Abstract: Objective: To assess the neural activity associated with mindfulness-based alterations of pain perception. Methods: The Cochrane Central, EMBASE, Ovid Medline, PsycINFO, Scopus, and Web of Science databases were searched on 2 February 2016. Titles, abstracts, and full-text articles were independently screened by two reviewers. Data were independently extracted from records that included topics of functional neuroimaging, pain, and mindfulness interventions. Results: The literature search produced 946 total records, of which five met the inclusion criteria. Records reported pain in terms of anticipation (n = 2), unpleasantness (n = 5), and intensity (n = 5), and how mindfulness conditions altered the neural activity during noxious stimulation accordingly. Conclusions: Although the studies were inconsistent in relating pain components to neural activity, in general, mindfulness was able to reduce pain anticipation and unpleasantness ratings, as well as alter the corresponding neural activity. The major neural underpinnings of mindfulness-based pain reduction consisted of altered activity in the anterior cingulate cortex, insula, and dorsolateral prefrontal cortex.
Abstract: Perineuronal nets (PNNs) are specialized extracellular matrix molecules that are associated with the closing of the critical period, among other functions. In the adult brain, PNNs surround specific types of neurons, however the expression of PNNs in the auditory system of the mouse, particularly at the level of the midbrain and forebrain, has not been fully described. In addition, the association of PNNs with excitatory and inhibitory cell types in these structures remains unknown. Therefore, we sought to investigate the expression of PNNs in the inferior colliculus (IC), thalamic reticular nucleus (TRN) and primary auditory cortex (A1) of the mouse brain by labeling with wisteria floribunda agglutinin (WFA). To aid in the identification of inhibitory neurons in these structures, we employed the vesicular GABA transporter (VGAT)-Venus transgenic mouse strain, which robustly expresses an enhanced yellow-fluorescent protein (Venus) natively in nearly all gamma-amino butyric acid (GABA)-ergic inhibitory neurons, thus enabling a rapid and unambiguous assessment of inhibitory neurons throughout the nervous system. Our results demonstrate that PNNs are expressed throughout the auditory midbrain and forebrain, but vary in their local distribution. PNNs are most dense in the TRN and least dense in A1. Furthermore, PNNs are preferentially associated with inhibitory neurons in A1 and the TRN, but not in the IC of the mouse. These data suggest regionally specific roles for PNNs in auditory information processing.
Abstract: Alcohol consumption during pregnancy and its damaging consequences on the developing infant brain are significant public health, social, and economic issues. The major distinctive features of prenatal alcohol exposure in humans are cognitive and behavioral dysfunction due to damage to the central nervous system (CNS), which results in a continuum of disarray that is collectively called fetal alcohol spectrum disorder (FASD). Many rodent models have been developed to understand the mechanisms of and to reproduce the human FASD phenotypes. These animal FASD studies have provided several molecular pathways that are likely responsible for the neurobehavioral abnormalities that are associated with prenatal alcohol exposure of the developing CNS. Recently, many laboratories have identified several immediate, as well as long-lasting, epigenetic modifications of DNA methylation, DNA-associated histone proteins and microRNA (miRNA) biogenesis by using a variety of epigenetic approaches in rodent FASD models. Because DNA methylation patterns, DNA-associated histone protein modifications and miRNA-regulated gene expression are crucial for synaptic plasticity and learning and memory, they can therefore offer an answer to many of the neurobehavioral abnormalities that are found in FASD. In this review, we briefly discuss the current literature of DNA methylation, DNA-associated histone proteins modification and miRNA and review recent developments concerning epigenetic changes in FASD.
Abstract: In the past twenty years, evidence of neurotoxicity in the developing brain in animal studies from exposure to several general anesthetics has been accumulating. Propofol, a commonly used general anesthetic medication, administered during synaptogenesis, may trigger widespread apoptotic neurodegeneration in the developing brain and long-term neurobehavioral disturbances in both rodents and non-human primates. Despite the growing evidence of the potential neurotoxicity of different anesthetic agents in animal studies, there is no concrete evidence that humans may be similarly affected. However, given the growing evidence of the neurotoxic effects of anesthetics in laboratory studies, it is prudent to further investigate the mechanisms causing these effects and potential ways to mitigate them. Here, we review multiple studies that investigate the effects of in utero propofol exposure and the developmental agents that may modify these deleterious effects.
Abstract: Visual perception is constructive in nature; that is, a coherent whole is generated from ambiguous fragments that are encountered in dynamic visual scenes. Creating this coherent whole from fragmented sensory inputs requires one to detect, identify, distinguish and organize sensory input. The organization of fragments into a coherent whole is facilitated by the continuous interactions between lower level sensory inputs and higher order processes. However, age-related declines are found in both neural structures and cognitive processes (e.g., attention and inhibition). The impact of these declines on the constructive nature of visual processing was the focus of this study. Here we asked younger adults, young-old (65–79 years), and old-old adults (80+ years) to view a multistable figure (i.e., Necker cube) under four conditions (free, priming, volition, and adaptation) and report, via a button press, when percepts spontaneously changed. The oldest-olds, unlike young-olds and younger adults, were influenced by priming, had less visual stability during volition and showed less ability to adapt to multistable stimuli. These results suggest that the ability to construct a coherent whole from fragments declines with age. More specifically, vision is constructed differently in the old-olds, which might influence environmental interpretations and navigational abilities in this age group.
Abstract: (1) Background: Hyperkinetic syndrome of childhood (HKSoC) is an International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9) category in which the majority of the children are also diagnosed under the Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, Text Revision (DSM-IV-TR), where the umbrella term is “Attention-Deficit and Disruptive Behavior Disorders”. The diagnostic criteria for HKSoC are developmentally inappropriate inattention, hyperactivity, and impulsivity. Some studies have implicated mercury (Hg) exposure as a risk factor. (2) Methods: This hypothesis testing study; using the Vaccine Safety Datalink; assessed the toxicological effects of bolus exposure to organic-Hg from Thimerosal-containing vaccines (TCVs) by examining the relationship between Thimerosal-preserved hepatitis B vaccines (TM-HepB) given at varying levels and at specific intervals in the first six months after birth and the risk of a child being diagnosed with HKSoC. (3) Results: Children diagnosed with HKSoC were significantly more likely to be exposed to increased organic-Hg from TM-HepB doses given within the first month (odds ratio = 1.45; 95% confidence interval (CI) = 1.30–1.62); within the first two months (odds ratio = 1.43; 95% CI = 1.28–1.59); and within the first six months (odds ratio = 4.51; 95% CI = 3.04–6.71) than controls. (4) Conclusion: The results indicate that increasing organic-Hg exposure from TCVs heightens the risk of a HKSoC diagnosis.