Neuroscience
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Defining the markers corresponding to a high risk of developing depression in humans would have major clinical significance; however, few studies have been conducted since they are not only complex but also require homogeneous groups. This study compared congenital learned helpless (cLH) rats, selectively bred for high stress sensitivity and learned helplessness (LH) behavior, to congenital non-learned helpless (cNLH) rats that were bred for resistance to uncontrollable stress. Naïve cLH rats show some depression-like behavior but full LH behavior need additional stress, making this model ideal for studying vulnerability to depression. ⋯ These reductions corresponded primarily to reduced inter-hemispheric connectivity. The main reduction however was in the sensory system. It is argued that reduced connectivity and inter-hemispheric connectivity of the sensory system reflects an internal convergence state which may precede other depressive symptomatology and therefore could be used as markers for vulnerability to the development of depression.
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The complex neuronal circuitry of the cerebellum is embedded within its lamina, folia, and lobules, which together play an important role in sensory and motor function. Studies in mouse models have demonstrated that both cerebellar lamination and lobule/fissure development are under genetic control. The cerebellar vermis of C57BL/6 mice exhibits spontaneous malformations of neuronal migration of posterior lobules (VIII-IX; molecular layer heterotopia); however, the extent to which other inbred mice also exhibit these malformations is unknown. ⋯ These data indicate that heterotopia formation is a weakly penetrant trait requiring homozygosity of one or more C57BL/6 alleles outside of chromosome 1 and the sex chromosomes. Additional morphological analyses showed no relationship between heterotopia formation and other features of lobule/fissure organization. These data are relevant toward understanding normal cerebellar development and disorders affecting cerebellar foliation and lamination.
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The medial preoptic nucleus (MPN) is a sexually dimorphic cell group of the medial preoptic area that plays a central role in the integration of olfactory and hormonal stimuli that modulate sexually differentiated behaviors. The influence of sex steroids in these behaviors is mediated through activation of estrogen receptors (ERs), which are highly expressed in this nucleus. Little is known about the effects of progesterone (P) or the selective activation of each ER subtype on the expression of estrogen receptor alpha (ERα) in the MPN of female rats. ⋯ A similar effect was observed after the administration of EB, but not of P. Results also show that the estradiol-induced down-regulation of the ERα is mediated by activation of both ER subtypes, and that ERβ activation leads to a reduction in the total number of ERα-immunoreactive neurons that is twice that resulting from ERα activation. Present data suggest that ERα activation triggers a sort of negative feedback mechanism in MPN neurons that reduces its own expression, which might be of importance for the regulation of estradiol-dependent physiological and behavioral responses.
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Sickness behaviors have become the focus of great interest in recent years as they represent a clear case of how peripheral disturbances in immune signaling can disrupt quite complex behaviors. In the current study, we were interested in examining whether we could identify any significant morphological disturbances in microglia associated with these sickness-like behaviors in adult male Sprague-Dawley rats. We chose lipopolysaccharide (LPS 100 μg/kg/i.p.), to induce sickness-like behaviors as it is the most well-validated approach to do so in rodents and humans. ⋯ We undertook these complementary analysis of microglial cells in the both the pre- and infralimbic divisions of the PFC. Our results indicated that microglial soma size was significantly enlarged, while cell processes had contracted slightly following LPS administration. To our knowledge this study is to first to definitely demonstrate substantial microglial disturbances within the PFC following LPS delivered at a dose that was sufficient to induce significant sickness-like behavior.
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Contrast adaptation, generated by prolonged viewing of a high contrast spatial pattern, is known to reduce perceptual sensitivity to subsequently presented stimuli of similar spatial frequency (SF). Neural correlates of this pattern-specific contrast adaptation have been described in several classic studies in cat primary visual cortex (V1). ⋯ We found that adapting stimuli that drove a neuron more strongly generally produced more adaptation, implicating an intrinsic or fatigue-like process. Importantly, we also observed that slightly stronger contrast adaptation was produced when the adapting SF matched the test SF even when matched and nonmatched adapting gratings elicited similar spike rates indicating extrinsic or network processes contribute as well.