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[PMID]:28823729
[Au] Autor:Aguilar JI; Dunn M; Mingote S; Karam CS; Farino ZJ; Sonders MS; Choi SJ; Grygoruk A; Zhang Y; Cela C; Choi BJ; Flores J; Freyberg RJ; McCabe BD; Mosharov EV; Krantz DE; Javitch JA; Sulzer D; Sames D; Rayport S; Freyberg Z
[Ad] Endereço:Department of Pharmacology, Vanderbilt University, Nashville, TN 37232, USA.
[Ti] Título:Neuronal Depolarization Drives Increased Dopamine Synaptic Vesicle Loading via VGLUT.
[So] Source:Neuron;95(5):1074-1088.e7, 2017 Aug 30.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The ability of presynaptic dopamine terminals to tune neurotransmitter release to meet the demands of neuronal activity is critical to neurotransmission. Although vesicle content has been assumed to be static, in vitro data increasingly suggest that cell activity modulates vesicle content. Here, we use a coordinated genetic, pharmacological, and imaging approach in Drosophila to study the presynaptic machinery responsible for these vesicular processes in vivo. We show that cell depolarization increases synaptic vesicle dopamine content prior to release via vesicular hyperacidification. This depolarization-induced hyperacidification is mediated by the vesicular glutamate transporter (VGLUT). Remarkably, both depolarization-induced dopamine vesicle hyperacidification and its dependence on VGLUT2 are seen in ventral midbrain dopamine neurons in the mouse. Together, these data suggest that in response to depolarization, dopamine vesicles utilize a cascade of vesicular transporters to dynamically increase the vesicular pH gradient, thereby increasing dopamine vesicle content.
[Mh] Termos MeSH primário: Dopamina/metabolismo
Neurônios/metabolismo
Vesículas Sinápticas/metabolismo
Proteína Vesicular 2 de Transporte de Glutamato/fisiologia
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Dextroanfetamina/farmacologia
Drosophila
Proteínas de Drosophila/metabolismo
Concentração de Íons de Hidrogênio
Locomoção/efeitos dos fármacos
Mesencéfalo/metabolismo
Camundongos
Neurônios/fisiologia
Terminações Pré-Sinápticas/metabolismo
Proteína Vesicular 2 de Transporte de Glutamato/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Drosophila Proteins); 0 (Vesicular Glutamate Transport Protein 2); TZ47U051FI (Dextroamphetamine); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170822
[St] Status:MEDLINE


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[PMID]:28632508
[Au] Autor:Keser Z; Dehgan MW; Shadravan S; Yozbatiran N; Maher LM; Francisco GE
[Ad] Endereço:From the Department of Physical Medicine and Rehabilitation, University of Texas Health Science Center and TIRR Memorial Hermann NeuroRecovery Research Center, Houston, Texas (ZK, NY, GEF); Speech-Language Pathology Department, TIRR Memorial Hermann Hospital, Houston, Texas (MWD, SS); and Department of Communication Sciences and Disorders, University of Houston, Texas (LMM).
[Ti] Título:Combined Dextroamphetamine and Transcranial Direct Current Stimulation in Poststroke Aphasia.
[So] Source:Am J Phys Med Rehabil;96(10 Suppl 1):S141-S145, 2017 Oct.
[Is] ISSN:1537-7385
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:There is a growing need for various effective adjunctive treatment options for speech recovery after stroke. A pharmacological agent combined with noninvasive brain stimulation has not been previously reported for poststroke aphasia recovery. In this "proof of concept" study, we aimed to test the safety of a combined intervention consisting of dextroamphetamine, transcranial direct current stimulation, and speech and language therapy in subjects with nonfluent aphasia. Ten subjects with chronic nonfluent aphasia underwent two experiments where they received dextroamphetamine or placebo along with transcranial direct current stimulation and speech and language therapy on two separate days. The Western Aphasia Battery-Revised was used to monitor changes in speech performance. No serious adverse events were observed. There was no significant increase in blood pressure with amphetamine or deterioration in speech and language performance. Western Aphasia Battery-Revised aphasia quotient and language quotient showed a statistically significant increase in the active experiment. Comparison of proportional changes of aphasia quotient and language quotient in active experiment with those in placebo experiment showed significant difference. We showed that the triple combination therapy is safe and implementable and seems to induce positive changes in speech and language performance in the patients with chronic nonfluent aphasia due to stroke.
[Mh] Termos MeSH primário: Afasia/reabilitação
Estimulantes do Sistema Nervoso Central/administração & dosagem
Dextroanfetamina/administração & dosagem
Reabilitação do Acidente Vascular Cerebral/métodos
Estimulação Transcraniana por Corrente Contínua/métodos
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Afasia/etiologia
Afasia/fisiopatologia
Terapia Combinada
Estudos Cross-Over
Método Duplo-Cego
Feminino
Seres Humanos
Linguagem
Masculino
Meia-Idade
Recuperação de Função Fisiológica
Fala/fisiologia
Fonoterapia/métodos
Acidente Vascular Cerebral/complicações
Acidente Vascular Cerebral/fisiopatologia
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Central Nervous System Stimulants); TZ47U051FI (Dextroamphetamine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170621
[St] Status:MEDLINE
[do] DOI:10.1097/PHM.0000000000000780


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[PMID]:28373066
[Au] Autor:Banks ML; Snyder RW; Fennell TR; Negus SS
[Ad] Endereço:Department of Pharmacology & Toxicology, Virginia Commonwealth University, Richmond, VA 23298, USA. Electronic address: matthew.banks@vcuhealth.org.
[Ti] Título:Role of d-amphetamine and d-methamphetamine as active metabolites of benzphetamine: Evidence from drug discrimination and pharmacokinetic studies in male rhesus monkeys.
[So] Source:Pharmacol Biochem Behav;156:30-38, 2017 May.
[Is] ISSN:1873-5177
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Benzphetamine is a Schedule III anorectic agent that is a prodrug for d-amphetamine and d-methamphetamine and may have utility as an "agonist" medication for cocaine use disorder treatment. This study evaluated the pharmacokinetic-pharmacodynamic profile of benzphetamine using a drug discrimination procedure in rhesus monkeys. The potency and time course of cocaine-like discriminative stimulus effects were compared for benzphetamine (10-18mg/kg, intramuscular (IM)) and d-amphetamine (0.032-0.32mg/kg, IM) in monkeys (n=3-4) trained to discriminate IM cocaine (0.32mg/kg) from saline in a two-key food-reinforced discrimination procedure. Parallel pharmacokinetic studies in the same monkeys determined plasma benzphetamine, d-methamphetamine and/or d-amphetamine levels for correlation with behavioral effects. d-Amphetamine produced dose-dependent, time-dependent, and full cocaine-like effects, i.e. ≥90% cocaine-appropriate responding, in all monkeys without altering response rates. The time course of d-amphetamine's cocaine-like discriminative stimulus effects correlated with plasma d-amphetamine levels. Benzphetamine was 180-fold less potent than d-amphetamine and produced full cocaine-like effects in only 2 of 4 monkeys while significantly decreasing response rates. Benzphetamine administration increased plasma d-methamphetamine (peak at 100min) and d-amphetamine (peak at 24h) levels, but the time course of behavioral effects did not correlate with increased levels of benzphetamine, d-methamphetamine or d-amphetamine. These results suggest that benzphetamine yields d-amphetamine and d-methamphetamine as active metabolites in rhesus monkeys, but generation of these metabolites is not sufficient to account for benzphetamine behavioral effects. The incomplete cocaine substitution profile and protracted d-amphetamine plasma levels suggest that benzphetamine may still warrant further evaluation as a candidate pharmacotherapy for cocaine use disorder treatment.
[Mh] Termos MeSH primário: Benzfetamina/farmacologia
Dextroanfetamina/farmacologia
Metanfetamina/farmacologia
[Mh] Termos MeSH secundário: Animais
Comportamento Animal/efeitos dos fármacos
Benzfetamina/farmacocinética
Dextroanfetamina/farmacocinética
Macaca mulatta
Masculino
Metanfetamina/farmacocinética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0M3S43XK27 (Benzphetamine); 44RAL3456C (Methamphetamine); TZ47U051FI (Dextroamphetamine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170405
[St] Status:MEDLINE


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[PMID]:28287789
[Au] Autor:Boomhower SR; Newland MC
[Ad] Endereço:Department of Psychology.
[Ti] Título:Effects of adolescent exposure to methylmercury and d-amphetamine on reversal learning and an extradimensional shift in male mice.
[So] Source:Exp Clin Psychopharmacol;25(2):64-73, 2017 Apr.
[Is] ISSN:1936-2293
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Adolescence is associated with the continued maturation of dopamine neurotransmission and is implicated in the etiology of many psychiatric illnesses. Adolescent exposure to neurotoxicants that distort dopamine neurotransmission, such as methylmercury (MeHg), may modify the effects of chronic -amphetamine ( -AMP) administration on reversal learning and attentional-set shifting. Male C57Bl/6n mice were randomly assigned to two MeHg-exposure groups (0 ppm and 3 ppm) and two -AMP-exposure groups (saline and 1 mg/kg/day), producing four treatment groups (n = 10-12/group): control, MeHg -AMP, and MeHg + -AMP. MeHg exposure (via drinking water) spanned postnatal days 21-59 (the murine adolescent period), and once daily intraperitoneal injections of -AMP or saline spanned postnatal days 28-42. As adults, mice were trained on a spatial-discrimination-reversal (SDR) task in which the spatial location of a lever press predicted reinforcement. Following 2 SDRs, a visual-discrimination task (extradimensional shift) was instated in which the presence of a stimulus light above a lever predicted reinforcement. Responding was modeled using a logistic function, which estimated the rate (slope) of a behavioral transition and trials required to complete half a transition (half-max). MeHg, -AMP, and MeHg + -AMP exposure increased estimates of half-max on the second reversal. MeHg exposure increased half-max and decreased the slope term following the extradimensional shift, but these effects did not occur following MeHg + -AMP exposure. MeHg + -AMP exposure produced more perseverative errors and omissions following a reversal. Adolescent exposure to MeHg can modify the behavioral effects of chronic -AMP administration. (PsycINFO Database Record
[Mh] Termos MeSH primário: Dextroanfetamina/farmacologia
Dopamina/metabolismo
Compostos de Metilmercúrio/farmacologia
Reversão de Aprendizagem/efeitos dos fármacos
[Mh] Termos MeSH secundário: Fatores Etários
Animais
Comportamento Animal/efeitos dos fármacos
Dextroanfetamina/administração & dosagem
Aprendizagem por Discriminação/efeitos dos fármacos
Injeções Intraperitoneais
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Modelos Biológicos
Distribuição Aleatória
Reforço (Psicologia)
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Methylmercury Compounds); TZ47U051FI (Dextroamphetamine); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170717
[Lr] Data última revisão:
170717
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170314
[St] Status:MEDLINE
[do] DOI:10.1037/pha0000107


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[PMID]:28253393
[Au] Autor:Mustian KM; Alfano CM; Heckler C; Kleckner AS; Kleckner IR; Leach CR; Mohr D; Palesh OG; Peppone LJ; Piper BF; Scarpato J; Smith T; Sprod LK; Miller SM
[Ad] Endereço:Department of Surgery, Wilmot Cancer Institute, University of Rochester Medical Center, Rochester, New York.
[Ti] Título:Comparison of Pharmaceutical, Psychological, and Exercise Treatments for Cancer-Related Fatigue: A Meta-analysis.
[So] Source:JAMA Oncol;3(7):961-968, 2017 Jul 01.
[Is] ISSN:2374-2445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Importance: Cancer-related fatigue (CRF) remains one of the most prevalent and troublesome adverse events experienced by patients with cancer during and after therapy. Objective: To perform a meta-analysis to establish and compare the mean weighted effect sizes (WESs) of the 4 most commonly recommended treatments for CRF-exercise, psychological, combined exercise and psychological, and pharmaceutical-and to identify independent variables associated with treatment effectiveness. Data Sources: PubMed, PsycINFO, CINAHL, EMBASE, and the Cochrane Library were searched from the inception of each database to May 31, 2016. Study Selection: Randomized clinical trials in adults with cancer were selected. Inclusion criteria consisted of CRF severity as an outcome and testing of exercise, psychological, exercise plus psychological, or pharmaceutical interventions. Data Extraction and Synthesis: Studies were independently reviewed by 12 raters in 3 groups using a systematic and blinded process for reconciling disagreement. Effect sizes (Cohen d) were calculated and inversely weighted by SE. Main Outcomes and Measures: Severity of CRF was the primary outcome. Study quality was assessed using a modified 12-item version of the Physiotherapy Evidence-Based Database scale (range, 0-12, with 12 indicating best quality). Results: From 17 033 references, 113 unique studies articles (11 525 unique participants; 78% female; mean age, 54 [range, 35-72] years) published from January 1, 1999, through May 31, 2016, had sufficient data. Studies were of good quality (mean Physiotherapy Evidence-Based Database scale score, 8.2; range, 5-12) with no evidence of publication bias. Exercise (WES, 0.30; 95% CI, 0.25-0.36; P < .001), psychological (WES, 0.27; 95% CI, 0.21-0.33; P < .001), and exercise plus psychological interventions (WES, 0.26; 95% CI, 0.13-0.38; P < .001) improved CRF during and after primary treatment, whereas pharmaceutical interventions did not (WES, 0.09; 95% CI, 0.00-0.19; P = .05). Results also suggest that CRF treatment effectiveness was associated with cancer stage, baseline treatment status, experimental treatment format, experimental treatment delivery mode, psychological mode, type of control condition, use of intention-to-treat analysis, and fatigue measures (WES range, -0.91 to 0.99). Results suggest that the effectiveness of behavioral interventions, specifically exercise and psychological interventions, is not attributable to time, attention, and education, and specific intervention modes may be more effective for treating CRF at different points in the cancer treatment trajectory (WES range, 0.09-0.22). Conclusions and Relevance: Exercise and psychological interventions are effective for reducing CRF during and after cancer treatment, and they are significantly better than the available pharmaceutical options. Clinicians should prescribe exercise or psychological interventions as first-line treatments for CRF.
[Mh] Termos MeSH primário: Estimulantes do Sistema Nervoso Central/uso terapêutico
Terapia Cognitiva
Terapia por Exercício
Fadiga/terapia
Glucocorticoides/uso terapêutico
Neoplasias/complicações
Inibidores da Captação de Serotonina/uso terapêutico
Promotores da Vigília/uso terapêutico
[Mh] Termos MeSH secundário: Compostos Benzidrílicos/uso terapêutico
Cloridrato de Dexmetilfenidato/uso terapêutico
Dextroanfetamina/uso terapêutico
Fadiga/etiologia
Seres Humanos
Metilfenidato/uso terapêutico
Metilprednisolona/uso terapêutico
Paroxetina/uso terapêutico
Psicoterapia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (Benzhydryl Compounds); 0 (Central Nervous System Stimulants); 0 (Glucocorticoids); 0 (Serotonin Uptake Inhibitors); 0 (Wakefulness-Promoting Agents); 1678OK0E08 (Dexmethylphenidate Hydrochloride); 207ZZ9QZ49 (Methylphenidate); 41VRH5220H (Paroxetine); R3UK8X3U3D (modafinil); TZ47U051FI (Dextroamphetamine); V63XWA605I (armodafinil); X4W7ZR7023 (Methylprednisolone)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170828
[Lr] Data última revisão:
170828
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170303
[St] Status:MEDLINE
[do] DOI:10.1001/jamaoncol.2016.6914


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[PMID]:28241065
[Au] Autor:Schrantee A; Tremoleda JL; Wylezinska-Arridge M; Bouet V; Hesseling P; Meerhoff GF; de Bruin KM; Koeleman J; Freret T; Boulouard M; Desfosses E; Galineau L; Gozzi A; Dauphin F; Gsell W; Booij J; Lucassen PJ; Reneman L
[Ad] Endereço:Department of Radiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
[Ti] Título:Repeated dexamphetamine treatment alters the dopaminergic system and increases the phMRI response to methylphenidate.
[So] Source:PLoS One;12(2):e0172776, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Dexamphetamine (AMPH) is a psychostimulant drug that is used both recreationally and as medication for attention deficit hyperactivity disorder. Preclinical studies have demonstrated that repeated exposure to AMPH can induce damage to nerve terminals of dopamine (DA) neurons. We here assessed the underlying neurobiological changes in the DA system following repeated AMPH exposure and pre-treated rats with AMPH or saline (4 times 5 mg/kg s.c., 2 hours apart), followed by a 1-week washout period. We then used pharmacological MRI (phMRI) with a methylphenidate (MPH) challenge, as a sensitive and non-invasive in-vivo measure of DAergic function. We subsequently validated the DA-ergic changes post-mortem, using a.o. high-performance liquid chromatography (HPLC) and autoradiography. In the AMPH pre-treated group, we observed a significantly larger BOLD response to the MPH challenge, particularly in DA-ergic brain areas and their downstream projections. Subsequent autoradiography studies showed that AMPH pre-treatment significantly reduced DA transporter (DAT) density in the caudate-putamen (CPu) and nucleus accumbens, whereas HPLC analysis revealed increases in the DA metabolite homovanillic acid in the CPu. Our results suggest that AMPH pre-treatment alters DAergic responsivity, a change that can be detected with phMRI in rats. These phMRI changes likely reflect increased DA release together with reduced DAT binding. The ability to assess subtle synaptic changes using phMRI is promising for both preclinical studies of drug discovery, and for clinical studies where phMRI can be a useful tool to non-invasively investigate DA abnormalities, e.g. in neuropsychiatric disorders.
[Mh] Termos MeSH primário: Encéfalo/efeitos dos fármacos
Estimulantes do Sistema Nervoso Central/farmacologia
Dextroanfetamina/farmacologia
Dopamina/metabolismo
Metilfenidato/farmacologia
[Mh] Termos MeSH secundário: Animais
Encéfalo/metabolismo
Estimulantes do Sistema Nervoso Central/efeitos adversos
Cromatografia Líquida de Alta Pressão
Corpo Estriado/metabolismo
Dextroanfetamina/efeitos adversos
Proteínas da Membrana Plasmática de Transporte de Dopamina/metabolismo
Inibidores da Captação de Dopamina/farmacologia
Neurônios Dopaminérgicos/efeitos dos fármacos
Esquema de Medicação
Proteína Glial Fibrilar Ácida/metabolismo
Hemodinâmica
Imuno-Histoquímica
Imagem por Ressonância Magnética
Masculino
Ratos
Ratos Sprague-Dawley
Receptores de Dopamina D2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Central Nervous System Stimulants); 0 (DRD2 protein, rat); 0 (Dopamine Plasma Membrane Transport Proteins); 0 (Dopamine Uptake Inhibitors); 0 (Glial Fibrillary Acidic Protein); 0 (Receptors, Dopamine D2); 207ZZ9QZ49 (Methylphenidate); TZ47U051FI (Dextroamphetamine); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170228
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0172776


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[PMID]:27979580
[Au] Autor:Toce MS; Farias M; Bruccoleri R; Brown DW; Burns MM
[Ad] Endereço:Harvard Medical Toxicology Program, Boston Children's Hospital, Boston, MA. Electronic address: michael.toce@childrens.harvard.edu.
[Ti] Título:A Case Report of Reversible Takotsubo Cardiomyopathy after Amphetamine/Dextroamphetamine Ingestion in a 15-Year-Old Adolescent Girl.
[So] Source:J Pediatr;182:385-388.e3, 2017 Mar.
[Is] ISSN:1097-6833
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Stimulant medications are used in the treatment of attention deficit hyperactivity disorder and serious cardiac complications can occur when these medications are abused. We present a 15-year-old adolescent girl who was found to have a Takotsubo cardiomyopathy after acute amphetamine/dextroamphetamine ingestion.
[Mh] Termos MeSH primário: Estimulantes do Sistema Nervoso Central/envenenamento
Dextroanfetamina/envenenamento
Imagem Cinética por Ressonância Magnética/métodos
Cardiomiopatia de Takotsubo/induzido quimicamente
Cardiomiopatia de Takotsubo/diagnóstico por imagem
[Mh] Termos MeSH secundário: Adolescente
Eletrocardiografia/métodos
Feminino
Seres Humanos
Prognóstico
Recuperação de Função Fisiológica
Medição de Risco
Tentativa de Suicídio
Cardiomiopatia de Takotsubo/terapia
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Central Nervous System Stimulants); TZ47U051FI (Dextroamphetamine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170621
[Lr] Data última revisão:
170621
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161217
[St] Status:MEDLINE


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[PMID]:27001613
[Au] Autor:van de Giessen E; Weinstein JJ; Cassidy CM; Haney M; Dong Z; Ghazzaoui R; Ojeil N; Kegeles LS; Xu X; Vadhan NP; Volkow ND; Slifstein M; Abi-Dargham A
[Ad] Endereço:Department of Psychiatry, Columbia University College of Physicians and Surgeons, New York, NY, USA.
[Ti] Título:Deficits in striatal dopamine release in cannabis dependence.
[So] Source:Mol Psychiatry;22(1):68-75, 2017 Jan.
[Is] ISSN:1476-5578
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Most drugs of abuse lead to a general blunting of dopamine release in the chronic phase of dependence, which contributes to poor outcome. To test whether cannabis dependence is associated with a similar dopaminergic deficit, we examined striatal and extrastriatal dopamine release in severely cannabis-dependent participants (CD), free of any comorbid conditions, including nicotine use. Eleven CD and 12 healthy controls (HC) completed two positron emission tomography scans with [ C]-(+)-PHNO, before and after oral administration of d-amphetamine. CD stayed inpatient for 5-7 days prior to the scans to standardize abstinence. Magnetic resonance spectroscopy (MRS) measures of glutamate in the striatum and hippocampus were obtained in the same subjects. Percent change in [ C]-(+)-PHNO-binding potential (ΔBP ) was compared between groups and correlations with MRS glutamate, subclinical psychopathological and neurocognitive parameters were examined. CD had significantly lower ΔBP in the striatum (P=0.002, effect size (ES)=1.48), including the associative striatum (P=0.003, ES=1.39), sensorimotor striatum (P=0.003, ES=1.41) and the pallidus (P=0.012, ES=1.16). Lower dopamine release in the associative striatum correlated with inattention and negative symptoms in CD, and with poorer working memory and probabilistic category learning performance in both CD and HC. No relationships to MRS glutamate and amphetamine-induced subclinical positive symptoms were detected. In conclusion, this study provides evidence that severe cannabis dependence-without the confounds of any comorbidity-is associated with a deficit in striatal dopamine release. This deficit extends to other extrastriatal areas and predicts subclinical psychopathology.
[Mh] Termos MeSH primário: Cannabis/efeitos adversos
Corpo Estriado/efeitos dos fármacos
Abuso de Maconha/fisiopatologia
[Mh] Termos MeSH secundário: Adulto
Anfetamina/farmacologia
Encéfalo/efeitos dos fármacos
Cannabis/metabolismo
Dextroanfetamina/farmacologia
Dopamina
Endocanabinoides/metabolismo
Feminino
Seres Humanos
Imagem por Ressonância Magnética
Masculino
Abuso de Maconha/metabolismo
Tomografia por Emissão de Pósitrons/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endocannabinoids); CK833KGX7E (Amphetamine); TZ47U051FI (Dextroamphetamine); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160323
[St] Status:MEDLINE
[do] DOI:10.1038/mp.2016.21


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[PMID]:28044946
[Au] Autor:Mattingly GW; Anderson RH
[Ad] Endereço:1Washington University School of Medicine,Department of Psychiatry and Behavioral Neurosciences,St. Charles,Missouri,USA.
[Ti] Título:Optimizing outcomes in ADHD treatment: from clinical targets to novel delivery systems.
[So] Source:CNS Spectr;21(S1):45-59, 2016 12.
[Is] ISSN:1092-8529
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Our knowledge and understanding of the underlying neurobiology and symptomatic expression of ADHD has advanced dramatically over the past decade. Associated with these advances has been a similar explosion of new treatment options to individualize treatment for our patients. This article will: ∙ review strategies to measure ADHD symptoms and functional difficulties while seeking to achieve full symptomatic remission throughout the day ∙ summarize recent findings regarding the management and prioritization of ADHD and comorbid conditions and ∙ discuss the various pharmacologic treatment options with a focus on recently developed molecules and novel delivery systems.
[Mh] Termos MeSH primário: Inibidores da Captação Adrenérgica/uso terapêutico
Agonistas de Receptores Adrenérgicos alfa 2/uso terapêutico
Transtorno do Deficit de Atenção com Hiperatividade/tratamento farmacológico
Estimulantes do Sistema Nervoso Central/administração & dosagem
[Mh] Termos MeSH secundário: Transtornos de Ansiedade/epidemiologia
Transtornos de Ansiedade/terapia
Cloridrato de Atomoxetina/uso terapêutico
Transtorno do Deficit de Atenção com Hiperatividade/epidemiologia
Transtorno Bipolar/epidemiologia
Transtorno Bipolar/terapia
Clonidina/uso terapêutico
Comorbidade
Preparações de Ação Retardada
Transtorno Depressivo/epidemiologia
Transtorno Depressivo/terapia
Dextroanfetamina/administração & dosagem
Guanfacina/uso terapêutico
Seres Humanos
Metilfenidato/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Adrenergic Uptake Inhibitors); 0 (Adrenergic alpha-2 Receptor Agonists); 0 (Central Nervous System Stimulants); 0 (Delayed-Action Preparations); 207ZZ9QZ49 (Methylphenidate); 30OMY4G3MK (Guanfacine); 57WVB6I2W0 (Atomoxetine Hydrochloride); MN3L5RMN02 (Clonidine); TZ47U051FI (Dextroamphetamine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170629
[Lr] Data última revisão:
170629
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170104
[St] Status:MEDLINE
[do] DOI:10.1017/S1092852916000808


  10 / 6496 MEDLINE  
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[PMID]:27754966
[Au] Autor:Kapellen TM; Reimann R; Kiess W; Kostev K
[Ti] Título:Prevalence of medically treated children with ADHD and type 1 diabetes in Germany - Analysis of two representative databases.
[So] Source:J Pediatr Endocrinol Metab;29(11):1293-1297, 2016 Nov 01.
[Is] ISSN:2191-0251
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The aim of this study was to analyze the prevalence of attention deficit hyperactivity disorder (ADHD) in children and adolescents with type 1 diabetes mellitus (T1DM) in Germany. METHODS: Two different representative German databases - IMS®-Disease Analyzer, a database that includes diagnoses as well as other information, and IMS®-LRx, a database that documents prescriptions - were used to conduct a retrospective analysis. We searched the LRx database for patients who received both insulin and ADHD-specific medication. RESULTS: In 2014, 677,587 children and adolescents aged 0-18 years were treated by a pediatrician and documented in the Disease Analyzer database. Of these patients, 16,833 received the International Statistical Classification of Diseases and Related Health Problems (ICD-10) diagnosis of ADHD (2.5%) and 3668 patients were treated for T1DM (0.1%). Of these 3668 patients, a total of 153 children were also diagnosed with ADHD (4.2%; p<0.05). In the LRx database, the overall prevalence of children in Germany who received both drugs for the treatment of ADHD and insulin in 2014 amounted to 2.9%. Diagnosis of ADHD is 2.4-3.3 times more frequent in boys than in girls. The highest prevalence was seen in the age group of 12-15 years (3.5%) and the lowest in the age group of 6-11 years (2.5%). CONCLUSIONS: Children with diabetes suffer from ADHD significantly more frequently than children without diabetes. The prevalence of medically treated children with ADHD and diabetes is similar to that documented in a recent report by the Barmer GEK health insurance body. However, it is possible that children with T1DM are much more frequently seen by medical care providers and are thus more likely to be evaluated and receive an appropriate diagnosis.
[Mh] Termos MeSH primário: Transtorno do Deficit de Atenção com Hiperatividade/tratamento farmacológico
Diabetes Mellitus Tipo 1/tratamento farmacológico
Hipoglicemiantes/uso terapêutico
Insulina/uso terapêutico
Inibidores da Captação de Neurotransmissores/uso terapêutico
[Mh] Termos MeSH secundário: Adolescente
Fatores Etários
Cloridrato de Atomoxetina/uso terapêutico
Transtorno do Deficit de Atenção com Hiperatividade/epidemiologia
Criança
Estudos de Coortes
Comorbidade
Dextroanfetamina/uso terapêutico
Diabetes Mellitus Tipo 1/epidemiologia
Prescrições de Medicamentos
Feminino
Alemanha/epidemiologia
Seres Humanos
Masculino
Metilfenidato/uso terapêutico
Prevalência
Estudos Prospectivos
Fatores de Risco
Fatores Sexuais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hypoglycemic Agents); 0 (Insulin); 0 (Neurotransmitter Uptake Inhibitors); 207ZZ9QZ49 (Methylphenidate); 57WVB6I2W0 (Atomoxetine Hydrochloride); TZ47U051FI (Dextroamphetamine)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170503
[Lr] Data última revisão:
170503
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161105
[St] Status:MEDLINE



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