Electrochemical sensing of transient ascorbate fluctuation under hypoxic stress in live rat brain.

Hypoxia, a common cause of programmed cell death or apoptosis, represents a neuropathological process. Although certain response proteins to hypoxic stress and their effects on cell status and fate have been identified, the real-time quantification of smaller neurochemicals to understand pathogenic mechanism in live rat brain during such stress remains unexplored. In this study, by employing a cutting-edge electrochemical tool developed with carbon nanotube-sheathed carbon fiber microelectrode that offers remarkable selectivity and temporal/spatial resolution for monitoring ascorbate, we observed a substantial efflux of ascorbate in response to hypoxic stress in live rat brain.

Correction: Polydopamine-capped AgNPs as a novel matrix overcoming the ion suppression of phosphatidylcholine for MALDI MS comprehensive imaging of glycerophospholipids and sphingolipids in impact-induced injured brain.

Correction for 'Polydopamine-capped AgNPs as a novel matrix overcoming the ion suppression of phosphatidylcholine for MALDI MS comprehensive imaging of glycerophospholipids and sphingolipids in impact-induced injured brain' by Chao Han , , 2019, , 6304-6312, https://doi.org/10.1039/C9AN01361J.

Activation of Kv7 channels normalizes hyperactivity of the VTA-NAcLat circuit and attenuates methamphetamine-induced conditioned place preference and sensitization in mice.

The brain circuit projecting from the ventral tegmental area (VTA) to the nucleus accumbens lateral shell (NAcLat) has a key role in methamphetamine (MA) addiction. As different dopamine (DA) neuron subpopulations in the VTA participate in different neuronal circuits, it is a challenge to isolate these DA neuron subtypes. Using retrograde tracing and Patch-seq, we isolated DA neurons in the VTA-NAcLat circuit in MA-treated mice and performed gene expression profiling.

Dopamine D1 receptor in orbitofrontal cortex to dorsal striatum pathway modulates methamphetamine addiction.

The orbitofrontal cortex (OFC)-dorsal striatum (DS) is an important neural circuit that contributes to addictive behavior, including compulsive reinforcement, yet the specific types of neurons that play a major role still need to be further elucidated. Here, we used a place conditioning paradigm to measure the conditioned responses to methamphetamine (MA). The results demonstrated that MA increases the expression of c-Fos, synaptic plasticity in OFC and DS.

Astrocyte-derived lactate/NADH alters methamphetamine-induced memory consolidation and retrieval by regulating neuronal synaptic plasticity in the dorsal hippocampus.

Drug memory is associated with drug-taking experience and environmental cues, which mainly contribute to addiction. Recent studies report that glycogenolysis-derived lactate from astrocyte transport to neurons is necessary for long-term potentiation and memory formation instead of its function as an energy substrate. However, the role of astrocyte-neuron lactate transfer in neuronal plasticity and methamphetamine (METH)-induced addiction memory consolidation and retrieval, especially the underlying mechanisms, are not clear.

Exploring the role and mechanism of gut microbiota in methamphetamine addiction using antibiotic treatment followed by fecal microbiota transplantation.

Recently, the role of the gut microbiota in the context of drug addiction has attracted the attention of researchers; however, the specific effects and underlying mechanisms require further exploration. To accomplish this, C57BL/6 mice were firstly treated with methamphetamine (MA). Conditioned place preference (CPP) behavior changes, gut permeability and function, microglial activation, and inflammatory cytokine expression were systematically analyzed in antibiotics-treated mice with microbiota depletion and in fecal microbiota transplantation mice with microbiota reconstitution.

Inactivation of the Lateral Hypothalamus Attenuates Methamphetamine-Induced Conditioned Place Preference through Regulation of Kcnq3 Expression.

Repeated administration of methylamphetamine (MA) induces MA addiction, which is featured by awfully unpleasant physical and emotional experiences after drug use is terminated. Neurophysiological studies show that the lateral hypothalamus (LH) is involved in reward development and addictive behaviors. Here, we show that repeated administration of MA activates the expression of c-Fos in LH neurons responding to conditioned place preference (CPP).

Single-Vesicle Electrochemistry Reveals Sex Difference in Vesicular Storage and Release of Catecholamine.

Quantitative measurements of sex difference in vesicle chemistry (i.e., chemical storage and release) at the single-vesicle level are essential to understand sex differences in cognitive behaviors; however, such measurements are very challenging to conventional analytical methods.

Nicotinamide adenine dinucleotide promotes synaptic plasticity gene expression through regulation N-methyl-D-aspartate receptor/Ca/Erk1/2 pathway.

Nicotinamide adenine dinucleotide (NADH) has been reported to regulate synaptic plasticity recently, while its role in this process remains unclear. To explore the contribution and the underlying mechanisms of NADH regulating synaptic plasticity, here, we examined NADH's effect on immediate-early response genes (IEGs) expressions, including C-Fos and Arc in primary cultured cortical neurons and the frontal cortex of mouse brain. Our results showed that NADH promoted IEGs expression and that the C-Fos and Arc levels are increased in primary cultured cortical neurons, which is almost completely blocked by N-methyl-D-aspartate receptor (NMDAR) inhibitor, MK-801.

Simultaneous Monitoring of Intracellular Temperature and Norepinephrine Variation by Fluorescent Probes during Norepinephrine Reuptake.

A long-standing challenge has been the simultaneous sensing of intracellular temperature and norepinephrine (NE) variations to explore signaling pathways and depression pathogeny. Here, we designed a fluorescent probe using poly(-isopropylacrylamide) and 1-[4-(7-nitro-benzo [1,2,5]oxadiazol-4-yl)-piperazin-1-yl]-propenone (PNIPAm-AANBD) and ()-1-(4-boronobenzyl)-2-(2-(1,3-dioxo-1,3-benzo[]isochromen-6-yl)vinyl)pyridin-1-ium bromide (PHE) for simultaneously measuring the temperature and NE with high selectivity. The fluorescence intensity of the PNIPAm-AANBD moiety exhibited a good response to temperature changes.

Unveiling the Role of DJ-1 Protein in Vesicular Storage and Release of Catecholamine with Nano/Micro-Tip Electrodes.

DJ-1 protein deficiency caused by PARK7 gene mutation has been suggested to closely relate to Parkinson's disease (PD), mainly through the attenuation D2 dopamine receptor activity in mice; however, whether or how it affects the vesicular storage and exocytosis of neurochemicals remains unclear. By using electrochemical methods at a single vesicle/cell level with nano/micro-tip electrodes, we for the first time find that DJ-1 protein deficiency caused by PARK7 gene knockout (KO) in mice has little effect on vesicular catecholamine content but significantly prolongs the exocytotic events, especially the closing time of exocytotic fusion pores. Further studies suggest the inhibition of α-synuclein aggregation by DJ-1 protein might be one way that DJ-1 protein acts on neurotransmission.

Polydopamine-capped AgNPs as a novel matrix overcoming the ion suppression of phosphatidylcholine for MALDI MS comprehensive imaging of glycerophospholipids and sphingolipids in impact-induced injured brain.

Matrix-assisted laser desorption/ionization mass spectrometry imaging (MALDI MSI) is a powerful tool for the characterization and localization of analytes without the need for extraction, purification, separation or labeling of samples. However, in tissue sections the most abundant lipids, phosphatidylcholines (PCs), could suppress the signals of other classes of coexisting lipids. In this work, polydopamine (PDA)-capped AgNPs (AgNPs@PDA) were synthesized as a matrix of MALDI MSI to analyze lipids in both positive and negative ion modes.

In Vivo Monitoring of Oxygen Fluctuation Simultaneously at Multiple Sites of Rat Cortex during Spreading Depression.

Spreading depression (SD) is a common pathological process in the brain shown as propagating neuronal depolarization followed by activity depression over the brain, and it is closely related to migraines and epilepsy. Although O is known to fluctuate during SD, the difference of O responses at different sites in the same brain region remains unknown. In this study, we develop an in vivo electrochemical method with microelectrode arrays (MEAs) to monitor, in real time, O fluctuation at multiple sites of rat cortex during SD with high spatial/temporal resolution.

Selective Amperometric Recording of Endogenous Ascorbate Secretion from a Single Rat Adrenal Chromaffin Cell with Pretreated Carbon Fiber Microelectrodes.

Quantitative description of ascorbate secretion at a single-cell level is of great importance in physiological studies; however, most studies on the ascorbate secretion have so far been performed through analyzing cell extracts with high performance liquid chromatography, which lacks time resolution and analytical performance on a single-cell level. This study demonstrates a single-cell amperometry with carbon fiber microelectrodes (CFEs) to selectively monitor amperometric vesicular secretion of endogenous ascorbate from a single rat adrenal chromaffin cell. The CFEs are electrochemically pretreated in a weakly basic solution (pH 9.

Neuroprotection of resveratrol against neurotoxicity induced by methamphetamine in mouse mesencephalic dopaminergic neurons.

Resveratrol is originally extracted from huzhang, a Chinese herbal medicine. Recently, resveratrol has attracted a great of attention due to its antioxidant and antiapoptotic properties. Although the neuroprotection of resveratrol on neural damages in various models has been well characterized, little is known about the role of resveratrol in methamphetamine (MA) induced neurotoxicity in mesencephalic dopaminergic neurons.

Paliperidone protects SK-N-SH cells against glutamate toxicity via Akt1/GSK3β signaling pathway.

Schizophrenia is a heterogeneous psychotic illness and its etiology remains poorly understood. Recent studies have suggested that neurodegeneration is a component of schizophrenia pathology and some atypical antipsychotics appear to slow progressive morphological brain changes. In addition, the atypical antipsychotics were reported to have a superior therapeutic efficacy in treating schizophrenia and have a low incidence of extrapyramidal side effects (EPS) compared to typical antipsychotics.

Neuroprotective effects of resveratrol on damages of mouse cortical neurons induced by β-amyloid through activation of SIRT1/Akt1 pathway.

Resveratrol (3,5,4'-tihydroxy-trans-stilbene), a polyphenolic phytoalexin found in the skin and seeds of grapes, has been reported to possess a wide range of biological and pharmacological activities including antioxidant, anti-inflammatory, and antimutagenic effects. The present study intended to explore the neuroprotective effects of resveratrol against Aβ25-35 -induced neurotoxicity of cultured mouse cortical neurons and the possible mechanisms involved. For this purpose, mouse cortical neurons were cultured and exposed to 30 μM Aβ25-35 in the absence or presence of resveratrol (5, 10, and 25 μM).

Paliperidone protects prefrontal cortical neurons from damages caused by MK-801 via Akt1/GSK3β signaling pathway.

Recent studies have suggested that neurodegeneration is involved in the pathogenesis of schizophrenia, and some atypical antipsychotics appear to prevent or retard progressive morphological brain changes. However, the underlying molecular mechanisms are largely unknown. Whether changes in intracellular signaling pathways are related to their neuroprotective effects remains undefined.

Resveratrol inhibits β-amyloid-induced neuronal apoptosis through regulation of SIRT1-ROCK1 signaling pathway.

Alzheimer's disease (AD) is characterized by the accumulation of β-amyloid peptide (Aβ) and loss of neurons. Recently, a growing body of evidences have indicated that as a herbal compound naturally derived from grapes, resveratrol modulates the pathophysiology of AD, however, with a largely unclear mechanism. Therefore, we aimed to investigate the protection of resveratrol against the neurotoxicity of β-amyloid peptide 25-35 (Aβ(25-35)) and further explore its underlying mechanism in the present study.