Neuroscience
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Parkinson's disease (PD) is the second most common neurodegenerative disorder. Despite its high frequency the etiology is still unclear; several lines of evidence show that an inflammatory process is implicated in the pathogenesis of this disorder; where activation of brain microglia plays a central role in the damage of dopaminergic neurons of the substantia nigra. ⋯ This exposure may be enhanced by increased permeability of the intestinal ("leaky gut") and the blood brain barrier; enhancing the entrance of microbiota-produced substances into the central nervous system. In this manuscript, we explore the evidence from clinical and basic science implicating microglia activation by gut dysbiosis and how this phenomenon may impact in the symptomatology and progression of PD.
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Hubs emerge in structural and resting state network analysis as areas highly connected to other parts of the brain and have been shown to respond to several task domains in functional imaging studies. A cognitive explanation for this multi-functionality is still wanting. We propose, that hubs subserve domain-general meta-cognitive functions, relevant to a variety of domain-specific networks and test this hypothesis for the example of processing explicit identity information. ⋯ Indeed, the two contrasts showed significant conjunctions in the left inferior parietal lobe (IPL), precuneus (PC), and posterior cingulate. Accordingly, identity processing may well be one domain-general meta-cognitive function that hub-areas provide to domain-specific networks. For the parietal lobe we back up our hypothesis further with existing reports of activation peaks for other tasks that depend on identity processing, e.g., episodic recollection, theory of mind, and visual perspective taking.
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A single brief noise exposure can cause a significant loss of cochlear afferent synapses without causing permanent threshold shift. Previously we reported that the initial synaptic loss is partially reversible in Guinea pigs, indicating that synaptic loss can be categorized as either temporary or permanent. Since synaptic loss is biased to innervating auditory nerve fibers (ANFs) with low spontaneous spike rates (SSR), which are critical to the coding of in-background noise, coding-in-noise deficits (CIND) have been predicted to result from noise-induced synaptic damage. ⋯ The present study sought to determine the effects of repeated noise exposure on temporary and permanent synaptic loss in Guinea pigs and C57 mice, whether such effects were additive, and whether repeated noise exposure induced CIND in Guinea pigs. The results show that the second noise exposure caused much less temporary synaptic loss and no additional permanent loss in Guinea pigs; however, an additional permanent loss was seen after the second noise was in the mice, although it was not significant. In Guinea pigs, the observed increased masking of the AM CAP provides evidence for CIND after repeated noise exposure.
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The mesopontine tegmental anesthesia area (MPTA) is a small brainstem nucleus that, when exposed to minute quantities of GABAA receptor agonists, induces a state of general anesthesia. In addition to immobility and analgesia this state is accompanied by widespread suppression of neural activity in the cerebral cortex and high delta-band power in the electroencephalogram. Collectively, MPTA neurons are known to project to a variety of forebrain targets which are known to relay to the cortex in a highly distributed manner. ⋯ Results indicated that double-labeling was rare, occurring on average in only 1.3% of the neurons sampled. The overwhelming majority of individual MPTA neurons showed specific connectivity, contributing to only one of the major ascending pathways, either ipsilaterally or contralaterally, but not bilaterally. This architecture would permit particular functional aspects of anesthetic loss-of-consciousness to be driven by specific subpopulations of MPTA neurons.
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Survivals after prenatal hypoxia-ischemia (HI) usually suffer long-lasting cognitive defects. Reduced blood-oxygen supplies and the following reperfusion cause mitochondrial injury. Damaged mitochondria could be replaced by mitochondrial biogenesis program and peroxisome proliferator-activated receptor γ co-activator 1α (PGC-1α) is the specific up-regulator. ⋯ Postnatal administration of pioglitazone further promoted PGC-1α and mitochondrial biogenesis, alleviated hippocampal injury, and improved performance in the behavioral tasks after intrauterine HI. Our investigation implicated activation of PGC-1α, and mitochondrial biogenesis is a neuroprotective mechanism against brain injury caused by systemic prenatal HI. Promotion of PGC-1α by pioglitazone might be a potential treatment for protecting against hippocampal injury and cognitive defects after intrauterine HI.