Substance use disorders involve long-term changes in the brain that lead to compulsive drug seeking, craving, and a high probability of relapse. Recent findings have highlighted the role of epigenetic regulations in controlling chromatin access and regulation of gene expression following exposure to drugs of abuse. In the present review, we focus on data investigating genome-wide epigenetic modifications in the brain of addicted patients or in rodent models exposed to drugs of abuse, with a particular focus on DNA methylation and histone modifications associated with transcriptional studies. We highlight critical factors for epigenomic studies in addiction. We discuss new findings related to psychostimulants, alcohol, opiate, nicotine and cannabinoids. We examine the possible transmission of these changes across generations. We highlight developing tools, specifically those that allow investigation of structural reorganization of the chromatin. These have the potential to increase our understanding of alteration of chromatin architecture at gene regulatory regions. Neuroepigenetic mechanisms involved in addictive behaviors could explain persistent phenotypic effects of drugs and, in particular, vulnerability to relapse.

The retinoid family members, including vitamin A and derivatives like 13-cis-retinoic acid (ITT) and all-trans retinoic acid (ATRA), are essential for normal functioning of the developing and adult brain. When vitamin A intake is excessive, however, or after ITT treatment, increased risks have been reported for depression and suicidal ideation. Here, we review pre-clinical and clinical evidences supporting association between retinoids and depressive disorders and discuss several possible underlying neurobiological mechanisms. Clinical evidences include case reports and studies from healthcare databases and government agency sources. Preclinical studies further confirmed that RA treatment induces hyperactivity of the hypothalamus-pituitary-adrenal (HPA) axis and typical depressive-like behaviors. Notably, the molecular components of the RA signaling are widely expressed throughout adult brain. We further discuss three most important brain systems, hippocampus, hypothalamus and orbitofrontal cortex, as major brain targets of RA. Finally, we highlight altered monoamine systems in the pathophysiology of RA-associated depression. A better understanding of the neurobiological mechanisms underlying RA-associated depression will provide new insights in its etiology and development of effective intervention strategies.

Introduction: Persistent tic disorders (PTDs) and attention-deficit hyperactivity disorder (ADHD) are common neurodevelopmental conditions which tend to co-occur. Both diagnoses are associated with sleep problems. This systematic review and meta-analysis investigates overlaps and distinctions in objective sleep parameters based on diagnosis (PTD-only, PTD + ADHD, and ADHD-only). Methods: Databases were searched to identify studies with objective sleep measures in each population. Metaanalyses were conducted using a random effects model. Results: Polysomnography was the only measure included in all three groups. Twenty studies met final inclusion criteria, combining PTD-only (N = 108), PTD + ADHD (N = 79), and ADHD-only (N = 316). Compared to controls (N = 336), PTD-only and PTD + ADHD groups had significantly lower sleep efficiency and higher sleep onset latency. PTD + ADHD also had significantly increased time in bed and total sleep time. No significant differences were observed between ADHD-only groups and controls. Discussion: Different sleep profiles appear to characterise each population. PTD + ADHD was associated with more pronounced differences. Further research is required to elucidate disorder-specific sleep problems, ensuring appropriate identification and monitoring of sleep in clinical settings.

This review presents state-of-the-art knowledge about the roles of the basal ganglia (BG) in action-selection, cognition, and motivation, and how this knowledge has been used to improve deep brain stimulation (DBS) treatment of neurological and psychiatric disorders. Such pathological conditions include Parkinson's disease, Huntington's disease, Tourette syndrome, depression, and obsessive-compulsive disorder. The first section presents evidence supporting current hypotheses of how the cortico-BG circuitry works to select motor and emotional actions, and how defects in this circuitry can cause symptoms of the BG diseases. Emphasis is given to the role of striatal dopamine on motor performance, motivated behaviors and learning of procedural memories. Next, the use of cutting-edge electrochemical techniques in animal and human studies of BC functioning under normal and disease conditions is discussed. Finally, functional neuroimaging studies are reviewed; these works have shown the relationship between cortico-BG structures activated during DBS and improvement of disease symptoms. (C) 2015 Elsevier Ltd. All rights reserved.

Serotonin plays a modulatory role in central control of the autonomic nervous system (ANS). The nucleus tractus solitarii (NTS) in the medulla is an area of viscerosomatic integration innervated by both central and peripheral serotonergic fibers. Influences from different origins therefore trigger the release of serotonin into the NTS and exert multiple influences on the ANS. This major influence on the ANS is also mediated by activation of several receptors in the NTS. In particular, the NTS is the central zone with the highest density of serotonin(3) (5-HT3) receptors. In this review, we present evidence that 5-HT3 receptors in the NTS play a key role in one of the crucial homeostatic responses to acute and chronic stress: inhibitory modulation of the parasympathetic component of the ANS. The possible functional interactions of 5-(HT3) receptors with GABA(A) and NK1 receptors in the NTS are also discussed. (C) 2016 Elsevier Ltd. All rights reserved.

Intellectual disability (ID) and autism spectrum disorder (ASD) are the most common developmental disorders present in humans. Combined, they affect between 3 and 5% of the population. Additionally, they can be found together in the same individual thereby complicating treatment. The causative factors (genes, epigenetic and environmental) are quite varied and likely interact so as to further complicate the assessment of an individual patient. Nonetheless, much valuable information has been gained by identifying candidate genes for ID or ASD. Understanding the etiology of either ID or ASD is of utmost importance for families. It allows a determination of the risk of recurrence, the possibility of other comorbidity medical problems, the molecular and cellular nature of the pathobiology and hopefully potential therapeutic approaches. (C) 2014 Elsevier Ltd. All rights reserved.