Neuroscience
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Epilepsy is one of the most common chronic neurological diseases. It is characterized by recurrent epileptic seizures, where one-third of patients are refractory to existing treatments. Evidence revealed the association between neuroinflammation and increased susceptibility to seizures since there is a pronounced increase in the expression of key inflammatory mediators, such as prostaglandin E2 (PGE2), during seizures. ⋯ Indeed, galangin prevented behavioral and electroencephalographic seizures, reactive species production, decreased microglial and astrocytic immunocontent, as well as decreased VCAM-1 immunocontent and p-PKA/PKA ratio induced by PGE2/PTZ. Therefore, this study suggests galangin may have an antagonizing role on PGE2-induced effects, reducing cerebral inflammation and protecting from excitatory effects evidenced by administrating PGE2 and PTZ. However, further studies are needed to investigate the clinical implications of the findings and their underlying mechanisms.
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Decision-making in the mammalian brain typically involves multiple brain structures within the midbrain, thalamus, striatum, limbic system, and cortex. Although task specific contributions of each brain region have been identified, neurons responding to reinforcement have been found throughout these structures. We sought to determine if any brain area, or cluster of areas, are the source of information, and if the fidelity of information varies among the areas. ⋯ Analysis of FPs prior to reward revealed most regions reflected the prior probability of reward. Lastly, analyses of information flow suggested reinforcement information does not originate within a single structure of the network, within the resolution afforded by FP recordings. These data suggest reward delivery information is rapidly distributed non-uniformly across the network, and there is no canonical flow of information about reward events in the recorded structures.
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Rett Syndrome (RTT) is a neurological disorder mainly associated with mutations in the X-linked gene coding for the methyl-CpG binding protein 2 (MECP2). To assist in studying MECP2's function, researchers have generated Mecp2 mouse mutants showing that MECP2's product (MeCP2) mostly functions as a transcriptional regulator. ⋯ In the present review, we describe the findings of these transcriptomic studies, and highlight differences between them, and discuss how studies on these genetic models can sharpen our understanding of the human disorder. We conclude that - while there's large variability regarding the number of differentially expressed genes identified - there are overlapping features that inform on the biology of RTT.
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Genetic factors significantly contribute to the risk for developing alcoholism. To study these factors and other associated phenotypes, rodent lines have been developed using selective breeding for high alcohol preference. One of these models, the alcohol preferring (P) rat, has been used in hundreds of preclinical studies over the last few decades. ⋯ Intra-CeA infusion of NK1R antagonist attenuates yohimbine-induced reinstatement in P rats. Conversely, upregulation of NK1R within the CeA of Wistar rats increases alcohol consumption and sensitivity to yohimbine-induced reinstatement. These findings suggest that NK1R upregulation in the CeA contributes to multiple alcohol-related phenotypes in the P rat, including alcohol consumption and sensitivity to relapse.
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Few animal studies focus on consequences of nicotine postnatal exposure, particularly through lactation. We have recently shown that forced nicotine drinking elevates maternal care, paradoxically provoking arousal and stress in pups. Present work aimed to evaluate the specific contribution of altered maternal cares, compared to the sequelae merely due to nicotine effects. ⋯ Brain analyses at adulthood suggest that, in prefrontal cortex, nicotine per se reduced serotonin, while the maternal overcare reduced CHRN-B2 gene-expression. As a whole, unescapable nicotine-enhanced maternal care could have an impact on the offspring arousal by acting on prefrontal CHRN-B2 gene-expression. When present results are translated to consequences of non-voluntary exposure in humans, we propose that children receiving altered attentions by a smoking caregiver might undergo a neuro-behavioural development biased towards emotional shyness.