Neuroscience
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Controlled Clinical Trial
Bilateral Prefrontal Cortex Anodal tDCS Effects on Self-reported Aggressiveness in Imprisoned Violent Offenders.
Reduced activity of the frontal lobes, and particularly of the prefrontal cortex, has been related with violent behavior, aggression and crime. The causal importance of prefrontal cortex activity for aggressive behaviors and the self-perception of aggressiveness needs however to be clarified. The aim of this study was to explore the effect of an anodal transcranial direct current stimulation protocol (tDCS, 1.5 mA, 15 min), which, according to previous studies, enhances cortical excitability, applied bilaterally over the prefrontal cortex on self-reported aggressiveness. ⋯ In both inmate groups the results revealed an aggression-reducing effect of tDCS on the Physical aggression, Anger, and Verbal aggression dimensions of the BAQ. In the Hostility dimension, tDCS significantly reduced aggression only in the group of murderers. These results suggest that modulation of prefrontal cortex excitability by 3 consecutive sessions of tDCS reduces self-reported aggressiveness similarly in murderer and non-murderer samples.
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Response preparation in simple reaction time (RT) tasks has been modeled as an increase in neural activation to a sub-threshold level, which is maintained until the go-signal. However, the amount of time required for response preparation following a warning signal (WS) is currently unclear, as experiments typically employ long foreperiods to ensure maximal preparation. The purpose of the present experiments was to examine the time course of motor preparation in a simple RT task when given a limited amount of time to engage in preparatory processing. ⋯ To probe response preparation, a startling acoustic stimulus (SAS), which involuntarily triggers the release of sufficiently prepared responses, was randomly presented during the foreperiod at one of six equally spaced time points between 0 and 500 ms prior to the go-signal. Results showed that the long inter-trial interval was not always effective at preventing participants from engaging in preparatory processing between trials; thus, in Experiment 2 participants performed wrist flexion or extension movements in an instructed delay paradigm, where the required movement was cued by the WS. Results showed that the proportion of startle trials where the intended response was elicited by the SAS at short latency significantly increased until 100 ms prior to the go-signal, indicating response preparation can take up to 300-400 ms following the WS in a simple RT task with a short fixed foreperiod.
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Sensitivity to anticonvulsant effects of the γ-aminobutyric acidA receptor-active neurosteroid allopregnanolone (ALLO) during ethanol withdrawal varies across genotypes, with high sensitivity in genotypes with mild withdrawal and low sensitivity in genotypes with high withdrawal. The present studies determined whether the resistance to ALLO during withdrawal in mouse genotypes with high handling-induced convulsions (HICs) during withdrawal could be overcome with use of ganaxolone (GAN), the metabolically stable derivative of ALLO. In separate studies, male and female Withdrawal Seizure-Prone (WSP-1) and DBA/2J (D2) mice were exposed to air (controls) or 72-h ethanol vapor and then were scored for HICs during withdrawal (hourly for the first 12 h, then at hours 24 and 25). ⋯ AUC was decreased by 81% (males) and 70% (females) in controls and by 35% (males) and 21% (females) during withdrawal. The significant anticonvulsant effect of GAN during withdrawal in D2 but not WSP-1 mice suggests that different mechanisms may contribute to ALLO insensitivity during withdrawal in these two genotypes. Importantly, the results in D2 mice suggest that GAN may be a useful treatment for ethanol withdrawal-induced seizures.
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The use of anabolic androgenic steroids (AASs) among non-athletes is a public health-problem, as abusers underestimate the negative effects associated with these drugs. The present study investigated the toxic effects of testosterone, nandrolone, stanozolol, and trenbolone, and aimed to understand how AAS abuse affects the brain. Mixed cortical cultures from embryonic rats were grown in vitro for 7 days and thereafter treated with increasing concentrations of AASs for 24 h (single-dose) or 3 days (repeated exposure). ⋯ Flutamide almost completely prevented AAS-induced toxicity by maintaining mitochondrial function, cellular integrity, and inhibition of apoptosis. Overall, we found that supra-physiological concentrations of AASs induce cell death in mixed primary cortical cultures, but to different extents, and possibly through various mechanisms. The data presented herein suggest that the molecular interactions of the AASs with the AR are primarily responsible for the toxic outcomes observed.
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B4GALNT1 is an enzyme essential for the synthesis of complex gangliosides, whose absence leads to progressive neurodegeneration with aging in mice. Recently, eleven cases of hereditary spastic paraplegia with mutation in the coding region of B4GALNT1 were reported. However, changes in the enzymatic activity of their products have never been studied. ⋯ Western immunoblotting of cell lysates from transfectants with cDNA plasmids revealed 67-kDa bands except those containing premature termination codons or frame-shift mutation. Taken together with the clinical findings of patients, loss of enzyme activity may be responsible for the clinical features of hereditary spastic paraplegia, whereas the intensity of neurological disorders was relatively milder than expected. These clinical features of patients including those with male hypogonadism are very similar to the abnormal phenotypes detected in B4galnt1-deficient mice.