Human Psychopharmacology: Clinical and Experimental最新文献

This study aimed to determine if belief in caffeine's ergogenic potential influences choice reaction time (CRT) and/or running performance. Twenty-nine healthy individuals (23.7 ± 5 years, 16 males) completed two trials (one week apart). Before the trials, participants indicated their "belief" in caffeine's ergogenic effects and previous "experience" using caffeine for performance. On arrival, participants randomly received either sham "Low (100mg; LD)" or "High (300mg; HD)" dose caffeine capsules 30-min before commencing the CRT test, followed by a 10km run. Paired samples t-tests determined differences between trials for CRT latency (Ex-Gaussian analysis; μ-, σ- and τ-) and running performance using the entire cohort and sub-groups exhibiting strong "beliefs"+/-"experience". Sham caffeine dose did not influence CRT (μ-, σ- and τ-respectively, LD: 400 ± 53ms vs. HD: 388 ± 41ms; LD: 35 ± 18ms vs. HD: 34 ± 17ms; LD: 50 ± 24ms vs. HD: 52 ± 19ms, all p's > 0.05). Neither belief (n = 6), nor belief + experience (n = 4), influenced this effect. Furthermore, caffeine dose did not influence run time (LD: 49.05 ± 3.75min vs. HD: 49.06 ± 3.85min, p = 0.979). Belief (n = 9) (LD: 48.93 ± 3.71min vs. HD: 48.9 ± 3.52min, p = 0.976), and belief + experience (n = 6) (LD: 48.68 ± 1.87min vs. HD: 49.55 ± 1.75min, p = 0.386) didn't influence this effect. A dose-response to sham caffeine ingestion was not evident on cognitive or endurance performance in healthy individuals, regardless of their convictions about caffeine's ergogenicity.

Background: Patients with schizophrenia have an increased prevalence of type 2 diabetes mellitus that has shown a significant association with the rs7754840 polymorphism in the gene encoding the cyclin-dependent kinase 5 (CDK5) regulatory subunit-associated protein 1-like 1 (CDKAL1).

Objective: To examine whether this polymorphism was involved in the susceptibility in first-episode drug-naive schizophrenic patients (FDSP), and further influenced their clinical symptoms.

Methods: This polymorphism was genotyped in 239 FDSP and 368 healthy controls. The clinical symptoms in FDSP were assessed using the Positive and Negative Syndrome Scale (PANSS) five-factor models.

Results: There was no significant difference in the allelic and genotypic frequencies of this polymorphism between two groups (both p > 0.05) after adjusting for covariates. However, the PANSS depressive score significantly differed by genotype in FDSP after adjusting for covariates (F = 5.25, p = 0.006). This significant difference also persisted after Bonferroni correction (p < 0.05). FDSP with C/C genotype had significantly higher PANSS depressive score than those with C/G genotype (p = 0.007) and those with G/G genotype (p = 0.005). Moreover, further stepwise multivariate regression analysis showed the significant association between the rs7754840 polymorphism and PANSS depressive score in FDSP (β = -1.07, t = -2.75, p = 0.007).

Conclusions: Our findings demonstrated that although the CDKAL1 rs7754840 polymorphism did not contribute to the susceptibility to FDSP, it might be implicated in depressive symptoms in this patient group.

Objective: To establish in an exploratory neuroimaging study whether γ-hydroxybutyrate (sodium oxybate [SO]), a sedative, anti-narcoleptic drug with abuse potential, transiently inhibits striatal dopamine release in the human.

Methods: Ten healthy participants (30 years; 6M, 4F) and one participant with narcolepsy received a baseline positron emission tomography scan of [C-11]raclopride, a D2/3 dopamine receptor radioligand sensitive to dopamine occupancy, followed approximately one week later by an oral sedative 3g dose of SO and two [C-11]raclopride scans (1 h, 7 h post SO). Plasma SO levels and drowsiness duration were assessed.

Results: No significant changes were detected in [C-11]raclopride binding in striatum overall 1 or 7 h after SO, but a small non-significant increase in [C-11]raclopride binding, implying decreased dopamine occupancy, was noted in limbic striatal subdivision at one hour (+6.5%; p uncorrected = 0.045; +13.2%, narcolepsy participant), returning to baseline at 7 h. A positive correlation was observed between drowsiness duration and percent change in [C-11]raclopride binding in limbic striatum (r = 0.73; p = 0.017).

Conclusions: We did not find evidence in this sample of human subjects of a robust striatal dopamine change, as was reported in non-human primates. Our preliminary data, requiring extension, suggest that a 3g sedative SO dose might cause slight transient inhibition of dopamine release in limbic striatum.

Objective: Synthetic cannabinoids (SCs) have become increasingly popular in recent years, especially among adolescents. The first aim of the current study was to examine resting-state functional connectivity (rsFC) in SC users compared to controls. Our second aim was to examine the influence of comorbid attention-deficit/hyperactivity disorder (ADHD) symptomatology on rsFC changes in SC users compared to controls.

Methods: Resting-state functional magnetic resonance imaging (fMRI) analysis included 25 SC users (14 without ADHD and 11 with ADHD combined type) and 12 control subjects.

Results: We found (i) higher rsFC between the default mode network (DMN) and salience network, dorsal attention network and cingulo-opercular network, and (ii) lower rsFC within the DMN and between the DMN and visual network in SC users compared to controls. There were no significant differences between SC users with ADHD and controls, nor were there any significant differences between SC users with and without ADHD.

Conclusions: We found the first evidence of abnormalities within and between resting state networks in adolescent SC users without ADHD. In contrast, SC users with ADHD showed no differences compared to controls. These results suggest that comorbidity of ADHD and substance dependence may show different rsFC alterations than substance use alone.