Neurochemistry international
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Both insulin and tau, promoting neuronal differentiation (neurite outgrowth, neuronal polarity, and myelination) and cell survival, are associated with neurodegenerative disease (e.g., Alzheimer's disease). The aim of this study was to explore relation between insulin-induced activation of insulin signal and expression of tau protein on neurite-like process outgrowth in adrenal chromaffin cells. Primary cultured bovine adrenal chromaffin cells were incubated with insulin to determine whether stimulant of insulin signal could affect tau expression and neurite-like process outgrowth. ⋯ Pulse-label followed by polyacrylamide gel electrophoresis revealed that insulin accelerated tau protein synthesis rate (t(1/2)) from 2.6 to 1.9h. Insulin did not change tau mRNA level. Taken together, these results suggest that insulin-induced activation of PI3K∼mTOR pathway up-regulated tau protein via acceleration of protein synthesis, on which insulin promoted neurite-like process outgrowth.
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Much evidence exists for the involvement of vesicular zinc in neurotransmission and cortical plasticity. Recent studies have reported that mice deficient in zinc transporter-3 protein (ZnT3) and thus, vesicular zinc, have significant behavioural and biochemical deficits. Here, we examined whether phenotypic differences existed in the barrel cortices of ZnT3 KO mice using functional proteomics and quantitative PCR. ⋯ The reduced expression of Nrtkb persisted with whisker plucking. These data demonstrate that fundamental changes in the expression of proteins and genes important in neurotransmission occur in the absence of vesicular zinc. Furthermore, the complement of experience-dependent changes were different between WT and KO mice, indicating that the lack of vesicular zinc affects the process of cortical plasticity.
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Rapid eye movement (REM) sleep rebound following REM deprivation using the platform-on-water method is characterized by increased time spent in REM sleep and activation of melanin-concentrating hormone (MCH) expressing neurons. Orexinergic neurons discharge reciprocally to MCH-ergic neurons across the sleep-wake cycle. However, the relation between REM architecture and the aforementioned neuropeptides remained unclear. ⋯ A negative reciprocal correlation was also found between the activation of MCH- and orexin-immunoreactive neurons during REM rebound. Furthermore, difference between the activation of CART-immunoreactive (CART-IR) and non-CART-immunoreactive MCH-ergic neuron subpopulations was found only after selective REM deprivation, it was absent in the large platform (stress control) rebound group. These results support the role of CART-IR subpopulation of MCH-ergic neurons and the inverse relationship of MCH and orexin in the regulation of REM sleep after REM sleep deprivation.
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EGb761 is a well-defined mixture of active compounds extracted from Ginkgo biloba leaves. This extract is used clinically due to its neuroprotective effects, exerted probably via its potent antioxidant or free radical scavenger action. Previous studies suggest that oxidative stress, via free radical production, may play an important role in depression and animal models for depression-like behavior. ⋯ This antidepressant-like effect of EGb761 was associated with a reduction in lipid peroxidation and superoxide radical production (indicated by a downregulation of Mn-superoxide dismutase activity), both of which are indicators of oxidative stress. The protective effect of EGb761 is not related to excitatory or inhibitory effects in locomotor activity, and was also associated with the modulation of serotonergic and dopaminergic neurotransmission. It is suggested that EGb761 produces an antidepressant-like effect, and that an antioxidant effect against oxidative stress may be partly responsible for its observed neuroprotective effects.
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The goal of our work was a throughout characterization of the pharmacology of the TIPP-analog, Tyr-Tic-(2S,3R)-β-MePhe-Phe-OH and see if putative δ-opioid receptor subtypes can be distinguished. Analgesic latencies were assessed in mouse tail-flick assays after intrathecal administration. In vitro receptor autoradiography, binding and ligand-stimulated [(35)S]GTPγS functional assays were performed in the presence of putative δ(1)-(DPDPE: agonist, BNTX: antagonist), δ(2)-(agonist: deltorphin II, Ile(5,6)-deltorphin II, antagonist: naltriben) and μ-(DAMGO: agonist) opioid ligands. ⋯ Deletion of the DOR-1 gene resulted in no residual binding of the radioligand and no significant DPDPE effect on G-protein activation. Tyr-Tic-(2S,3R)-β-MePhe-Phe-OH is a highly potent and δ-opioid specific antagonist both in vivo and in vitro. However, the putative δ(1)- and δ(2)-opioid receptors could not be unequivocally distinguished in vitro.