Neuroscience
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Major depressive disorder (MDD) is a heterogeneous mental disorder for which the precise assessment of symptom severity remains challenging. Studies have consistently found that the microbiota-gut-brain (MGB) axis is profoundly altered in MDD, but whether MGB-relevant clinical parameters are applicable to depression subphenotyping remains largely unexplored. In this prospective study, we assessed the taxonomic and metabolic signatures of fecal microbiota from 45 unmedicated MDD patients and explored their associations with the severity of depression and anxiety symptoms as measured by Hamilton depression scale-17 (HAMD-17) and Hamilton anxiety scale-14 (HAMA-14), respectively. ⋯ Patients with severe depression symptoms showed significantly higher abundance of Phascolarctobacterium and Akkermansia, while enrichment of Akkermansia, Coprococcus and Streptococcus were observed with severe anxiety symptoms. In addition, fecal microbial metabolite indole-3-carboxyaldehyde proved useful to discriminate the severity of depression or anxiety symptoms. Together, our results support the utility of microbial taxa and metabolites as potential MGB-based biomarker panel for stratifying the symptom severity of MDD patients.
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Alzheimer's disease (AD) is characterized by global cognitive impairment in multiple cognitive domains. Thalamic dysfunction during AD progression has been reported. However, there are limited studies regarding dysfunction in the functional connectivity (FC) of thalamic subdivisions and the relationship between such dysfunction and clinical assessments. ⋯ The abnormal FC of the medial nuclei with the left precuneus was correlated with the Mini Mental State Examination score in the patient group. Using the FC values showing between-group differences, the linear support vector machine classifier achieved quite good in accuracy, sensitivity, specificity and area under the curve. Dysfunction in the FC of the intralaminar and medial thalamus with the precuneus may comprise a potential neural substrate for cognitive impairment during AD progression, which in turn may provide new treatment targets.
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Neurons cultured on a multi-electrode array show not only spontaneous firing, but also network-specific burst firing, the latter of which develops into synchronous bursting. Such synchronous bursting can be suppressed by exposure to xenon (Xe) gas. To better understand such suppression of bursting by Xe, we investigate here whether signal transmission between neurons is also suppressed under these conditions. ⋯ The pressure dependence of the response ratio to the stimulus suggests that Xe suppresses multiple points of action simultaneously when suppressing synaptic signal transduction, as observed in the suppression of the synchronized bursting. In addition, we find that the signal that transmits not via synaptic bonding (axon conduction) is also suppressed under Xe gas pressures over 0.3 MPa. Therefore, we conclude that Xe-induced suppression of synchronized bursting is caused mainly by a decrease in the apparent number of active neurons that contribute to the neuronal network, a decrease due to inhibition of signal transmission via synaptic connections.
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To determine detrimental effects of estrogen and insulin deficiencies on hippocampus, we examined apoptosis-induced neuronal damage and cholinergic system in ovariectomized and/or diabetic rat hippocampus. Possible neuroprotective effects of treadmill exercise were also investigated. Adult female Wistar rats were randomly divided into four groups (n = 5 rats/group) as follows: control, ovariectomized (Ovx), diabetic (Dia, streptozotocin (STZ) 60 mg/kg; i.p.), and Ovx + Dia groups. ⋯ Treadmill exercise attenuated apoptosis-induced neuropathology in the Ovx and Dia groups and recovered AChE activity in the Dia group. Neuroprotective effects of treadmill exercise were mediated by inhibition of apoptosis. Moderate exercise protocol had no beneficial anti-apoptotic and neuroprotective effects in ovariectomized-diabetic rats.
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Tone-evoked synaptic excitation and inhibition are highly correlated in many neurons with V-shaped tuning curves in the primary auditory cortex of pentobarbital-anesthetized rats. In contrast, there is less correlation between spontaneous excitation and inhibition in visual cortex neurons under the same anesthetic conditions. However, it was not known whether the primary auditory cortex resembles visual cortex in having spontaneous excitation and inhibition that is less correlated than tone-evoked excitation and inhibition. ⋯ We use the ratio of the excitatory event rate to the inhibitory event rate, and the assumption that the excitatory and inhibitory synaptic currents can each be reasonably described as a filtered Poisson process, to estimate the maximum spontaneous excitatory-inhibitory correlation for each neuron. In a subset of neurons, we also measured tone-evoked excitation and inhibition. In neurons with V-shaped tuning curves, although tone-evoked excitation and inhibition were highly correlated, the spontaneous inhibitory event rate was typically sufficiently lower than the spontaneous excitatory event rate to indicate a lower excitatory-inhibitory correlation for spontaneous activity than for tone-evoked responses.