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Fourteen people were arrested by the anti-drug squad and Rapid Intervention Unit throughout the weekend. Those arrested, all men aged between 18 and 40 years of age, were in possession of suspected heroin, cocaine, ecstasy and cannabis. The suspects were arrested during a routine of searches in a number of localities, includinf St. Two of the men are expected to be arraigned in court later today, with one of the suspects in question found in possession of around ecstasy pills, and the other who resisted arrest. Fourteen arrested for drug possession Fourteen people, aged between 18 and 40 were arrested for drug possession. More from Staff Reporter. By using this site, you agree to our Privacy Policy including the use of cookies to enhance your experience.

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Official websites use. Share sensitive information only on official, secure websites. This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author s and source are credited. Recently we demonstrated that genetic or pharmacological suppression of the central ghrelin signaling system, involving the growth hormone secretagogue receptor 1A GHS-R1A , lead to a reduced reward profile from alcohol. As the target circuits for ghrelin in the brain include a mesolimbic reward pathway that is intimately associated with reward-seeking behaviour, we sought to determine whether the central ghrelin signaling system is required for reward from drugs of abuse other than alcohol, namely cocaine or amphetamine. We found that amphetamine—as well as cocaine-induced locomotor stimulation and accumbal dopamine release were reduced in mice treated with a GHS-R1A antagonist. Moreover, the ability of these drugs to condition a place preference was also attenuated by the GHS-R1A antagonist. Thus GHS-R1A appears to be required not only for alcohol-induced reward, but also for reward induced by psychostimulant drugs. Our data suggest that the central ghrelin signaling system constitutes a novel potential target for treatment of addictive behaviours such as drug dependence. Since its discovery in Kojima et al. It seems clear that ghrelin exerts its orexigenic and pro-obesity effects by interacting with discrete hypothalamic cell groups that include leptin-responsive circuits in the arcuate nucleus, such as the neuropeptide Y cell group Dickson and Luckman ; Hewson et al. Recently, however, we and others have reported that ghrelin also activates key CNS pathways involved in reward, that include the mesolimbic dopamine system Abizaid et al. By this route, ghrelin may increase the incentive value of both natural and artificial rewards and hence, increase reward-seeking behavior. The emerging neurobiology of central ghrelin signaling system indicates that it may serve as a common denominator to enhance search for rewards such as drugs of abuse and rewarding foods. This is evidenced, in part, by human function imaging studies in which ghrelin was shown to alter the brain response to visual food cues, most markedly in the ventral striatum, an area also activated by psychostimulant drugs see e. Wise and Bozarth ; Malik et al. In rodents, ghrelin has been shown to increase foraging for food Keen-Rhinehart and Bartness , to enhance cocaine-induced locomotor stimulation, to condition a place preference for cocaine, and to induce cocaine-seeking behaviors Wellman et al. Recently, we demonstrated that central ghrelin signaling system is required for alcohol reward; we found that the ability of alcohol to increase locomotor activity, to induce accumbal dopamine release, and to condition a place preference were abolished in ghrelin receptor growth hormone secretagogue receptor 1A GHS-R1A in knockout mice and also in mice treated with two different GHS-R1A antagonists Jerlhag et al. In the present study, such tests were also used to determine whether the central ghrelin signaling system is required for the rewarding properties of cocaine and amphetamine in mice treated peripherally with a GHS-R1A antagonist. Tap water and food Normal chow; Harlan Teklad; Norfolk, England were supplied ad libitum, except during the experimental setups. Similar doses have been used previously to induce an activation of the mesolimbic dopamine system, as measured by locomotor activity and accumbal dopamine release in rats Wise and Bozarth Jerlhag et al. This dose was used in all studies and was always administered 10 min prior to drug exposure. Indeed, it has been established that this compound, when administered peripherally, is a GHS-R1A antagonist and suppresses food intake induced by ghrelin or by the GHS-R1A agonist, hexarelin Moulin et al. JMV was dissolved in vehicle 0. All drug challenges were part of a balanced design with regard to both the treatment order and the number of subjects per treatment. For all drug challenges, 0. Amphetamine- or cocaine-induced locomotor stimulation was measured as most drugs of abuse cause locomotor stimulation, an effect mediated, at least in part, by their ability to enhance the extracellular concentration of accumbal dopamine Engel et al. Such parameters have been suggested to be homologous effects evolving from a common mechanism involving the dopaminergic reward system, implying that these parameters reflect reward induced by drugs of abuse Engel et al. It should, however, be emphasized that several other neurostransmitter systems may mediate drug-induced locomotor stimulation Engel et al. Whereas CPP-testing demonstrates drug-induced reward more directly, locomotor stimulation provides an indirect, yet supportive measure. Locomotor activity was recorded as described previously Jerlhag et al. Five by five rows of photocell beams, at the floor level of the box, creating photocell detection allowed a computer-based system to register the activity of the mice. Locomotor activity was defined as the accumulated number of new photocell beams interrupted during a min period. Mice were allowed to habituate to the locomotor activity box 1 h prior to drug challenge. In separate experiments, the effects of the i. Neither water nor food was available to the mice during the locomotor experiments. The activity registration started 5 min after the last injection and was subsequently measured for a min period. For measurements of extracellular dopamine levels that reflect dopamine release , mice were implanted unilaterally with a microdialysis probe positioned in the nucleus accumbens NAcc. The surgery was performed as described thoroughly elsewhere Jerlhag et al. The scull bone was exposed and one hole for the probe and one for the anchoring screw were drilled. The probe was randomly alternated to either the left or right side. The coordinates for NAcc were 1. All probes were surgically implanted 2 days prior to the experiment. After surgery, the mice were kept in individual cages Macrolon III. In separate experiments, the effects of JMV i. After 1 h of habituation to the microdialysis set-up, perfusion samples were collected every 20 min. After the baseline samples, mice were injected with JMV i. The dopamine levels in the dialysates were determined by HPLC with electrochemical detection. The mobile phase pH 5. The mobile phase was delivered at a flow rate of 0. After the completion of the microdialysis experiments, the locations of the probe were verified Jerlhag et al. Only mice with probe placement in the NAcc were included in the statistical analysis. After the microdialysis experiments were completed, the location of the probe was verified. The mice were decapitated, probes were perfused with pontamine sky blue 6BX to facilitate probe localization, and the brains were mounted on a vibroslice device M Vibroslice; Campden Instruments Ltd. One compartment was defined by black- and white-striped walls and by a dark laminated floor, whereas the other had a white unlaminated floor and walls of wooden texture. Compartments were illuminated by 45 lux. The procedure consisted of pre-conditioning day 1 , conditioning days 2—5 , and post-conditioning day 6. On day 1 pre-conditioning , mice were i. Conditioning 20 min per session was done using a biased procedure in which amphetamine or cocaine was paired to the least preferred compartment. In this biased procedure, it should be more difficult to obtain a positive CPP response. The mice received a total of two i. After drug injection, the mice were placed in the appropriate compartment. On day 6, the mice were placed between the two compartments and were thereafter given free access to both compartments for 20 min. Prior to this test session, the mice were acutely injected with JMV i. As animals that receive vehicle in both compartments are not drug-conditioned, and, therefore, have no drug-induced CPP response to block using an antagonist, such experiments were not conducted. CPP was calculated as the difference in percentage of total time spent in the drug-paired i. All locomotor activity data were evaluated by a two-way ANOVA followed by Bonferroni post-hoc tests comparing treatments. The microdialysis experiments were evaluated by a two-way ANOVA followed by Bonferroni post-hoc test for comparisons between different treatments and specifically at given time points. As expected, amphetamine increased locomotor activity, accumbal dopamine release, and induced a CPP. All of these effects of amphetamine were attenuated by peripheral administration of JMV Figs. Even though JMV does not completely block the amphetamine-induced dopamine release, this increase fails to reach statistical significance compared to vehicle treatment. Suppressed ghrelin signaling by ghrelin receptor GHS-R1A antagonist JMV attenuates amphetamine, and cocaine-induced locomotor stimulation and accumbal dopamine release. Even though JMV does not completely block the amphetamine-induced accumbal dopamine release, this increase fails to reach statistical significance compared to vehicle treatment. Even though JMV does not completely block the cocaine-induced accumbal dopamine release, this increase fails to reach statistical significance compared to vehicle treatment. In studies parallel to those described for amphetamine, we found that JMV also suppressed the effect of the powerful psychostimulant drug cocaine on activation of the mesolimbic dopamine system Figs. Even though JMV does not completely block cocaine-induced accumbal dopamine release, this increase failed to reach statistical significance compared to vehicle treatment. Control experiments showed that neither i. After the experiment, the location of the probe was verified and only mice with probe placement in the NAcc were included in the statistical analysis. It should be emphasized that in a few mice, the probe was located outside the NAcc shell, and in these mice, no effect of amphetamine or cocaine on accumbal dopamine release was observed data not shown. Given that only amphetamine and cocaine increase accumbal dopamine compared to vehicle, it appears less likely that the probes causes structural defects within the NAcc that may influence the possibility to detect dopamine release. Verification of probe placement. A coronal mouse brain section showing ten representative probe placements vertical lines in the NAcc of mice used in the present study Franklin and Paxinos Ten representative placements are illustrated, but all other placements were within the NAcc shell. Placements outside this area were not included in the statistical analysis. The present study demonstrates that the ghrelin signaling system, involving GHS-R1A, is required for indirect measures of the rewarding properties of the psychostimulant drugs, amphetamine and cocaine. Hence, we found that the ability of these drugs to induce locomotor stimulation, accumbal dopamine release, and to condition a place preference is reduced in mice treated peripherally with a GHS-R1A antagonist. These effects of drugs of abuse, considered to constitute part of the addiction process, are intimately associated with its reinforcing properties Wise and Bozarth The GHS-R1A was administered peripherally in the present study, but it seems likely that it gains access to the CNS and acts at the level of the mesolimbic dopamine system Jerlhag et al. Taken together with our recent studies showing that the central ghrelin signaling system is required for alcohol- induced locomotor stimulation, accumbal dopamine release, and CPP Jerlhag et al. Supporting a role of ghrelin signaling in drug reinforcement are data demonstrating that food restriction, a state which is associated with elevated ghrelin levels, augments cocaine, as well as amphetamine-induced locomotor stimulation facilitates the acquisition of cocaine-seeking behavior and enhances self-administration of cocaine or amphetamine in rats Carroll et al. However, a role of stress should not be excluded. Moreover, in rats, an elevated plasma level of ghrelin enhances cocaine-seeking and augments cocaine-induced reward, assessed by locomotor stimulation, as well as CPP testing Wellman et al. Neurotransmitters in areas such as the NAcc and the ventral tegmental area VTA collectively regulate this activation Samson et al. Here it was shown that GHS-R1A, possibly at the level of the mesolimbic dopamine system, mediates the stimulatory, dopamine releasing, and CPP properties of psychostimulant drugs. By this route, GHS-R1A may modulate the ability and sensitivity of the mesolimbic dopamine neurons to be activated by psychostimulant drugs. The possibility that GHS-R1A influences the synthesis and release of dopamine should also be considered. In the NAcc, the dopamine released by amphetamine and cocaine activates dopamine receptors, and it should therefore be considered that the GHS-R1A antagonist attenuates psychostimulant-induced reinforcement by inhibiting the dopamine receptors in the NAcc. GHS-R1A in the NAcc may also be of importance for psychostimulant-induced locomotor stimulation, dopamine release, and CPP even though they do not appear to regulate alcohol consumption Schneider et al. The possibility remains, however, that downstream mechanisms independent of the mesolimbic dopamine system also may have important roles for the rewarding properties of cocaine and amphetamine. Our collective findings regarding the role of the central ghrelin signaling system, including the GHS-R1A, in alcohol Jerlhag et al. Furthermore, one study has demonstrated that a single-nucleotide polymorphism in the GHS-R1A gene is associated with high alcohol consumption Landgren et al. Collectively, these findings rise important questions regarding the physiological role of ghrelin influencing not only food intake and appetite, but also clearly having a broader role in reward induced by addictive drugs such as alcohol, amphetamine, and cocaine. Our data suggest that the central ghrelin signaling system, including the GHS-R1A, constitutes a novel potential target for treatment of addictive behaviors such as drug dependence. The authors are grateful for the excellent help of Mrs. Gun Andersson and Mr. Kenn Johannessen. Jean Martinez and Dr. As a library, NLM provides access to scientific literature. Psychopharmacology Berl. Ghrelin receptor antagonism attenuates cocaine- and amphetamine-induced locomotor stimulation, accumbal dopamine release, and conditioned place preference Elisabet Jerlhag Elisabet Jerlhag 1 Section for Pharmacology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, SE 30 Gothenburg, Sweden. Find articles by Elisabet Jerlhag. Find articles by Emil Egecioglu. Find articles by Suzanne L Dickson. Received Dec 22; Accepted Jun 3; Issue date Open in a new tab. Similar articles. Add to Collections. Create a new collection. Add to an existing collection. Choose a collection Unable to load your collection due to an error Please try again. Add Cancel.

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