Neuroscience
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The adverse consequences of early-life sleep deprivation on mental health are well recognized, yet many aspects remain unknown, therefore, animal studies can offer useful insights. Male Sprague-Dawley rats at postnatal day (PND) 19 were subjected to sleep deprivation (SD) for 14 days (6-8 hours/day). Control (CON) rats were gently handled. ⋯ Our postulation is that SD by increasing PFC oxido-inflammation, negatively affects glutamate receptor subunits and PSD95 expression, which disrupts synapse formation and maturation, potentially causing anxiety-like behavior at PND33. Oxido-inflammation further results in MKP-1 and CaMKII-mediated blockade of ERK1/2 activation, which inhibits CREB dependent BDNF expression. This most likely disrupts neuronal circuit development, leading to depression-like behavior at PND90.
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Ethanol ingestion by a mother during pregnancy entails adverse consequences for her offspring. In this study, adult female rats were given access to ethanol from 8 days prior to mating to post-parturition weaning, and the effects on her offspring were evaluated. We investigated changes in the cocaine- and amphetamine-regulated transcript peptide (CART), a neuropeptide involved in the central effects of ethanol in the frame of reward and stress processing circuits. ⋯ Their brains showed decreased CART-immunoreactivity in nucleus accumbens shell, lateral bed nucleus of stria terminalis, PVN, ARC, LH, hippocampus and LC as compared to age-matched control offspring. However, CART-immunoreactive profile in EW and fibers in VTA of 85-day-old offspring was similar to that in the control. Thus, regional imbalance in the CART system of the offspring of alcoholic dams seems correlated with the affective and emotional abnormalities and memory deficits.
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Peripheral diabetic neuropathy (PDN) is one of the most common complications of diabetes mellitus. Previous studies showed an association between dietary iron load and inflammation in the development of PDN in a rat model of type 1 diabetes (T1D). Here we investigated the role of iron and neural inflammation in development of PDN in a animal model of obesity and type 2 diabetes (T2D). 3-month-old db/db mice were fed with a high, standard or low iron diet for 4 months. ⋯ Numbers of pro-inflammatory M1 macrophages were reduced in nerve sections, and anti-inflammatory M2 macrophages were increased in db/db mice on high iron diet compared to other groups. These results confirm and extend our previous findings in STZ-diabetic rats by showing that dietary non-hem iron supplementation may partly prevent the development of PDN in opposition to iron restriction. The identification of these dietary iron effects on the metabolic and inflammatory mechanisms of PDN supports a role of dietary iron and leads us to suggest testing for iron levels in human diabetic patients.
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In the developing brain, microglial cells play an important role in shaping neuronal circuits. These immune cells communicate with neurons through fractalkine (CX3CL1), a neuronal cytokine that acts on microglial CX3CR1 receptor. Among various functions, this signaling pathway has been implicated in the postnatal maturation of glutamatergic synapses. ⋯ In CX3CR1-deficient mice, GABAergic currents were slightly altered, whereas the developmental changes of these currents were comparable with wild-type animals. Despite these minor changes in GABAergic transmission, the GDP frequency was strikingly reduced in CX3CR1-deficient mice compared to wild-type, with no change in the GDP shape and ending period. Collectively, it emerges that, in the neonate hippocampus, the fractalkine signaling pathway tunes GDP activities and is marginally involved in the maturation of GABAergic synapses, suggesting that microglial cells have distinct impact on maturing GABAergic, glutamatergic, and network functions.
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There is now widespread consensus that social biases often influence actions independently of the actor's intention or awareness. The notion that we are sometimes blind to the origins of our thoughts, attitudes, and behaviors also features prominently in research into domain-general human memory systems, which has a long history of distinguishing between implicit and explicit repercussions of past experience. A shared challenge across these fields of study is thus to identify techniques for effectively managing the contents of our memory stores, particularly those aspects into which we have limited metacognitive insight. ⋯ A second body of work concerns breakthroughs in understanding memory consolidation, which determines the fate of newly encoded memories. We discuss the promise of each of these developments for identifying ways to become better stewards of our social minds. More generally, we suggest that, as with other forms of learning and memory, intentional practice and rehearsal may be critical in learning to minimize unwanted biases.