Neuroscience
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Obstructive sleep apnea patients face episodes of chronic intermittent hypoxia (CIH), which has been suggested as a causative factor for increased sympathetic activity (SNA) and hypertension. Female rats exposed to CIH develop hypertension and exhibit changes in respiratory-sympathetic coupling, marked by an increase in the inspiratory modulation of SNA. We tested the hypothesis that enhanced inspiratory-modulation of SNA is dependent on carotid bodies (CBs) and are associated with changes in respiratory network activity. ⋯ Post-inspiratory neurons are active for a longer period during expiration in CIH-female rats. Further, using the computational model of a brainstem respiratory-sympathetic network, we demonstrate that a reduction in Pre-I/I neuron firing frequency simulates the enhanced inspiratory SNA modulation in CIH-female rats. We conclude that changes in respiratory-sympathetic coupling in CIH-female rats is dependent on CBs and it is associated with changes in firing properties of specific respiratory neurons types.
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Previous work from our lab revealed that adult female rats have increased levels of myelin basic protein (MBP), a marker for myelination, in the orbitofrontal cortex (OFC) as compared to adult males. The goal of the present study was to determine the role of gonadal hormones, acting either in adulthood or at puberty, in the development of an adult sex difference in OFC levels of MBP. In an initial experiment, we replicated our previous results demonstrating that gonadally intact female rats have increased levels of MBP in the OFC as compared to males. ⋯ This reduction eliminated the sex difference in adult MBP levels in the OFC. These results reveal puberty to be an organizational time point for a sex difference in the OFC of adult rats in levels of a marker of myelination. This neuroanatomical difference may contribute to observed sex differences in OFC-associated behaviors including in inhibitory control.
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The comparative roles of the human amygdala and orbitofrontal cortex in emotional processing are under substantial debate, supported prominently by invasive primate studies. Noninvasive studies in humans are restricted by the limitations of electro- and magneto-encephalographic methods, which are hampered by the closed-field architecture and deep location of these structures. Here we employ whole-brain functional magnetic resonance imaging at an effective sampling rate of 300 ms to define the latency of enhanced blood oxygen level dependent (BOLD) contrast within structures activated by emotionally evocative relative to neutral scenes, in an effort to assess the hypothesized primacy of amygdala-inferotemporal co-activity in human emotional perception, relative to orbitofrontal cortex. ⋯ Subcortical structures including the amygdala, locus coeruleus, and basal forebrain also showed reliably increased activity during emotional scene perception. The latency at which emotional BOLD signal enhancement varied considerably across structures, ranging from 2 to 6 seconds after scene onset. Though coarse, the spatiotemporal pattern of emotion-enhanced activity identified here is consistent with the idea that the amygdala and inferior temporal fusiform gyrus are the first regions to discriminate scene emotionality, which may then distribute this categorical information to other cortical and subcortical structures.
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The article studies the effect of melatonin on the intensity of free radical oxidation, the functioning of the enzymatic components of the antioxidant system and their transcriptional regulation in rats with experimental cerebral ischemia/reperfusion of the brain. The development of ischemia/reperfusion was characterized by the activation of apoptotic processes and the accumulation of mRNA of the genes Sod1, Cat, Gpx1, Gsr, Hif-1α, Nrf2, Nfkb2, and Foxo1 in the rats' brains. ⋯ At the same time, there was a shift in the activity of superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase, which increased in the presence of a pathology, towards the control values. The revealed changes may be accounted for by antioxidant and neuroprotective properties of melatonin, which provided a decrease in the degree of mobilization of the protective systems in animal organism.
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Exploring sexual dimorphisms in the brain morphology is important for their impact and therapeutic implications for several neurological diseases. The hypothesis that sex could influence the transcriptome of brain cells could be the basis regarding the different response to cognitive decline identified in men and women. In this paper, we analyzed several prefrontal cortices (PFC) microarrays datasets of young/middle-aged healthy subjects and then Alzheimer's disease (AD) patients, according to the sex. ⋯ In addition, the sex-matched analysis of transcriptome identified a convergent molecular signature in men and women AD patients. Furthermore, the WPSEG belonging to CNS cells in PFC of healthy middle-aged subjects was correlated to AD profiles according to the sex. Since our results, it is possible to conclude that during the aging the PFC' cells adopt transcriptional strategies sex-dependent that could potentially control the development of neurodegenerative diseases.