Neurotoxicity in Vitro Cultured Neuronal Cell Lines and Electrophysiological Approach

1995 ◽  
pp. 311-330
Author(s):  
H. P. M. Vijverberg ◽  
M. Oortgiesen ◽  
T. Leinders ◽  
R. Zwart
Keyword(s):  
Cell Lines ◽  
Neuronal Cell ◽  
Neuronal Cell Lines

scholarly journals Paternally Inherited DLK1 Deletion Associated With Familial Central Precocious Puberty

2017 ◽  
Vol 102 (5) ◽  
pp. 1557-1567 ◽  
Author(s):  
Andrew Dauber ◽  
Marina Cunha-Silva ◽  
Delanie B. Macedo ◽  
Vinicius N. Brito ◽  
Ana Paula Abreu ◽  
...  
Keyword(s):  
Cell Lines ◽  
Precocious Puberty ◽  
Medical Center ◽  
Academic Medical Center ◽  
Neuronal Cell ◽  
Central Precocious Puberty ◽  
Long Term Follow Up ◽  
Neuronal Cell Lines ◽  
Translational Start

Abstract Context: Central precocious puberty (CPP) results from premature activation of the hypothalamic–pituitary–gonadal axis. Few genetic causes of CPP have been identified, with the most common being mutations in the paternally expressed imprinted gene MKRN3. Objective: To identify the genetic etiology of CPP in a large multigenerational family. Design: Linkage analysis followed by whole-genome sequencing was performed in a family with five female members with nonsyndromic CPP. Detailed phenotyping was performed at the time of initial diagnosis and long-term follow-up, and circulating levels of Delta-like 1 homolog (DLK1) were measured in affected individuals. Expression of DLK1 was measured in mouse hypothalamus and in kisspeptin-secreting neuronal cell lines in vitro. Setting: Endocrine clinic of an academic medical center. Patients: Patients with familial CPP were studied. Results: A complex defect of DLK1 (∼14-kb deletion and 269-bp duplication) was identified in this family. This deletion included the 5′ untranslated region and the first exon of DLK1, including the translational start site. Only family members who inherited the defect from their father have precocious puberty, consistent with the known imprinting of DLK1. The patients did not demonstrate additional features of the imprinted disorder Temple syndrome except for increased fat mass. Serum DLK1 levels were undetectable in all affected individuals. Dlk1 was expressed in mouse hypothalamus and in kisspeptin neuron-derived cell lines. Conclusion: We identified a genomic defect in DLK1 associated with isolated familial CPP. MKRN3 and DLK1 are both paternally expressed imprinted genes. These findings suggest a role of genomic imprinting in regulating the timing of human puberty.

scholarly journals Synergic Therapeutic Potential of PEA-Um Treatment and NAAA Enzyme Silencing In the Management of Neuroinflammation

2020 ◽  
Vol 21 (20) ◽  
pp. 7486
Author(s):  
Giovanna Casili ◽  
Marika Lanza ◽  
Michela Campolo ◽  
Rosalba Siracusa ◽  
Irene Paterniti ◽  
...  
Keyword(s):  
Cell Lines ◽  
Therapeutic Potential ◽  
Neuronal Cells ◽  
Neuronal Cell ◽  
In Vitro Study ◽  
Protective Role ◽  
Point Of View ◽  
Concomitant Treatment ◽  
Neuronal Cell Lines

Inflammation is a key element in the pathobiology of neurodegenerative diseases and sees the involvement of different neuronal and non-neuronal cells as players able to respond to inflammatory signals of immune origin. Palmitoylethanolamide (PEA) is an endogenous potent anti-inflammatory agent, in which activity is regulated by N-acylethanolamine acid amidase (NAAA), that hydrolyzes saturated or monounsaturated fatty acid ethanolamides, such as PEA. In this research, an in vitro study was performed on different neuronal (SH-SY5Y) and non-neuronal cell lines (C6, BV-2, and Mo3.13) subjected to NAAA enzyme silencing and treated with PEA ultra-micronized (PEA-um) (1, 3, and 10 μM) to increase the amount of endogenous PEA available for counteract neuroinflammation provoked by stimulation with lipopolysaccharide (LPS) (1 μg/mL) and interferon gamma (INF-γ )(100 U/mL). Cell viability was performed by MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide) staining, suggesting a protective effect of PEA-um (3 and 10 μM) on all cell lines studied. Western Blot analysis for inflammatory markers (Inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2)) was carried out in control and NAAA-silenced cells, highlighting how the concomitant treatment of the neuronal and non-neuronal cells with PEA-um after NAAA genic downregulation is satisfactory to counteract neuroinflammation. These in vitro findings support the protective role of endogenous PEA availability in the neuronal field, bringing interesting information for a translational point of view.

Stably transfected rat neuronal cell lines expressing alpha-Synuclein GFP Fusion Proteins as an in vitro model of Parkinson's Disease

2004 ◽  
Vol 2004 (Fall) ◽  
Author(s):  
Gert Schwach ◽  
M. Tschemmernegg ◽  
E. Schreiner ◽  
M. Windisch ◽  
R. Pfragner ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Lines ◽  
Fusion Proteins ◽  
In Vitro Model ◽  
Neuronal Cell ◽  
Alpha Synuclein ◽  
Neuronal Cell Lines ◽  
Vitro Model

Gynura Procumbens (Lour.) Merr Inhibits the Glutamate Induced Toxicity in Neuronal Cell Lines.

2017 ◽  
Author(s):  
W Lee Hyeon ◽  
H Ryu Ga ◽  
S Yang Woo ◽  
J Ma Choong
Keyword(s):  
Cell Lines ◽  
Neuronal Cell ◽  
Neuronal Cell Lines

scholarly journals Human Neuronal Cell Lines as An In Vitro Toxicological Tool for the Evaluation of Novel Psychoactive Substances

2021 ◽  
Vol 22 (13) ◽  
pp. 6785
Author(s):  
Valeria Sogos ◽  
Paola Caria ◽  
Clara Porcedda ◽  
Rafaela Mostallino ◽  
Franca Piras ◽  
...  
Keyword(s):  
Cell Death ◽  
Neuronal Cell ◽  
In Vitro Study ◽  
Dependent Manner ◽  
Novel Psychoactive Substances ◽  
Psychoactive Substances ◽  
Concentration Dependent Manner ◽  
Mechanisms Of Toxicity ◽  
Neuronal Cell Lines

Novel psychoactive substances (NPS) are synthetic substances belonging to diverse groups, designed to mimic the effects of scheduled drugs, resulting in altered toxicity and potency. Up to now, information available on the pharmacology and toxicology of these new substances is very limited, posing a considerable challenge for prevention and treatment. The present in vitro study investigated the possible mechanisms of toxicity of two emerging NPS (i) 4′-methyl-alpha-pyrrolidinoexanophenone (3,4-MDPHP), a synthetic cathinone, and (ii) 2-chloro-4,5-methylenedioxymethamphetamine (2-Cl-4,5-MDMA), a phenethylamine. In addition, to apply our model to the class of synthetic opioids, we evaluated the toxicity of fentanyl, as a reference compound for this group of frequently abused substances. To this aim, the in vitro toxic effects of these three compounds were evaluated in dopaminergic-differentiated SH-SY5Y cells. Following 24 h of exposure, all compounds induced a loss of viability, and oxidative stress in a concentration-dependent manner. 2-Cl-4,5-MDMA activates apoptotic processes, while 3,4-MDPHP elicits cell death by necrosis. Fentanyl triggers cell death through both mechanisms. Increased expression levels of pro-apoptotic Bax and caspase 3 activity were observed following 2-Cl-4,5-MDMA and fentanyl, but not 3,4-MDPHP exposure, confirming the different modes of cell death.

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