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Abstract Background Athletes are expected to consider multiple factors when making informed decision about nutritional supplement use. Besides rules, regulations and potential health hazards, the efficacy of different nutritional supplements in performance enhancement is a key issue. The aim of this paper was to find evidence for informed decision making by investigating the relationship between specific performance-related reasons for supplement use and the reported use of nutritional supplements. Methods The 'UK Sport 2005 Drug Free Survey' data (n = 874) were re-analysed using association [χ2] and 'strength of association' tests [ϕ] to show the proportion of informed choices and to unveil incongruencies between self-reported supplement use and the underlying motives. Results Participants (n = 520) reported supplement use in the pattern of: vitamin C (70.4%), creatine (36.1%), whey protein (30.6%), iron (29.8%), caffeine (23.8%), and ginseng (8.3%) for the following reasons: strength maintenance (38.1%), doctors' advice (24.2%), enhancing endurance (20.0%), ability to train longer (13.3%), and provided by the governing body (3.8%). Of thirty possible associations between the above supplements and reasons, 11 were predictable from literature precedents and only 8 were evidenced and these were not strong (ϕ < .7). The best associations were for the ability to train longer with creatine (reported by 73.9%, χ2 = 49.14, p < .001; ϕ = .307, p < .001), and maintaining strength with creatine (reported by 62.6%, χ2 = 97.08, p < .001; ϕ = .432, p < .001) and whey protein (reported by 56.1%, χ2 = 97.82, p < .001; ϕ = .434, p < .001). Conclusion This study provided a platform for assessing congruence between athletes' reasons for supplement use and their actual use. These results suggest that a lack of understanding exists in supplement use. There is an urgent need to provide accurate information which will help athletes make informed choices about the use of supplements.

Abstract Background The widespread use of nutritional supplements among athletes is poorly understood. The prevalence of supplement intake and users' knowledge have been researched independently leading to useful, but disconnected, information on supplement use. Methods The 'UK Sport 2005 Drug Free Survey' data (n = 874) were re-analysed using association [χ2] and 'strength of association' tests [φ], to discover observed incongruencies between self-reported supplement use and the underlying motives. Results are given for test pairs between 'motive for use' [doctor's advice, avoiding sickness, overcoming injuries and enhancement of diet] and each supplement used and these were categorized as strong (φ > .7), intermediate (7 < φ > .3) and weak (φ < .3). Results The use of selected supplements varied widely as follows: multivitamin (72.7%), vitamin C (70.4%), echinacea (30.8%), iron (29.8%), magnesium (11.0%) and ginseng (8.3%). Associations with motive were found in 8 of the 10 test pairs which were expected from literature precedents, however only weak associations exist. Of these, four were associated with avoidance of sickness [iron (χ2 = 11.94, p < .001; φ = .15, p = .001), multivitamin (χ2 = 6.43, p < .001; φ = .11, p = .011), vitamin C (χ2 = 54.67, p < .001; φ = .32, p < .001) and echinacea (χ2 = 40.34, p < .001; φ = .28, p < .001)]. The remaining 4 associations were: no time to prepare meals with ginseng (χ2 = 7.64, p = .006; φ = .12, p = .006) and multivitamin (χ2 = 9.103, p = .003; φ = .13, p = .003); overcoming injuries with magnesium (χ2 = 6.99, p = .008; φ = .11, p = .008); doctors' advice and iron (χ2 = 35.00, p < .001; φ = .25, p = .001). Conclusion These results suggest a lack of understanding regarding supplements and health maintenance, except for vitamin C and echinacea. Furthermore, supplement use is apparently independent of physicians/dieticians' advice, except for iron. This may suggest a widespread circumvention of expert advice in the growing area of supplement use and therefore should be addressed to underscore potential health risks.

Among the central goals of stress neurobiology research is to understand the mechanisms by which stressors change neural circuit function to precipitate or exacerbate psychiatric symptoms. Yet despite decades of effort, psychiatric medications that target the biological substrates of the stress response are largely lacking. We propose that the clinical advancement of stress response-based therapeutics for psychiatric disorders may be hindered by 'hidden variables' in stress research, including considerations of behavioral study design (stressors and outcome measures), individual variability, sex differences, and the interaction of the body's stress hormone system with endogenous circadian and ultradian rhythms. We highlight key issues and suggest ways forward in stress neurobiology research that may improve the ability to assess stress mechanisms and translate preclinical findings., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2023 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Major depressive disorder (MDD) is a leading cause of disability worldwide. Individuals with MDD exhibit decreased motivation and deficits in reward processing. In a subset of MDD patients, chronic dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis occurs, resulting in increased levels of the 'stress hormone' cortisol during the normal rest period (i.e., evening and night). However, the mechanistic relationship between chronically elevated resting cortisol and behavioral deficits in motivation and reward processing remains unclear. Given that women are diagnosed with MDD at twice the rate of men, it is important to understand whether the mechanisms linking cortisol to the symptoms of MDD differ by sex. In this study, we used subcutaneous implants to chronically elevate free plasma corticosterone (the rodent homolog of cortisol; 'CORT') during the rest period in male and female mice and examined changes in behavior and dopamine system function. We found that chronic CORT treatment impaired motivated reward-seeking in both sexes. In female but not male mice, CORT treatment reduced dopamine content in the dorsomedial striatum (DMS). In male but not female mice, CORT treatment impaired the function of the dopamine transporter (DAT) in DMS. From these studies, we conclude that chronic CORT dysregulation impairs motivation by impairing dopaminergic transmission in the DMS, but via different mechanisms in male and female mice. A better understanding of these sex-specific mechanisms could lead to new directions in MDD diagnosis and treatment., (© 2023. The Author(s).)

Dopamine neurons have been intensely studied for their roles in reinforcement learning. A dominant theory of how these neurons contribute to learning is through the encoding of a reward prediction error (RPE) signal. Recent advances in dopamine research have added nuance to RPE theory by incorporating the ideas of sensory prediction error, distributional encoding, and belief states. Further nuance is likely to be added shortly by convergent lines of research on dopamine neuron diversity. Finally, a major challenge is to reconcile RPE theory with other current theories of dopamine function to account for dopamine's role in movement, motivation, and goal-directed planning., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

New studies examine how the different sub-structures in the cerebellum are organized to receive information during complex behavioral tasks., Competing Interests: AH, TL No competing interests declared, (© 2019, Holloway and Lerner.)

Depression after traumatic brain injury (TBI) is common but the mechanisms by which TBI causes depression are unknown. TBI decreases glutamate transporters GLT-1 and GLAST and allows extravasation of thrombin. We examined the effects of thrombin on transporter expression in primary hippocampal astrocytes. Application of a PAR-1 agonist caused down-regulation of GLT-1, which was prevented by inhibition of Rho kinase (ROCK). To confirm these mechanisms in vivo, we subjected mice to closed-skull TBI. Thrombin activity in the hippocampus increased one day following TBI. Seven days following TBI, expression of GLT-1 and GLAST was reduced in the hippocampus, and this was prevented by administration of the PAR-1 antagonist SCH79797. Inhibition of ROCK attenuated the decrease in GLT-1, but not GLAST, after TBI. We measured changes in glutamate levels in the hippocampus seven days after TBI using an implanted biosensor. Stress-induced glutamate levels were significantly increased following TBI and this was attenuated by treatment with the ROCK inhibitor fasudil. We quantified depressive behavior following TBI and found that inhibition of PAR-1 or ROCK decreased these behaviors. These results identify a novel mechanism by which TBI results in down-regulation of astrocyte glutamate transporters and implicate astrocyte and glutamate transporter dysfunction in depression following TBI.

Transcranial direct current stimulation (tDCS) is a popular brain stimulation method that is used to modulate cortical excitability, producing facilitatory or inhibitory effects upon a variety of behaviors. There is, however, a current lack of consensus between studies, with many results suggesting that polarity-specific effects are difficult to obtain. This article explores some of these differences and highlights the experimental parameters that may underlie their occurrence. We provide a general, practical snapshot of tDCS methodology, including what it is used for, how to use it, and considerations for designing an effective and safe experiment. Our aim is to equip researchers who are new to tDCS with the essential knowledge so that they can make informed and well-rounded decisions when designing and running successful experiments. By summarizing the varied approaches, stimulation parameters, and outcomes, this article should help inform future tDCS research in a variety of fields.

Recent evidence suggests that wheel running can abolish conditioned place preference (CPP) for cocaine in mice. Running significantly increases the number of new neurons in the hippocampus, and new neurons have been hypothesised to enhance plasticity and behavioral flexibility. Therefore, we tested the hypothesis that increased neurogenesis was necessary for exercise to abolish cocaine CPP. Male nestin-thymidine kinase transgenic mice were conditioned with cocaine, and then housed with or without running wheels for 32 days. Half of the mice were fed chow containing valganciclovir to induce apoptosis in newly divided neurons, and the other half were fed standard chow. For the first 10 days, mice received daily injections of bromodeoxyuridine (BrdU) to label dividing cells. On the last 4 days, mice were tested for CPP, and then euthanized for measurement of adult hippocampal neurogenesis by counting the number of BrdU-positive neurons in the dentate gyrus. Levels of running were similar in mice fed valganciclovir-containing chow and normal chow. Valganciclovir significantly reduced the numbers of neurons (BrdU-positive/NeuN-positive) in the dentate gyrus of both sedentary mice and runner mice. Valganciclovir-fed runner mice showed similar levels of neurogenesis as sedentary, normal-fed controls. However, valganciclovir-fed runner mice showed the same abolishment of CPP as runner mice with intact neurogenesis. The results demonstrate that elevated adult hippocampal neurogenesis resulting from running is not necessary for running to abolish cocaine CPP in mice., (© 2014 Federation of European Neuroscience Societies and John Wiley & Sons Ltd.)

Daily levels of physical activity vary greatly across individuals and are strongly influenced by genetic background. While moderate levels of physical activity are associated with improved physical and mental health, extremely high levels of physical activity are associated with behavioral disorders such as attention deficit hyperactivity disorder (ADHD). However, the genetic and neurobiological mechanisms relating hyperactivity to ADHD or other behavioral disorders remain unclear. Therefore, we conducted a selective breeding experiment for increased home cage activity starting with a highly genetically variable population of house mice and evaluated the line for correlated responses in other relevant phenotypes. Here we report results through Generation 10. Relative to the Control line, the High-Active line traveled approximately 4 times as far in the home cage (on days 5 and 6 of a 6-day test), displayed reduced body mass at maturity, reduced reproductive success, increased wheel running and open field behavior, decreased performance on the rotarod, decreased performance on the Morris water maze that was not rescued by acute administration of d-amphetamine, reduced hyperactivity from chronically administered low clinical doses of d-amphetamine, and increased numbers of new cells and neuronal activation of the dentate gyrus. Standardized phenotypic differences between the lines were compared to estimates expected from genetic drift to evaluate whether the line differences could have resulted from random effects as opposed to correlated responses to selection. Results indicated line differences in body mass and locomotor responses to low doses of amphetamine were more likely due to selection than drift. The efficacy of low doses of d-amphetamine in ameliorating hyperactivity support the High-Active line as a useful model for exploring the etiology of hyperactivity-associated comorbid behavioral disorders.

Absolute quantum yields for the radical (H + HCO) channel of HCHO photolysis, Phi(HCO), have been measured for the tropospherically relevant range of wavelengths (lambda) between 300 and 330 nm. The HCO photoproduct was directly detected by using a custom-built, combined ultra-violet (UV) absorption and cavity ring down (CRD) detection spectrometer. This instrument was previously employed for high-resolution (spectral resolution approximately 0.0035 nm) measurements of absorption cross-sections of HCHO, sigma(HCHO)(lambda), and relative HCO quantum yields. Absolute Phi(HCO) values were measured at seven wavelengths, lambda = 303.70, 305.13, 308.87, 314.31, 320.67, 325.59, and 329.51 nm, using an independent calibration technique based on the simultaneous UV photolysis of HCHO and Cl(2). These Phi(HCO) measurements display greater variability as a function of wavelength than the current NASA-JPL recommendations for Phi(HCO). The absolute Phi(HCO)(lambda) determinations and previously measured sigma(HCHO)(lambda) were used to scale an extensive set of relative HCO yield measurements. The outcome of this procedure is a full suite of data for the product of the absolute radical quantum yield and HCHO absorption cross-section, Phi(HCO)(lambda)sigma(HCHO)(lambda), at wavelengths from 302.6 to 331.0 nm with a wavelength resolution of 0.005 nm. This product of photochemical parameters is combined with high-resolution solar photon flux data to calculate the integrated photolysis rate of HCHO to the radical (H + HCO) channel, J(HCO). Comparison with the latest NASA-JPL recommendations, reported at 1 nm wavelength resolution, suggests an increased J(HCO) of 25% at 0 degrees solar zenith angle (SZA) increasing to 33% at high SZA (80 degrees). The differences in the calculated photolysis rate compared with the current HCHO data arise, in part, from the higher wavelength resolution of the current data set and highlight the importance of using high-resolution spectroscopic techniques to achieve a complete and accurate picture of HCHO photodissociation processes. All experimental Phi(HCO)(lambda)sigma(HCHO)(lambda) data are available for the wavelength range 302.6-331.0 nm (at 294 and 245 K and under 200 Torr of N(2) bath gas) as Supporting Information with wavelength resolutions of 0.005, 0.1, and 1.0 nm. Equivalent data sets of Phi(H(2)+CO)(lambda)sigma(HCHO)(lambda) for the molecular (H(2) + CO) photofragmentation channel, produced using the measured Phi(HCO)(lambda) sigma(HCHO)(tau) values, are also provided at 0.1 and 1.0 nm resolution.