• Energy Research
• Open Access close
• Restricted close
• FR close
• NL close
• Neuroscience close

Neuroimaging studies have demonstrated gray matter (GM) volume abnormalities in substance users. While the majority of substance users are polysubstance users, very little is known about the relation between GM volume abnormalities and polysubstance use.In this study we assessed the relation between GM volume, and the use of alcohol, tobacco, cocaine and cannabis as well as the total number of substances used, in a sample of 169 males: 15 non-substance users, 89 moderate drinkers, 27 moderate drinkers who also smoke tobacco, 13 moderate drinkers who also smoke tobacco and use cocaine, 10 heavy drinkers who smoke tobacco and use cocaine and 15 heavy drinkers who smoke tobacco, cannabis and use cocaine.Regression analyses showed that there was a negative relation between the number of substances used and volume of the dorsal medial prefrontal cortex (mPFC) and the ventral mPFC. Without controlling for the use of other substances, the volume of the dorsal mPFC was negatively associated with the use of alcohol, tobacco, and cocaine. After controlling for the use of other substances, a negative relation was found between tobacco and cocaine and volume of the thalami and ventrolateral PFC, respectively.These findings indicate that mPFC alterations may not be substance-specific, but rather related to the number of substances used, whereas, thalamic and ventrolateral PFC pathology is specifically associated with tobacco and cocaine use, respectively. These findings are important, as the differential alterations in GM volume may underlie different cognitive deficits associated with substance use disorders.

We present a protocol for the biosensor Cell-Fit-HD4D. It enables long-term monitoring and correlation of single-cell fate with subcellular-deposited energy of ionizing radiation. Cell fate tracking using widefield time-lapse microscopy is uncoupled in time from confocal ion track imaging. Registration of both image acquisition steps allows precise ion track assignment to cells and correlation with cellular readouts. For complete details on the use and execution of this protocol, please refer to Niklas et al. (2022).

γ-aminobutyric acid (GABA) is an amino acid used for mitigating the detrimental effects of heat stress in broilers. In addition, a growing body of literature suggests that the in ovo feeding of various nutrients can enhance the post-hatch thermotolerance of broilers. Therefore, we hypothesized that the supplementation of GABA during incubation might have positive effects in heat-stressed broilers. Chicks hatched from eggs were divided into three groups described as follows: chicks hatched from eggs incubated at normal temperature and then raised under thermoneutral temperature (CON); chicks hatched from eggs incubated at normal temperature but raised under cyclic heat stress (HS) (CON+HS); and chicks hatched from eggs injected with 60 mg of GABA dissolved in 0.6 mL of distilled water but raised under cyclic HS (G10+HS). The HS was applied between 28 and 31 days of age with ambient temperatures raised from 22 ± 1 °C to 33 ± 1 °C for 6 h daily. Compared to the CON group, average daily weight gain was significantly lower in the CON+HS but not in the G10+HS group. Feed intake was significantly decreased in both the CON+HS and G10+HS groups. Compared to the CON group, plasma corticosterone levels were significantly increased in the CON+HS group, but not the G10+HS group. Hepatic mRNA levels of the acetyl-CoA carboxylase gene (ACC) were significantly reduced in the G10+HS group compared to the CON group. In addition, positive Pearson correlation coefficients were found in mRNA levels between fatty acid synthase (FAS) and nicotinamide adenine dinucleotide phosphate oxidase 1 (NOX1) (r = 0.55, p < 0.05), NOX1 and NOX4 (r = 0.65, p < 0.01), and catalase (CAT) and superoxide dismutase (SOD) (r = 0.62, p < 0.05). Taken together, the results suggest that this study can serve as a basis for future work focusing on the in ovo feeding of GABA as a technique to combat heat stress in broilers.

While the harmful effects of alcohol abuse are well documented, experimental and clinical data support a potential benefit of light to moderate alcohol consumption. Cross-sectional studies have suggested an association between alcohol consumption and multiple sclerosis (MS) disability. In the absence of prospective, longitudinal studies, the causal nature of this relationship cannot be established. It remains possible that patients with increased disability progression reduce their alcohol intake. Even though there is substantial evidence for anti-inflammatory effects of low-to-moderate doses of alcohol, the associations need to be interpreted very cautiously. This study discusses the current state of knowledge about MS and alcohol consumption, and the limitations in conducting research with retrospective data in patients with MS.

Prenatal restraint stress (PRS) in rats is associated with hippocampal dysfunctions and several behavioural and endocrine disorders related to this brain area. Recently, we have reported that the PRS modifies the hypothalamic-pituitary-adrenal (HPA) response to an ethanol challenge in adolescent animals. Since hippocampus is particularly sensitive to the deleterious effects of ethanol during adolescence, we investigated in this study the combined effects of PRS and ethanol administration on the oxidative status in the hippocampus of 28-day-old male rats. Thirty minutes after an intraperitoneal (i.p.) injection of ethanol (1.5 g/kg), the activities of several antioxidant enzymes (superoxide dismutase, catalase and glutathione peroxidase) but also non-enzymatic antioxidant (reduced glutathione) were assayed. Thiobarbituric acid reactive substances (TBARS) levels were also measured as a marker of lipid peroxidation. Ethanol enhanced superoxide dismutase activity in control rats but not in PRS rats. At basal level, catalase activity was lower in PRS rats than in control rats, indicating a potentially higher sensitivity to oxidative damages after this early stress. However, the hippocampal TBARS levels were not significantly affected by the ethanol administration, showing that an acute ethanol exposure does not induce oxidative damage in adolescent male rats. In conclusion, our data suggest that PRS affects both basal antioxidant status in the hippocampus and antioxidant response after an acute ethanol exposure. These findings extend previous works showing that PRS leads to hippocampal dysfunctions and raise the question of the potential increase of the hippocampal oxidative damage in PRS rats after repeated exposure to ethanol.

Our study aims at comparing in C57/Bl male mice, the impact of repeated injections of baclofen (an agonist of GABAB receptor) or diazepam (a benzodiazepine acting through a positive allosteric modulation of GABAA receptor) administered during the alcohol-withdrawal period on hippocampus-dependent memory impairments and brain regional glucocorticoid dysfunction after a short (1-week) or a long (4-week) abstinence. Hence, mice were submitted to a 6-month alcohol consumption (12%v/v) and were progressively withdrawn to water. Then, after a 1- or 4-weeks abstinence, they were submitted to a contextual memory task followed by measurements of corticosterone concentrations in the dorsal hippocampus (dHPC), the ventral hippocampus (vHPC) and the prefrontal cortex (PFC). Results showed that 1- and 4-week withdrawn mice exhibited a severe memory deficit and a significant abnormal rise of the test-induced increase of corticosterone (TICC) in the dHPC, as compared to water-controls or to mice still under alcohol consumption. Repeated daily systemic administrations of decreasing doses of diazepam (ranged from 0.5 to 0.12 mg/kg) or baclofen (ranged from 1.5 to 0.37 mg/kg) during the last 15 days of the withdrawal period, normalized both memory and TICC scores in the dHPC in 1-week withdrawn animals; in contrast, only baclofen-withdrawn mice showed both normal memory performance and TICC scores in the dHPC after a 4-week withdrawal period. In conclusion, the memory improvement observed in 4-week withdrawn mice administered with baclofen stem from the protracted normalization of glucocorticoid activity in the dHPC, a phenomenon encountered only transitorily in diazepam-treated withdrawn mice.

Activity pacing (AP) is a concept that is central to many chronic pain theories and treatments, yet there remains confusion regarding its definition and effects.To review the current knowledge concerning AP and integrate this knowledge in a manner that allows for a clear definition and useful directions for future research.A narrative review of the major theoretical approaches to AP and of the empirical evidence regarding the effects of AP interventions, followed by an integrative discussion.The concept of AP is derived from 2 main traditions: operant and energy conservation. Although there are common elements across these traditions, significant conceptual and practical differences exist, which has led to confusion. Little empirical evidence exists concerning the efficacy of AP as a treatment for chronic pain.Future research on AP should be based on a clear theoretical foundation, consider the context in which the AP behavior occurs and the type of pacing problem ("underactivity" vs. "overactivity"), and should examine the impact of AP treatment on multiple clinical outcomes. We provide a provisional definition of AP and specific recommendations that we believe will move the field forward.