school age population. Int J Eat Disord ; 5: Eating disorder symptoms among adolescents in the United States and Spain: A comparative study. Int J Eat Disord ; 11 1 : J Consult Clin Psychol ; 56 2 : Behavioral and psychological implications of body image dissatisfaction: Do men and women differ? Sex Roles ; Interactions between eating disorders and drug abuse. J Nerv Ment Dis ; 7 : Eating disorders and drug and alcohol problems. In: Baker A, Velleman R, editors. Clinical handbook of co-existing mental health and drug and alcohol problems. Florence K : Routledge; Servicios Personalizados Revista. Eating attitudes and their relation with drug consumption in a university sample Manuel Herrero, Ph. Introduction High co-morbidity rates between abnormal eating behaviours and attitudes, and other psychological disorders are commonly found in the literature. Results Pearson correlations between EAT scales and subscales scores, and the different drugs were calculated, and no correlation emerged with statistical significance. Discussion In this study, the correlations between eating attitudes and drug consumption pointed out by authors mentioned above have not been found. References 1.

How can I buy cocaine online in Vina del Mar