Troubleshooting in LC-MS/MS method for determining endocannabinoid and endocannabinoid-like molecules in rat brain structures applied to assessing the brain endocannabinoid/endovanilloid system significance

2014 ◽  
Vol 24 (4) ◽  
pp. 315-322 ◽  
Author(s):  
Beata Bystrowska ◽  
Irena Smaga ◽  
Małgorzata Tyszka-Czochara ◽  
Małgorzata Filip
Keyword(s):  
Rat Brain ◽  
Brain Structures ◽  
The Brain

scholarly journals Long-Term Social Isolation Reduces Expression of the BDNF Precursor and Prolyl Endopeptidase in the Rat Brain

2021 ◽  
Vol 86 (6) ◽  
pp. 704-715
Author(s):  
Sofie D. Shirenova ◽  
Nadezhda N. Khlebnikova ◽  
Nataliya A. Krupina
Keyword(s):  
Western Blot ◽  
Frontal Cortex ◽  
Rat Brain ◽  
Social Isolation ◽  
Early Life ◽  
Wistar Rats ◽  
Cognitive Impairments ◽  
Brain Structures ◽  
Prolyl Endopeptidase ◽  
The Brain

Abstract Early-life stress is a risk factor for the development of behavioral and cognitive disorders in humans and animals. Such stressful situations include social isolation in early postnatal ontogenesis. Behavioral and cognitive impairments associated with neuroplastic changes in brain structures. We have found that after ten weeks of social isolation, male Wistar rats show behavioral abnormalities and cognitive deficit, accompanied by an increase in the relative expression of gene encoding serine protease prolyl endopeptidase (PREP, EC 3.4.21.26) in the brain frontal cortex. The present study aimed to assess synaptophysin (SYP), brain-derived neurotrophic factor precursor (proBDNF), and PREP expression using Western blot in the brain structures – the hippocampus, frontal cortex, and striatum of the rats subjected to prolonged social isolation compared with group-housed animals. Twenty Wistar rats were used for this study (10 males and 10 females). Experimental animals (5 males and 5 females) were kept one per cage for nine months, starting from the age of one month. Ten-month-old socially isolated rats showed memory deficit in passive avoidance paradigm and Morris Water Maze and reactivity to novelty reduction. We used monoclonal antibodies for the Western blot analysis of the expression of SYP, proBDNF, and PREP in the rat brain structures. Social isolation caused a proBDNF expression reduction in the frontal cortex in females and a reduction in PREP expression in the striatum in males. These data suppose that neurotrophic factors and PREP are involved in the mechanisms of behavioral and cognitive impairments observed in the rats subjected to prolonged social isolation with an early life onset.

scholarly journals Expression of somatostatine in ischemia of rat brain

2013 ◽  
Vol 66 (11-12) ◽  
pp. 476-482
Author(s):  
Sinisa Babovic ◽  
Biljana Srdic-Galic ◽  
Branislava Soldatovic-Stajic ◽  
Mina Cvjetkovic-Bosnjak ◽  
Bojana Krstonosic ◽  
...  
Keyword(s):  
Rat Brain ◽  
Pyramidal Cells ◽  
Brain Structures ◽  
Immunohistochemical Method ◽  
Protein Distribution ◽  
Cortex Area ◽  
Histological Data ◽  
Bipolar Type ◽  
Ischemic Attack ◽  
The Brain

Introduction. This study used the immunohistochemical method to follow the expression of cytoplasmatic protein somatostanin in the course of ischemia of rat brain. The aim of the study was to define all the areas of expression of somatostain and to show the protein distribution on the map. Material and Methods. All the sections of telencephalon, diencephalon and midbrain were studied in resistant, and transitory ischemia, which enabled us to observe the reaction of neurons to an ischemic attack or to repeated attacks. Results and Discussion. The results of this study show that there is a difference in the reaction between the resistant and transitory ischemia groups of rats, especially in the parietofrontal cortex, area amygdaloidea anterior, clastrum, nc. reuniens and nc. suprachiasmaticus. The mapping shows the reaction in the structures of motor, sensitive and sensory cortex, mostly in the laminae II/III and V/VI, hippocampus - gyrus dentatus and CA1, CA2, CA3, endopiriform nucleus, paraventricular and periventricular nucleus of hypothalamus, corpus amygdaloideum, claustrum and caudoputamen. The more primitive sections of the brain - rhinencephalon, also showed a reaction, which led us to conclude that both newer and older brain structures reacted immunohistochemically. Histological data showed that small neurons are most commonly found while the second most common are big pyramidal cells of multipolar and bipolar type, with the different body shape. Conclusion. Our findings have confirmed the results of rare studies that dealt with these issues, and offered a precise and detailed map of cells expressing somatostanin in the rat brain following ischemic attack.

HMGB1gene expression changes in the striatum and amigdal of the rat's brain under alcoholization and ethanol withdrawal

2021 ◽  
Vol 67 (1) ◽  
pp. 95-99
Author(s):  
M.I. Airapetov ◽  
S.O. Eresko ◽  
E.R. Bychkov ◽  
A.A. Lebedev ◽  
P.D. Shabanov
Keyword(s):  
Rat Brain ◽  
Alcohol Withdrawal ◽  
Intracellular Signaling ◽  
Molecular Mechanisms ◽  
Brain Structures ◽  
Ethanol Withdrawal ◽  
Hmgb1 Protein ◽  
Neuroimmune System ◽  
The Brain

Intracellular signaling mediated by the HMGB1 protein, an agonist of TLRs, is considered as a possible target for the correction of pathologies of the neuroimmune system, however, the expression level of the Hmgb1 gene has not been previously studied in various brain structures of rats exposed to prolonged alcoholization followed by ethanol withdrawal. The study showed that long-term use of ethanol caused to an increase in the level of Hmgb1 mRNA in the striatum of rat brain. Alcohol withdrawal changed the level Hmgb1 mRNA in the striatum and amygdala on the 1st and 14th day. The data obtained may indicate that in different structures of the brain there are multidirectional changes in the molecular mechanisms of the neuroimmune response with prolonged use of ethanol and its withdrawal.

scholarly journals Expression of Toll-like receptors in emotiogenic structures of rat brain is changed under longterm alcohol consumption and ethanol withdrawal

2020 ◽  
Vol 22 (1) ◽  
pp. 77-86 ◽  
Author(s):  
M. I. Airapetov ◽  
S. O. Eresko ◽  
E. R. Bychkov ◽  
A. A. Lebedev ◽  
P. D. Shabanov
Keyword(s):  
Rat Brain ◽  
Alcohol Withdrawal ◽  
Drug Exposure ◽  
Brain Structures ◽  
Ethanol Consumption ◽  
Ethanol Withdrawal ◽  
Toll Like Receptors ◽  
Tlr3 Mrna ◽  
The Brain

Recent studies have provided strong evidence that long-term ethanol consumption leads to activation the mechanisms of neuroimmune signaling. Recently, much attention has been focused on the study of toll-like receptors (Toll-like receptors, TLRs), which play one of the key roles in the mechanisms of activation of the innate immune system in brain structures subsequently ethanol consumption. It is known that the activation of TLRs leads to the release of many proinflammatory cytokines with the resulting neuroinflammatory process. There are suggestions that TLRs may also be involved in the modulation of neurotransmitter systems of the brain, thereby contributing to the formation of pathological dependence on ethanol. The goal of our work was to study the level of expression the genes of TLRs (TLR3, TLR4, TLR7) and pro-inflammatory cytokine genes (IL-1β, CCL2) in the rat brain (amygdala, hippocampus, medial entorhinal cortex, striatum) under conditions of prolonged alcoholization and on different periods of alcohol withdrawal, which was previously not studied by researchers. Prolonged alcoholization of rats with ethanol did not lead to changes in levels mRNA of TLRs in the studied structures of the rat brain, with the exception of a small increase in the level of TLR3 mRNA in the hippocampus of prolonged alcoholized rats and a slight increase in the level of TLR3 mRNA in mEC. However, gene expression of TLRs undergoes changes in all the structures of the rat brain studied by us at different periods of alcohol withdrawal. The increased level of expression of both TLRs and proinflammatory genes in the period of alcohol withdrawal in the rat brain hippocampus deserves special attention, which indicates the presence of a persistent neuroinflammatory process in this brain structure in the period of alcohol withdrawal, which is probably supported with the participation of TLR-dependent signaling. The study of the mechanisms of inflammatory process activation by TLR-dependent signaling in different brain structures can open new targets for drug exposure. Such drugs can be used in the treatment of alcoholism.

Liquid Chromatography Analysis of Clozapine in Rat Brain Tissue, Using its Molecularly Imprinted Polymer after Administration of Toxic Dose of Drug and Lipid Emulsion Therapy

2019 ◽  
Vol 15 (3) ◽  
pp. 251-257
Author(s):  
Bahareh Sadat Yousefsani ◽  
Seyed Ahmad Mohajeri ◽  
Mohammad Moshiri ◽  
Hossein Hosseinzadeh
Keyword(s):  
Rat Brain ◽  
Brain Tissue ◽  
Molecularly Imprinted Polymer ◽  
Lipid Emulsion ◽  
Limit Of Detection ◽  
Imprinted Polymer ◽  
Toxic Dose ◽  
Molecularly Imprinted ◽  
The Brain ◽  
Rat Brain Tissue

Background:Molecularly imprinted polymers (MIPs) are synthetic polymers that have a selective site for a given analyte, or a group of structurally related compounds, that make them ideal polymers to be used in separation processes.Objective:An optimized molecularly imprinted polymer was selected and applied for selective extraction and analysis of clozapine in rat brain tissue.Methods:A molecularly imprinted solid-phase extraction (MISPE) method was developed for preconcentration and cleanup of clozapine in rat brain samples before HPLC-UV analysis. The extraction and analytical process was calibrated in the range of 0.025-100 ppm. Clozapine recovery in this MISPE process was calculated between 99.40 and 102.96%. The limit of detection (LOD) and the limit of quantification (LOQ) of the assay were 0.003 and 0.025 ppm, respectively. Intra-day precision values for clozapine concentrations of 0.125 and 0.025 ppm were 5.30 and 3.55%, whereas inter-day precision values of these concentrations were 9.23 and 6.15%, respectively. In this study, the effect of lipid emulsion infusion in reducing the brain concentration of drug was also evaluated.Results:The data indicated that calibrated method was successfully applied for the analysis of clozapine in the real rat brain samples after administration of a toxic dose to animal. Finally, the efficacy of lipid emulsion therapy in reducing the brain tissue concentration of clozapine after toxic administration of drug was determined.Conclusion:The proposed MISPE method could be applied in the extraction and preconcentration before HPLC-UV analysis of clozapine in rat brain tissue.

Effect of Prenatal Hypoxia on Activity of the Soluble Forms of Cholinesterases in Rat Brain Structures during Early Postnatal Ontogenesis

2020 ◽  
Vol 56 (6) ◽  
pp. 531-540
Author(s):  
A. Yu. Morozova ◽  
A. V. Arutyunyan ◽  
P. Yu. Morozova ◽  
L. S. Kozina ◽  
I. A. Zhuravin ◽  
...  
Keyword(s):  
Rat Brain ◽  
Brain Structures ◽  
Prenatal Hypoxia ◽  
Postnatal Ontogenesis ◽  
Early Postnatal Ontogenesis

scholarly journals Peptides Derived from Growth Factors to Treat Alzheimer’s Disease

2021 ◽  
Vol 22 (11) ◽  
pp. 6071
Author(s):  
Suzanne Gascon ◽  
Jessica Jann ◽  
Chloé Langlois-Blais ◽  
Mélanie Plourde ◽  
Christine Lavoie ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Growth Factors ◽  
Signaling Pathways ◽  
Brain Structures ◽  
Therapeutic Strategies ◽  
Native Proteins ◽  
Receptor Sites ◽  
The Brain

Alzheimer’s disease (AD) is a devastating neurodegenerative disease characterized by progressive neuron losses in memory-related brain structures. The classical features of AD are a dysregulation of the cholinergic system, the accumulation of amyloid plaques, and neurofibrillary tangles. Unfortunately, current treatments are unable to cure or even delay the progression of the disease. Therefore, new therapeutic strategies have emerged, such as the exogenous administration of neurotrophic factors (e.g., NGF and BDNF) that are deficient or dysregulated in AD. However, their low capacity to cross the blood–brain barrier and their exorbitant cost currently limit their use. To overcome these limitations, short peptides mimicking the binding receptor sites of these growth factors have been developed. Such peptides can target selective signaling pathways involved in neuron survival, differentiation, and/or maintenance. This review focuses on growth factors and their derived peptides as potential treatment for AD. It describes (1) the physiological functions of growth factors in the brain, their neuronal signaling pathways, and alteration in AD; (2) the strategies to develop peptides derived from growth factor and their capacity to mimic the role of native proteins; and (3) new advancements and potential in using these molecules as therapeutic treatments for AD, as well as their limitations.

scholarly journals High-Cholesterol Diet Decreases the Level of Phosphatidylinositol 4,5-Bisphosphate by Enhancing the Expression of Phospholipase C (PLCβ1) in Rat Brain

2020 ◽  
Vol 21 (3) ◽  
pp. 1161 ◽  
Author(s):  
Yoon Sun Chun ◽  
Sungkwon Chung
Keyword(s):  
Neurodegenerative Diseases ◽  
Rat Brain ◽  
Phospholipase C ◽  
Cultured Cells ◽  
Cell Interaction ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
Amyloid Aβ ◽  
The Brain

Cholesterol is a critical component of eukaryotic membranes, where it contributes to regulating transmembrane signaling, cell–cell interaction, and ion transport. Dysregulation of cholesterol levels in the brain may induce neurodegenerative diseases, such as Alzheimer’s disease, Parkinson disease, and Huntington disease. We previously reported that augmenting membrane cholesterol level regulates ion channels by decreasing the level of phosphatidylinositol 4,5-bisphosphate (PIP2), which is closely related to β-amyloid (Aβ) production. In addition, cholesterol enrichment decreased PIP2 levels by increasing the expression of the β1 isoform of phospholipase C (PLC) in cultured cells. In this study, we examined the effect of a high-cholesterol diet on phospholipase C (PLCβ1) expression and PIP2 levels in rat brain. PIP2 levels were decreased in the cerebral cortex in rats on a high-cholesterol diet. Levels of PLCβ1 expression correlated with PIP2 levels. However, cholesterol and PIP2 levels were not correlated, suggesting that PIP2 level is regulated by cholesterol via PLCβ1 expression in the brain. Thus, there exists cross talk between cholesterol and PIP2 that could contribute to the pathogenesis of neurodegenerative diseases.

scholarly journals The Brain Resting-State Functional Connectivity Underlying Violence Proneness: Is It a Reliable Marker for Neurocriminology? A Systematic Review

2019 ◽  
Vol 9 (1) ◽  
pp. 11 ◽  
Author(s):  
Ángel Romero-Martínez ◽  
Macarena González ◽  
Marisol Lila ◽  
Enrique Gracia ◽  
Luis Martí-Bonmatí ◽  
...  
Keyword(s):  
Functional Connectivity ◽  
Effective Treatment ◽  
Resting State ◽  
Brain Structures ◽  
Prevention Programs ◽  
Angular Gyrus ◽  
Resting State Functional Connectivity ◽  
Treatment And Prevention ◽  
Reliable Marker ◽  
The Brain

Introduction: There is growing scientific interest in understanding the biological mechanisms affecting and/or underlying violent behaviors in order to develop effective treatment and prevention programs. In recent years, neuroscientific research has tried to demonstrate whether the intrinsic activity within the brain at rest in the absence of any external stimulation (resting-state functional connectivity; RSFC) could be employed as a reliable marker for several cognitive abilities and personality traits that are important in behavior regulation, particularly, proneness to violence. Aims: This review aims to highlight the association between the RSFC among specific brain structures and the predisposition to experiencing anger and/or responding to stressful and distressing situations with anger in several populations. Methods: The scientific literature was reviewed following the PRISMA quality criteria for reviews, using the following digital databases: PubMed, PsycINFO, Psicodoc, and Dialnet. Results: The identification of 181 abstracts and retrieval of 34 full texts led to the inclusion of 17 papers. The results described in our study offer a better understanding of the brain networks that might explain the tendency to experience anger. The majority of the studies highlighted that diminished RSFC between the prefrontal cortex and the amygdala might make people prone to reactive violence, but that it is also necessary to contemplate additional cortical (i.e. insula, gyrus [angular, supramarginal, temporal, fusiform, superior, and middle frontal], anterior and posterior cingulated cortex) and subcortical brain structures (i.e. hippocampus, cerebellum, ventral striatum, and nucleus centralis superior) in order to explain a phenomenon as complex as violence. Moreover, we also described the neural pathways that might underlie proactive violence and feelings of revenge, highlighting the RSFC between the OFC, ventral striatal, angular gyrus, mid-occipital cortex, and cerebellum. Conclusions. The results from this synthesis and critical analysis of RSFC findings in several populations offer guidelines for future research and for developing a more accurate model of proneness to violence, in order to create effective treatment and prevention programs.

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