Neuroscience
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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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Several physiological processes in the CNS are regulated by the endocannabinoid system (ECS). Cannabinoid receptors (CBr) and CBr agonists have been involved in the modulation of the N-methyl-D-aspartate receptor (NMDAr) activation. Glutaric (GA), 3-hydroxyglutaric (3-OHGA), methylmalonic (MMA) and propionic (PA) acids are endogenous metabolites produced and accumulated in the brain of children affected by severe organic acidemias (OAs) with neurodegeneration. ⋯ Herein, we investigated the effects of the synthetic CBr agonist WIN 55,212-2 (WIN) on early markers of GA-, 3-OHGA-, MMA- and PA-induced toxicity in brain synaptosomes from adult (90-day-old) and adolescent (30-day-old) rats. As pre-treatment, WIN exerted protective effects on the GA- and MMA-induced mitochondrial dysfunction, and prevented the reactive oxygen species (ROS) formation and lipid peroxidation induced by all metabolites. Our findings support a protective and modulatory role of cannabinoids in the early toxic events elicited by toxic metabolites involved in OAs.
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High-intensity sound can induce seizures in susceptible animals. After repeated acoustic stimuli changes in behavioural seizure repertoire and epileptic EEG activity might be seen in recruited limbic and forebrain structures, a phenomenon known as audiogenic kindling. It is postulated that audiogenic kindling can produce synaptic plasticity events leading to the spread of epileptogenic activity to the limbic system. ⋯ These findings show that repeated high-intensity sound stimulation prevent LTP of Schaffer-CA1 synapses from Wistar rats, without affecting spatial memory. This effect was not seen in hippocampi from audiogenic seizure-prone WARs. In WARs the link between auditory stimulation and hippocampal LTP seems to be disrupted which could be relevant for the susceptibility to seizures in this strain.
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Arm movement control takes advantage of multiple inputs, including those originating from the contralateral arm. In the mirror paradigm, it has been suggested that control of the unseen arm, hidden by the mirror, is facilitated by the reflection of the other, moving arm. Although proprioceptive feedback originating from the moving arm, (the image of which is reflected in the mirror), is always coupled with visual feedback in the mirror paradigm, the former has received little attention. ⋯ Next (in Experiment 2), we masked proprioceptive afferents of the passively moved arm and specifically evaluated mirror feedback. We found that interlimb coupling through mirror feedback (though significant) was weaker than interlimb coupling through proprioceptive feedback. Overall, the present results show that in the mirror paradigm, proprioceptive feedback is stronger and more consistent than visual-mirror feedback in terms of the impact on interlimb coupling.
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Our previous studies demonstrated resveratrol (Res) administration protected Alzheimer's disease (AD) rats from developing memory decline by anti-oxidation. Beta-amyloid peptide 1-42 (Aβ1-42) is not only the primary protein component of senile plaques in AD but also is believed to play an important part in its pathology. ⋯ Rats were divided into six groups: (1) ovariectomized (OVX)+D-galactose (D-gal) 100mg/kg group (OVX+D-gal); (2-4) OVX, D-gal and Res 20, 40 and 80 mg/kg treated groups; and (5) OVX, D-gal and estradiol valerate 0.8 mg/kg treated group (ET); (6) Sham control group. 12 weeks later, Res 40 and 80 mg/kg treatment exhibited a significant decrease of Aβ1-42 compared with the OVX+D-gal rats of hippocampus, which was accompanied by decreased expression of advanced glycation endproducts (RAGE), matrix metalloprotein-9 (MMP-9), nuclear factor kappaB (NF-κB) and the increase of Claudin-5. These results suggest that Res is useful not only in protecting OVX+D-gal rats from neuroinflammation mediated by Aβ1-42 by decreasing the expression of NF-κB but also the integrity of BBB by increasing Claudin-5 and decreasing RAGE, MMP-9.