Journal of reward deficiency syndrome and addiction science最新文献

{"title":"Reward Deficiency Syndrome Solution Focused Brief Therapy to Begin Integrating the Sciences of Addiction & Reward Deficiency Syndrome (RDS)","authors":"E. Gilley","doi":"10.17756/jrdsas.2019-042","DOIUrl":"https://doi.org/10.17756/jrdsas.2019-042","url":null,"abstract":"Reward Deficiency Syndrome Solution Focused Brief Therapy (RDSSFBT), provided in both individual and group therapy formats, in the practice of Addiction Recovery Treatment, will help the client understand the importance of the challenge to achieve dopamine homeostasis in the recovery process. RDSSFBT introduces new Reward Deficiency Syndrome concepts and solutions to the practitioner-client world, helping to bridge the gap between the worlds of research and therapeutic practice [1]. Newly created RDS-SFBT will bring awareness of the advancements of cutting-edge global Reward Deficiency Syndrome research efforts [2], and expands the resource application available to the consumer.","PeriodicalId":91765,"journal":{"name":"Journal of reward deficiency syndrome and addiction science","volume":"41 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67653818","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pharmacological Inhibition of Brain Fatty Acid Binding Protein Reduces Ethanol Consumption in Mice","authors":"Antonio Figueiredo, John Hamilton, M. Marion, K. Blum, M. Kaczocha, S. Haj-Dahmane, D. Deutsch, P. Thanos","doi":"10.17756/JRDSAS.2017-037","DOIUrl":"https://doi.org/10.17756/JRDSAS.2017-037","url":null,"abstract":"The endocannabinoid (eCB) system is involved in a wide range of behavioral disorders including alcoholism. Inhibition of fatty acid amide hydrolase (FAAH), the principal enzyme that degrades the eCB anandamide (AEA), which enhances AEA levels in the brain, significantly increases ethanol consumption and preference. In the present study, we examined whether pharmacological inhibition of fatty acid binding proteins (FABPs) 5 and 7, which blocks the transport of AEA to FAAH, and increase AEA levels in vivo also alters ethanol consumption and preference. Using a limited access two-bottle choice paradigm, we evaluated ethanol consumption in both male and female C57Bl/6 mice. Results showed a significant decrease in ethanol consumption in both males and females treated with SBFI26, an inhibitor of FABPs. Specifically, male and female mice treated with SBFI26 consumed 24% and 42% less compared to mice receiving no injections, respectively. Subsequently, corticosterone was examined to evaluate the effects FABP5/7 inhibition upon the stress response. We observed a significant elevation in corticosterone levels following restraint stress in SBFI26 treated females, with a weak effect seen in males as compared to vehicle. Based on our results, targeting of FABPs appears to play an important role in ethanol consumption that is differentially regulated in males and females, which is mediated by the stress response.","PeriodicalId":91765,"journal":{"name":"Journal of reward deficiency syndrome and addiction science","volume":"3 1","pages":"21 - 27"},"PeriodicalIF":0.0,"publicationDate":"2017-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42769344","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Physical Exercise Interventions for Drug Addictive Disorders","authors":"T. Archer, R. Badgaiyan, K. Blum","doi":"10.17756/JRDSAS.2017-036","DOIUrl":"https://doi.org/10.17756/JRDSAS.2017-036","url":null,"abstract":"Physical exercise physical and psychological health positive through various different avenues, as example, through affecting positively cognitive performance based upon the relocation of cortical activity which seems to advancing the brain development, connectivity and resilience [1]. Any bodily activity that enhances or maintains physical fitness implies the engagement of regular and frequent exercise thereby maintaining physical fitness and the reduction of agents associated with health problems, e.g. cortisol. With regard to the large proportion of individuals with more-or-less sedentary occupations, physical exercise offers probably the most effective health-promoting lifestyle available with positive outcomes for both neurologic and psychiatric conditions [2–10]. The expressions of disorder emerging as consequences of exposure to reward loss have been neglected in approaches to the psychobiology of substance abuse disorders. This notion emphasizes the shared characteristics reward loss and addiction are reviewed, namely, the neural circuitry involved in reward devaluation, the influence of genetic and reward history on the behavioral vulnerability and resilience, the role of competing natural rewards, and emotional selfmedication as a backdrop [11] to the consequences evolving in the “Reward Deficiency Syndrome”. The Reward Deficiency Syndrome, characterized by expressions of rewardseeking behavior and/or addictions and involving a G protein-coupled receptor located on postsynaptic dopaminergic neurons that is centrally involved in reward-mediating mesocorticolimbic pathways, originates from genetic variations, most notably resulting from those carrying the D2A1 allele implicated in addiction and abuse [12, 13]. Individuals carrying the A1 allele tend to have insufficient numbers of D2 receptors in their brain, resulting in lack of pleasure and reward from activities that would provide others with pleasure. Dopamine subtype 2 receptor (D2DR) knockdown mice fail to gain weight or exhibit elevated appetitive motivation in comparison with the wild-type mice within standard environments yet in enriched environments incorporating voluntary exercise facilities, these D2DR knockdown mice expressed markedly lower activity with a rapid increase in obesity compared with the wild-type mice without being receptive of the protective benefit from exercise contingencies [14]. Thus, an underlying mechanism for conceptualizing and","PeriodicalId":91765,"journal":{"name":"Journal of reward deficiency syndrome and addiction science","volume":"3 1","pages":"17 - 20"},"PeriodicalIF":0.0,"publicationDate":"2017-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42143331","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pro-Dopamine Regulator – (KB220) to Balance Brain Reward Circuitry in Reward Deficiency Syndrome (RDS)","authors":"K. Blum, M. Febo, L. Fried, D. Baron, E. Braverman, K. Dushaj, Mona Li, Z. Demetrovics, R. Badgaiyan","doi":"10.17756/JRDSAS.2017-034","DOIUrl":"https://doi.org/10.17756/JRDSAS.2017-034","url":null,"abstract":"We are faced with a worldwide opiate/opioid epidemic that is devastating. According to the Centers for Disease Control and Prevention (CDC), at least 127 people, young and old, are dying every day in America due to narcotic overdose. The Food and Drug Administration (FDA) has approved Medication-Assisted Treatments (MATs) for opiate/opioids as well as alcohol and nicotine. The mechanism of action of most MATS favors either blocking of dopaminergic function or a form of Opiate Substitution Therapy (OST). These treatment options are adequate for short-term treatment of the symptoms of addiction and harm reduction but fail long-term to deal with the cause or lead to recovery. There is a need to continue to seek better treatment options. This mini-review is the history of the development of one such treatment; a glutaminergic-dopaminergic optimization complex called KB220. Growing evidence indicates that brain reward circuitry controls drug addiction, in conjunction with “anti-reward systems” as the “anti-reward systems” can be affected by both glutaminergic and dopaminergic transmission. KB220 may likely alter the function of these regions and provide for the possible eventual balancing the brain reward system and the induction of “dopamine homeostasis.” Many of these concepts have been reported elsewhere and have become an integral part of the addiction science literature. However, the concise review may encourage readership to reconsider these facts and stimulate further research focused on the impact that the induction of “dopamine homeostasis” may have on recovery and relapse prevention.","PeriodicalId":91765,"journal":{"name":"Journal of reward deficiency syndrome and addiction science","volume":"3 1","pages":"3 - 13"},"PeriodicalIF":0.0,"publicationDate":"2017-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45376343","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypothesizing Las Vegas and Sutherland Springs Mass Shooters Suffer from Reward Deficiency Syndrome: \"Born Bad\".","authors":"Thomas McLaughlin,&nbsp;Kenneth Blum,&nbsp;Bruce Steinberg,&nbsp;David Siwicki,&nbsp;Joseph Campione,&nbsp;Rajendra D Badgaiyan,&nbsp;Eric R Braverman,&nbsp;Edward J Modestino,&nbsp;Marjorie C Gondré-Lewis,&nbsp;David Baron,&nbsp;Deborah C Mash,&nbsp;John Giordano,&nbsp;Panayotis K Thanos","doi":"10.17756/jrdsas.2017-038","DOIUrl":"https://doi.org/10.17756/jrdsas.2017-038","url":null,"abstract":"<p><p>The slaughters in Las Vegas and Sutherland Springs demand explanation, in the face of the ineffable. An understanding of the shooters' motives could restore our trust in our mutually cooperative existence. In this short communication we provide post-hoc rationale of both Stephen Paddock (Las Vegas mass shooting) and Devin Kelley (Southerland Springs mass shooting) and hypothesize that these shooters had genetically induced \"Reward Deficiency Syndrome\" (RDS) and a hypodopaminergia trait/state. In this particular case we are in pursuit of trying to obtain postmortem samples of mass shooters for subsequent epigenetic and neurogenetic analyses. It is our contention that early genetic identification of RDS and its pathological behaviors including hyper - sexuality, violence, a love for guns, even in children, could be a giant step forward in potentially saving lives.</p>","PeriodicalId":91765,"journal":{"name":"Journal of reward deficiency syndrome and addiction science","volume":"3 2","pages":"28-31"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6022843/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36276346","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Physical Exercise Interventions for Drug Addictive Disorders.","authors":"Trevor Archer,&nbsp;Rajendra D Badgaiyan,&nbsp;Kenneth Blum","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":91765,"journal":{"name":"Journal of reward deficiency syndrome and addiction science","volume":"3 1","pages":"17-20"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5640325/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35453038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pharmacological Inhibition of Brain Fatty Acid Binding Protein Reduces Ethanol Consumption in Mice.","authors":"Antonio Figueiredo,&nbsp;John Hamilton,&nbsp;Matthew Marion,&nbsp;Kenneth Blum,&nbsp;Martin Kaczocha,&nbsp;Samir Haj-Dahmane,&nbsp;Dale Deutsch,&nbsp;Panayotis K Thanos","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The endocannabinoid (eCB) system is involved in a wide range of behavioral disorders including alcoholism. Inhibition of fatty acid amide hydrolase (FAAH), the principal enzyme that degrades the eCB anandamide (AEA), which enhances AEA levels in the brain, significantly increases ethanol consumption and preference. In the present study, we examined whether pharmacological inhibition of fatty acid binding proteins (FABPs) 5 and 7, which blocks the transport of AEA to FAAH, and increase AEA levels <i>in vivo</i> also alters ethanol consumption and preference. Using a limited access two-bottle choice paradigm, we evaluated ethanol consumption in both male and female C57Bl/6 mice. Results showed a significant decrease in ethanol consumption in both males and females treated with SBFI26, an inhibitor of FABPs. Specifically, male and female mice treated with SBFI26 consumed 24% and 42% less compared to mice receiving no injections, respectively. Subsequently, corticosterone was examined to evaluate the effects FABP5/7 inhibition upon the stress response. We observed a significant elevation in corticosterone levels following restraint stress in SBFI26 treated females, with a weak effect seen in males as compared to vehicle. Based on our results, targeting of FABPs appears to play an important role in ethanol consumption that is differentially regulated in males and females, which is mediated by the stress response.</p>","PeriodicalId":91765,"journal":{"name":"Journal of reward deficiency syndrome and addiction science","volume":"3 2","pages":"21-27"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5777574/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35764635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pro-Dopamine Regulator - (KB220) to Balance Brain Reward Circuitry in Reward Deficiency Syndrome (RDS).","authors":"Kenneth Blum,&nbsp;Marcelo Febo,&nbsp;Lyle Fried,&nbsp;David Baron,&nbsp;Eric R Braverman,&nbsp;Kristina Dushaj,&nbsp;Mona Li,&nbsp;Zsolt Demetrovics,&nbsp;Rajendra D Badgaiyan","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>We are faced with a worldwide opiate/opioid epidemic that is devastating. According to the Centers for Disease Control and Prevention (CDC), at least 127 people, young and old, are dying every day in America due to narcotic overdose. The Food and Drug Administration (FDA) has approved Medication-Assisted Treatments (MATs) for opiate/opioids as well as alcohol and nicotine. The mechanism of action of most MATS favors either blocking of dopaminergic function or a form of Opiate Substitution Therapy (OST). These treatment options are adequate for short-term treatment of the symptoms of addiction and harm reduction but fail long-term to deal with the cause or lead to recovery. There is a need to continue to seek better treatment options. This mini-review is the history of the development of one such treatment; a glutaminergic-dopaminergic optimization complex called KB220. Growing evidence indicates that brain reward circuitry controls drug addiction, in conjunction with \"anti-reward systems\" as the \"anti-reward systems\" can be affected by both glutaminergic and dopaminergic transmission. KB220 may likely alter the function of these regions and provide for the possible eventual balancing the brain reward system and the induction of \"dopamine homeostasis.\" Many of these concepts have been reported elsewhere and have become an integral part of the addiction science literature. However, the concise review may encourage readership to reconsider these facts and stimulate further research focused on the impact that the induction of \"dopamine homeostasis\" may have on recovery and relapse prevention.</p>","PeriodicalId":91765,"journal":{"name":"Journal of reward deficiency syndrome and addiction science","volume":"3 1","pages":"3-13"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5551501/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35316268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Clinically-Relevant Dose of Methylphenidate Enhances Synaptic Inhibition in the Juvenile Rat Prefrontal Cortex.","authors":"Kimberly R Urban,&nbsp;Yan-Chun Li,&nbsp;Bo Xing,&nbsp;Wen-Jun Gao","doi":"10.17756/jrdsas.2016-030","DOIUrl":"https://doi.org/10.17756/jrdsas.2016-030","url":null,"abstract":"<p><p>Methylphenidate (MPH) is perhaps the most commonly prescribed psychoactive substance for young children and adolescents; however, its effects on the immature brain are not well understood. MPH is increasingly abused by adolescents and prescriptions are being issued to increasingly younger children without rigorous psychological testing, raising the potential for misdiagnosis; it is therefore crucial to understand how this drug might impact a healthy, developing brain. Recently, we have shown that a clinically-relevant dose of MPH depresses the activity of pyramidal neurons in the prefrontal cortex of normal juvenile rats, but its effects on inhibitory synaptic transmission remain to be explored. We therefore recorded spontaneous (s), miniature (m), and evoked (e) inhibitory postsynaptic currents (IPSCs) in layer 5 pyramidal neurons in juvenile rat prefrontal cortex. We found a dose-dependent effect of MPH on sIPSC frequency but not amplitude, where 0.3 mg/kg significantly decreased frequency, but 1 mg/kg significantly increased frequency. Moreover, mIPSCs were not affected by either dose of MPH, whereas the amplitudes, as well as paired-pulse ratios and coefficient of variations of evoked IPSCs were significantly increased after MPH treatment, indicating a presynaptic action. Tonic GABA current was also not affected by MPH treatment. Taken together, these results suggest that MPH administration to a healthy juvenile may enhance excitation of GABAergic interneurons; thus shifting the excitation-inhibition balance in the prefrontal cortex towards inhibition, and depressing overall prefrontal cortical activity. Our findings also indicate that the adolescent brain is more sensitive to MPH than previously thought, and dose ranges need to be reconsidered for age as well as size.</p>","PeriodicalId":91765,"journal":{"name":"Journal of reward deficiency syndrome and addiction science","volume":"2 3","pages":"69-77"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6136665/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36497004","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypothesizing that, A Pro-Dopamine Regulator (KB220Z) Should Optimize, but Not Hyper-Activate the Activity of Trace Amine-Associated Receptor 1 (TAAR-1) and Induce Anti-Craving of Psychostimulants in the Long-Term.","authors":"Kenneth Blum, Rajendra D Badgaiyan, Eric R Braverman, Kristina Dushaj, Mona Li, Peter K Thanos, Zsolt Demetrovics, Marcelo Febo","doi":"10.17756/jrdsas.2016-023","DOIUrl":"10.17756/jrdsas.2016-023","url":null,"abstract":"<p><p>Unlike other drugs of abuse such as alcohol, nicotine, opiates/opioids, the FDA has not approved any agent to treat psychostimulant dependence. Certainly, it is widely acceptable that dopaminergic signaling is a key factor in both the initiation and continued motivation to abuse this class of stimulant substances. It is also well accepted that psychostimulants such as cocaine affect not only the release of neuronal dopamine at the nucleus accumbens (NAc), but also has powerful inhibitory actions on the dopamine transporter system. Understandably, certain individuals are at high risk and very vulnerable to abuse this class of substances. Trace-amine-associated receptor 1 (TAAR1) is a G -protein coupled receptor activated by trace amines. The encoded protein responds little or not at all to dopamine, serotonin, epinephrine, or histamine, but responds well to beta-phenylethylamine, p-tyramine, octopamine, and tryptamine. This gene is thought to be intronless. TAAR1 agonists reduce the neurochemical effects of cocaine and amphetamines as well as attenuate addiction and abuse associated with these two psychostimulants. The mechanism involves blocking the firing rate of dopamine in the limbic system thereby decreasing a hyperdopaminergic trait/state, whereby the opposite is true for TAAR1 antagonists. Based on many studies, it is accepted that in Reward Deficiency Syndrome (RDS), there is weakened tonic and improved phasic dopamine discharge leading to a hypodopaminergic/glutamatergic trait. The dopamine pro-complex mixture KB220, following many clinical trials including neuroimaging studies, has been shown to enhance resting state functional connectivity in humans (abstinent heroin addicts), naïve rodent models, and regulates extensive theta action in the cingulate gyrus of abstinent psychostimulant abusers. In this article, we are hypothesizing that KB220 may induce its action on resting state functional connectivity, for example, by actually balancing (optimizing) the effects of TAAR1 on the glutamatergic system allowing for optimization of this system. This will lead to a normalized and homeostatic release of NAc dopamine. This proposed optimization, and not enhanced activation of TAAR1, should lead to well-being of the individual. Hyper-activation instead of optimizing the TAAR1 system unfortunately will lead to a prolonged hypodopaminergic state and as such, will cause enhanced craving for not only psychoactive substances, but also other drug-related and even non-drug related RDS behaviors. This hypothesis will require extensive research, which seems warranted based on the global epidemic of drug and behavioral addictions.</p>","PeriodicalId":91765,"journal":{"name":"Journal of reward deficiency syndrome and addiction science","volume":"2 1","pages":"14-21"},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5351297/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34833374","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}