جستجوی مقالات مرتبط با کلیدواژه « neurons » در نشریات گروه « پزشکی »

As the repair capacity of the nervous system is low, stem cell therapy is a trend for replacement therapy. Dental pulp stem cells (DPSCs) have the potential to differentiate into many tissues, such as neurons. Harmine (7-methoxy-1methyl-9H-pyrido[3,4-b] indole) is an alkaloidal component of medicinal plants with a long history in traditional medicine. Alginate is a biocompatible hydrogel widely used as a biomaterial base in various scaffolds.

This study investigated whether harmine and encapsulation of cells in alginate hydrogel could improve DPSCs differentiation into neural cells.

DPSCs were cultured under standard stem cell culture conditions, then encapsulated in alginate hydrogel, and treated with differentiation medium with and without harmine. After 14 days, cell proliferation and differentiation were assessed by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay, real-time polymerase chain reaction (RT-PCR), and flow cytometry.

Harmine (5 and 10 M) significantly increased the proliferation and viability of DPSCs compared to the control group in both two-dimensional and three-dimensional culture systems (P < 0.05). The expression levels of three neural cell markers (nestin, microtubule-associated protein [MAP-2], and -tubulin III) in DPSCs-derived neural cells cultured in two-dimensional and three-dimensional culture systems were significantly increased in harmine-treated two-dimensionalandthree-dimensional culture systems compared to the control group (P < 0.05).

Either harmine or alginate hydrogel had an accelerating effect on DPSCs differentiation into neural cells. Harmine also increased the proliferation of the cells.

Glutamate, an excitatory neurotransmitter, plays a pivotal role in cellular phenomena in neurons, like synaptic plasticity and excitotoxicity. As the major glutamate receptors, N-methylD-aspartate receptors (NMDARs) undergo phosphorylation at Ser1303 on the GluN2B subunit upon glutamate binding. This effect results from the influx of calcium and subsequent activation of many known kinases that phosphorylate the receptor. However, the regulation of this phosphorylation at this site and the involved phosphatases have remained unknown, especially under excitotoxicity conditions induced by glutamate treatment.

This study attempts to investigate the regulation of phosphorylation at GluN2B-Ser1303 under excitotoxic conditions and identify the phosphatase responsible.

Primary cortical neurons prepared from embryonic rat brains were treated with glutamate, thereby inducing excitotoxicity in vitro. Then, the phosphorylation status of GluN2B-Ser1303 was studied using Western blots in the presence of various phosphatase inhibitors. Finally, the interaction of phosphatase with GluN2B was studied using immunostaining and coimmunoprecipitation analysis.

The results show that under excitotoxic conditions, there is a reduction in the phosphorylation of GluN2B-Ser1303, and protein phosphatase 1 (PP1) was the phosphatase responsible. PPI was found to interact with the receptor.

This study reports for the first time the regulation of phosphorylation at GluN2BSer1303 in vitro under excitotoxic conditions, which PP1 mediates. This site could be a potential drug target for designing novel compounds which could exacerbate excitotoxicity.

CA1, as a major structure involved in learning and memory, has been shown to be affected by tramadol addiction. Both orexin and endocannabinoid receptors express in CA1 and play an important role in drug dependency. The aim of this study was to evaluate the modulatory effects of orexin‑2 (OX2R) and endocannabinoid‑1 (CB1R) receptors on neuronal activity in CA1, in response to tramadol in rats.

Male Wistar rats were divided into 8 groups (n = 6–7); saline‑dimethyl sulfoxide (DMSO), tramadol‑DMSO, saline‑TCS‑OX2‑29, saline‑AM251, tramadol‑TCS‑OX2‑29, tramadol‑AM251, saline‑TCS‑OX2‑29‑AM251, tramadol‑TCS‑OX2‑29‑AM251. Tramadol was injected intraperitoneally, and then, AM251 (1 nmol/0.3 μL), CB1R antagonist and TCS‑OX2‑29 (1 nmol/0.3 μL), OX2R antagonist, were microinjected individually or concurrently into the CA1. Using in vivo extracellular single‑unit recording, the firing of CA1 pyramidal neurons was investigated.

Tramadol decreased neuronal activity in CA1 (P < 0.01) but increased it after micro‑injection of DMSO. TCS‑OX2‑29 increased neuronal activity in saline group (P < 0.05) but decreased it in tramadol group. AM251 had no effect on saline group but decreased neuronal activity in tramadol group (P < 0.05). Concurrent micro‑injection of TCS‑OX2‑29 and AM251 had no effect on saline group but decreased neuronal activity in tramadol group (P < 0.05).

Our findings suggest that neural activity in CA1 is rapidly affected by acute use of tramadol, and some of these effects may be induced through the endocannabinoid and orexin systems. Thus, the function of endocannabinoid and orexin systems in CA1 may play a role in tramadol addiction.

Tramadol is an opioid analgesic with monoamine reuptake inhibitory effects. Although tramadol has been widely used to control pain, there is controversy about the risk of abuse. Therefore, in the present study, the acute effects of tramadol on neuronal activity in the medial prefrontal cortex (mPFC), which is one of the important centers of the reward system, were investigated electrophysiologically.

Tramadol was injected interperitoneally (12.5 and 25 mk/kg) or subcutaneously (40 mg/kg) and its effect on the firing of mPFC neurons was investigated, using in vivo extracellular single unit recording.

Tramadol could not significantly affect neural activity in mPFC, suggesting no acute and rapid effect on mPFC.

The present results showed that neural activity in mPFC was not rapidly affected by acute application of tramadol. Since the role of mPFC in tramadol addiction has been elucidated, it can be concluded that these effects may be due to delayed responses or chronic use of tramadol.

A wide variety of cytokines are released from human amniotic membrane cells (hAMCs), which can increase the rate of differentiation of mesenchymal stem cells into the neurons. We studied the effect of Retinoic Acid (RA) on the differentiation rate of human Umbilical Cord Mesenchymal Stem Cells (hUMSCs) which were co-cultured with hAMCs. 

In this experimental study, both hUMSCs and hAMCs were isolated from postpartum human umbilical cords and placenta respectively. The expression of mesenchymal (CD73, CD90 and CD105), hematopoietic and endothelial (CD34 and CD45) markers in hUMSCs were confirmed by flow cytometry. The hUMSCs were cultured in four distinct groups: group 1) Control, group 2) Co-culture with hAMCs, group 3) RA treatment and group 4) Co-culture with hAMCs treated by RA. Twelve days after culturing, the expression of NSE, MAP2 and ChAT differentiation genes and their related proteins were examined by real-time PCR and immunocytochemistry respectively. 

The flow-cytometry analysis indicated increased expression of mesenchymal markers and a low expression of both hematopoietic and endothelial markers (CD73:98.24%, CD90: 97.32%, CD105: 90.75%, CD34: 2.96%, and CD45:1.74%). Moreover, the expression of both NSE and MAP2 markers was increased significantly in all studied groups in comparison to the control group  On the other hand, the expression of ChAT had a significant increase in the group 2 and 4 (RA and RA+ co-culture).

RA can be used as an effective inducer to differentiate hUMSCs into cholinergic-like cells, and hAMCs could increase the number of differentiated cells as an effective factor.

To elucidate the mechanism of Respiratory Syncytial Virus (RSV) infection and central neuronal disease and to understand the role of microglia in neuronal injuries during RSV infection.

The effects of RSV and the cytokines produced by RSV-infected CHME-5 microglial cells on SY5Y neuronal cells were evaluated based on an in vitro Transwell coculture system. Five treatment groups were established in this study, including the normal control SY5Y group, RSV+SY5Y infection group, (cytokine+CHME-5)+SY5Y Transwell group, (RSV+CHME-5)+SY5Y Transwell group, and (RSV+cytokine+CHME-5)+SY5Y Transwell group. The morphological and physical alterations in SY5Y cells and their synapses were analyzed by confocal microscopy. The mRNA and protein expression levels of TLR3/RIG-I, as well as the expression of Hv1, in microglia were measured by qRT-PCR and Western blot assays. In addition, the apoptosis ratio of neuronal cells was determined by flow cytometry.

RSV infection activated the protein expression of Hv1 protein in microglia in vitro (p <0.05), induced morphological changes in SY5Y cells, lengthened synapses (73.36±0.12 μm vs 38.10±0.11 μm), simultaneously activated TLR3 and RIG-I protein expression (p <0.05), upregulated the secretion of the inflammatory cytokines TNF-α, IL-6, and IL-8 (p <0.01), and increased the apoptosis rate of SY5Y cells (p <0.01).

The results demonstrate that RSV infection of microglia can induce SY5Y neuronal cell injury and stimulate apoptosis through inflammatory cytokine release.

Neurological coordination is essential for performing biological and mechanical activities achieved by the cooperation of biomolecules such as carbohydrates, lipids, and proteins. It plays an important role in energy production, which can be fascinatingly improved by ketone bodies. Ketone bodies are small, water-soluble lipid molecules by shifting the glycolytic phase KBs directly enters into the tricarboxylic acid cycle for ATP synthesis. It leads to the production of much more energy levels than a single molecule of glucose. Therefore, it could have a profound effect on neuro-metabolism as well as bioenergetics of ATP production. These neuro-enhancement properties are useful for epilepsy, Alzheimer's, and several neurocognitive disorders treatment. Interestingly, the cancer cells cannot use it for efficiently energy production results in decreasing cancer cells viability. This review summarized ketone bodies generation, related imperative effects on normal cells, and more importantly its application in various neurological disorders treatment by rising neuronal functions.

Cell culture is an important technique in cellular and molecular biology. There are two basic systems for culturing cells, adherent (monolayer) culture and suspension culture. In adherent cell culture, cellular adhesion molecules play a vital role in many physiological processes. Many cells, especially primary-obtained cells, hardly attach to plates, so coating agents are used for cell attachment and growth. There is no striking report on whether all cells need coated plates.

We investigated whether a coating plate is essential for primary spinal cord-obtained neuron culture.

Cells were separated and seeded in tissue culture plates coated with either Poly(L-lysine) or Poly(D-lysine), as well as without coating containing DMEM-F12 media with 10% FBS.

Interestingly, we found that neuron cells more potently attached to coating free plates.

These results provide strong evidence helping the researchers to optimize primary spinal cord cultures.