Notes

Burping in youngsters: Epidemic as well as association with gastroesophageal regurgitate condition.
In Study 1 (n = 13) we found strong activity for faces in multiple regions, including the previously described temporo-parietal and occipital regions when the control was a mono-colored, homogeneous surface. These differences disappeared in Study 2 (n = 11) when we compared faces to scrambled faces, controlling for low-level visual cues. Our results do not support the assumption that dogs rely on a specialized brain region for processing internal facial characteristics, which is in line with the behavioral findings regarding dogs inability to recognize human faces based on these features. Copyright © 2020 Szabó, Gábor, Gácsi, Faragó, Kubinyi, Miklósi and Andics.Dibutyryl cyclic adenosine monophosphate (dBcAMP) is a cell-permeable synthetic analog of cyclic adenosine monophosphate (cAMP). Although the elevation of cAMP levels was reported to promote the functional recovery in spinal cord injury, its role in neurogenesis or functional recovery after hippocampal injury is unknown. The objective of the study was to investigate the effects of dBcAMP on learning, memory, and hippocampal neurogenesis in the excitotoxically lesioned hippocampus. An excitotoxic lesion was induced in the hippocampi of 4-month-old male BALB/c mice by injecting 0.25 μg/μl into the lateral ventricles of both sides. The lesioned mice (L) were divided into L+dBcAMP and L+phosphate-buffered saline (PBS) groups. Sham surgery (S) was done by the injection of 1 μl of sterile saline into the lateral ventricles. The sham surgery mice were divided into S+dBcAMP and S+PBS groups. Mice in the L+dBcAMP and S+dBcAMP groups were treated with dBcAMP for 1 week (i.p., 50 mg/kg), whereas mice in the L+PBS and S+voidance tests and the number of neurons. In conclusion, dBcAMP protects the hippocampal neuron from degeneration and enhances hippocampal neurogenesis, learning, and memory. Copyright © 2020 Rao and Abd-El-Basset.Evidence regarding the association between early drinking (ED) and later dependence is controversial. It has been alternately hypothesized that ED either plays a causal role in the development of dependence or that it is an early marker of increased psychosocial vulnerabilities. Despite a clear rationale for delaying youth consumption, it is important to discern this relationship. However, most epidemiological evidence comes from individual studies and high-income countries. If there is a causal link between ED and dependence, an association at the aggregate level would be expected. Furthermore, if the link is due to biological mechanisms, the association should be rather invariable regardless of the drinking context, while if the association is due to psychosocial factors, a wider variability is to be expected. We explored whether the association between ED and dependence varied across countries clustered by their shared contextual drinking characteristics. We used data from 169 countries from the Global Inf for females, where no significant relationships were found after adjusting for income level. The association between ED and dependence varies according to the drinking context. Our findings either suggest that the ED-dependence association may be due to individual or environmental vulnerabilities that promote consumption outside cultural norms or that, if there is a causal link between ED and dependence, it is strongly moderated by psychosocial characteristics. Copyright © 2020 Conde, Peltzer, Gimenez and Cremonte.How are the complex maps for orientation selectivity (OS) created in the primary visual cortex (V1)? Rodents and rabbits have a random distribution of OS preferences across V1 while in cats, ferrets, and all primates cells with similar OS preferences cluster together into relatively wide cortical columns. Given other clear similarities in the organization of the visual pathways, why is it that maps coding OS preferences are so radically different? Prominent models have been created of cortical OS mapping that incorporate Hebbian plasticity, intracortical interactions, and the properties of growing axons. However, these models suggest that the maps arise primarily through intracortical interactions. Here we focus on several other features of the visual system and brain that may influence V1 structure. These are eye divergence, the total number of cells in V1, the thalamocortical networks, the topography of the retina and phylogeny. We outline the evidence for and against these factors contributing to map formaout the map structures of these species based on the organization of their brains and visual systems and, in doing so, set possible paths for future research. Copyright © 2020 Ibbotson and Jung.The propensity to engage in risky behaviors including excessive alcohol consumption may impose increased medical, emotional, and psychosocial burdens. Personality and behavioral traits of individuals may contribute in part to the involvement in risky behaviors, and therefore the classification of one's traits may help identify those who are at risk for future onset of the addictive disorder and related behavioral issues such as alcohol misuse. Personality and behavioral characteristics including impulsivity, anger, reward sensitivity, and avoidance were assessed in a large sample of healthy young adults (n = 475). Participants also underwent diffusion tensor imaging for the analysis of structural brain networks. A data-driven clustering using personality and behavioral traits of the participants identified four subtypes. As compared with individuals clustered into the neutral type, individuals with a high level of impulsivity (A subtype) and those with high levels of reward sensitivity, impulsivity, anger, anght © 2020 Yoon, Kim, Hong, Kim, Hong, Ha, Ma and Lyoo.Analog-digital facilitations (ADFs) have been described in local excitatory brain circuits and correspond to a class of phenomena describing how subthreshold variations of the presynaptic membrane potential influence spike-evoked synaptic transmission. In many brain circuits, ADFs rely on the propagation of somatic membrane potential fluctuations to the presynaptic bouton where they modulate ion channels availability, inducing modifications of the presynaptic spike waveform, the spike-evoked Ca2+ entry, and the transmitter release. Therefore, one major requirement for ADFs to occur is the propagation of subthreshold membrane potential variations from the soma to the presynaptic bouton. To date, reported ADFs space constants are relatively short (250-500 μm) which limits their action to proximal synapses. However, ADFs have been studied either in unmyelinated axons or in juvenile animals in which myelination is incomplete. We examined here the potential gain of ADFs spatial extent caused by myelination using a realistic model of L5 pyramidal cell. Myelination of the axon was found to induce a 3-fold increase in the axonal length constant. As a result, the different forms of ADF were found to display a much longer spatial extent (up to 3,000 μm). In addition, while the internodal length displayed a mild effect, the number of myelin wraps ensheathing the internodes was found to play a critical role in the ADFs spatial extents. We conclude that axonal myelination induces an increase in ADFs spatial extent in our model, thus making ADFs plausible in long-distance connections. Copyright © 2020 Zbili and Debanne.Exposure to toxic metals and metalloids is an important cause of preventable diseases worldwide. Inorganic arsenic (iAs) affects several organs and tissues, causing neurobehavioral alterations in the central nervous system (CNS) that might lead to neurodegeneration. In this work, we wanted to explore the time- and dose-related changes on glutathione (GSH) levels in several regions of the CNS, such as the cortex, striatum, hippocampus, and cerebellum, to identify the initial cellular changes associated to GSH depletion due to iAs exposure. Selleck Vorinostat Mice received a single intraperitoneal injection containing 5 or 14 mg/kg sodium arsenite. Animals were killed at 2, 6, and 24 h. Significant depletion of GSH levels was observed in the cortex at 2 and 6 h, while on the striatum, hippocampus, or cerebellum regions, no significant changes were observed. GSH depletion in the cortex was associated with the activation of the nuclear factor erythroid 2-related factor 2 (Nrf2) and nuclear factor kappa B (NFκB) pathways, which led to the upregulation of xCT, excitatory amino acid carrier 1 (EAAC1), glutamate/aspartate transporter (GLAST), and glial glutamate transporter 1 (GLT-1), and the activation of the transsulfuration pathways, which led to the overproduction of H2S in the cortex and increased levels of GSH in the cortex and cerebellum at 24 h. In the cortex, the N-methyl-D-aspartate (NMDA) receptor subunits NR2A and NR2B were also altered at 24 h. These early effects were not homogeneous among different brain regions and indicate early neurotoxic alterations in the cortex and cerebellum. Copyright © 2020 Silva-Adaya, Ramos-Chávez, Petrosyan, González-Alfonso, Pérez-Acosta and Gonsebatt.The cerebral ischemia injury can result in neuronal death and/or functional impairment, which leads to further damage and dysfunction after recovery of blood supply. Cerebral ischemia/reperfusion injury (CIRI) often causes irreversible brain damage and neuronal injury and death, which involves many complex pathological processes including oxidative stress, amino acid toxicity, the release of endogenous substances, inflammation and apoptosis. Oxidative stress and inflammation are interactive and play critical roles in ischemia/reperfusion injury in the brain. Oxidative stress is important in the pathological process of ischemic stroke and is critical for the cascade development of ischemic injury. Oxidative stress is caused by reactive oxygen species (ROS) during cerebral ischemia and is more likely to lead to cell death and ultimately brain death after reperfusion. During reperfusion especially, superoxide anion free radicals, hydroxyl free radicals, and nitric oxide (NO) are produced, which can cause lipid peroxidation, inflammation and cell apoptosis. Inflammation alters the balance between pro-inflammatory and anti-inflammatory factors in cerebral ischemic injury. Inflammatory factors can therefore stimulate or exacerbate inflammation and aggravate ischemic injury. Neuroprotective therapies for various stages of the cerebral ischemia cascade response have received widespread attention. At present, neuroprotective drugs mainly include free radical scavengers, anti-inflammatory agents, and anti-apoptotic agents. However, the molecular mechanisms of the interaction between oxidative stress and inflammation, and their interplay with different types of programmed cell death in ischemia/reperfusion injury are unclear. The development of a suitable method for combination therapy has become a hot topic. Copyright © 2020 Wu, Xiong, Wu, Ye, Jian, Zhi and Gu.Trace amine-associated receptors (TAARs) are a class of G-protein-coupled receptors found in mammals. While TAAR1 is expressed in several brain regions, all the other TAARs have been described mainly in the olfactory epithelium and the glomerular layer of the olfactory bulb and are believed to serve as a new class of olfactory receptors sensing innate odors. However, there is evidence that TAAR5 could play a role also in the central nervous system. In this study, we characterized a mouse line lacking TAAR5 (TAAR5 knockout, TAAR5-KO) expressing beta-galactosidase mapping TAAR5 expression. We found that TAAR5 is expressed not only in the glomerular layer in the olfactory bulb but also in deeper layers projecting to the limbic brain olfactory circuitry with prominent expression in numerous limbic brain regions, such as the anterior olfactory nucleus, the olfactory tubercle, the orbitofrontal cortex (OFC), the amygdala, the hippocampus, the piriform cortex, the entorhinal cortex, the nucleus accumbens, and the thalamic and hypothalamic nuclei.
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