scholarly journals МЕТАБОЛІЗМ МЕТАЛІВ У ГІПОКАМПІ ТА РОЛЬ ЦИНКУ В ПАТОГЕНЕЗІ ЕПІЛЕПТИФОРМНИХ СУДОМ

2016 ◽  
Vol 6 (2) ◽  
pp. 34-44
Author(s):  
O. M. Kuchkovsky
Keyword(s):  
Hippocampal Neurons ◽  
Zinc Content ◽  
Epileptic Activity ◽  
Endogenous Opioids ◽  
Common Mechanism ◽  
Zinc Metabolism ◽  
Glutamatergic Transmission ◽  
Secretory Material ◽  
Metabolism Regulation

<p>Physiological mechanisms of convulsions status during epilepsy or episindrom significantly different from the mechanisms, which were describe for other disorders associated with glutamatergic system, such as schizophrenia (a decrease of glutamate in neurons and increased dopaminergic load), drug addiction and alcoholism (the formation of endogenous opioids and dopamine, strengthening the role of GABA-ergic system).</p><p>With glutamatergic transmission are сconnect not only convulsive state, but also the realization of higher integrative functions. Therefore, the development of epilepsy, particularly  which caused glutamate, implemented by activating Zn-ergic hippocampal neurons, associate with complex changes in human mental functions. Based on a scientific literature about  of the role of chelating zinc in the mechanisms of glutamatergic transmission, we can  suggest it participation in the mechanisms of formation of epilepsy  convulsions.</p><p>In experience on animals, was show that in the animal organism of stressing correlative changes observe zinc content and secretory material in the hippocampus, Paneth cells  and B cells of pancreas. The nature of the changes depend on the stressor. When this change of zinc content in the hippocampus and hypothalamus (as the main regulator of stress reaction) were multidirectional that this can be explained by the release of metal together with secretory material in the hypothalamus into the bloodstream. Research epileptic activity  of hippocampus by administering to the animal chelate 8 BSQ allowed to establish the dependence between convulsant action  and first  stress condition of the animal. Evocation of stress by 8-BSQ and physical activity, immobilization and alcohol abuse found that the convulsive effect of this reagent during intravitreal research increased in the case of prior exposure by specified kinds of stressors. In this pre-convulsive effect on exertion increased by 266% and the zinc content was increased by 75%; in the case of pre-immobilization duration of seizures increased by 206% and the zinc content - 50%; in the case of pre-alcoholization duration of seizures increased by 234%, and a chelating zinc content - 75%. These results suggest a chelating zinc epileptiform participate in the mechanisms of seizures and, possibly, the development of mechanisms of temporal lobe epilepsy (hippocampal). The results of studies of zinc changes in central and peripheral organs of zinc-containing simulated at different functional states allow us to make the assumption that there is a common mechanism for coordination of functional activity as the hippocampus and other zinc-containing bodies with the help of changes in the chelating zinc metabolism, regulation is carried out by means of the hippocampus.</p>

scholarly journals Downregulation of miR-383 reduces depression-like behavior through targeting Wnt family member 2 (Wnt2) in rats

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Shanshan Liu ◽  
Qing Liu ◽  
Yanjie Ju ◽  
Lei Liu
Keyword(s):  
Inflammatory Response ◽  
Family Member ◽  
Chronic Stress ◽  
Hippocampal Neurons ◽  
Luciferase Reporter ◽  
Mild Stress ◽  
Neural Injury ◽  
Expression Levels ◽  
Qrt Pcr

AbstractThis study aimed to evaluate the role of miR-383 in the regulation of Wnt-2 signaling in the rat model of chronic stress. The male SD rats with depressive-like behaviors were stimulated with chronic unpredictable mild stress (CUMS) including ice-water swimming for 5 min, food deprivation for 24 h, water deprivation for 24 h, stimulating tail for 1 min, turning night into day, shaking for 15 min (once/s), and wrap restraint (5 min/time) every day for 21 days. The expression levels of miRNAs were detected by qRT-PCR, and the expression levels of Wnt2, depression-impacted proteins (GFAP, BDNF, CREB), brain neurotransmitters (5-HT, NE, DA) and apoptosis-related proteins (Bax and Bcl-2) were evaluated by qRT-PCR and western blot. Bioinformatic analysis and luciferase reporter assay were performed to determine the relationship between miR-383 and Wnt2. Ethological analysis was evaluated by sugar preference test, refuge island test and open field tests. Rescue experiments including knockdown of miR-383, overexpression and silencing of Wnt2 were performed to determine the role of miR-383. High expression levels of miR-383 were observed in the hippocampus of rats submitted to CUMS model. Downregulation of miR-383 significantly inhibited the apoptosis and inflammatory response of hippocampal neurons, and increased the expression levels of GFAP, BDNF and CREB which were impacted in depression, as well as neurotransmitters, then attenuated neural injury in rats induced by CUMS. Furthermore, Wnt family member 2 (Wnt2) was identified as a target of miR-383, and silencing of Wnt2 obviously attenuated the protective effect of miR-383 inhibitor on the apoptosis and inflammatory response in hippocampal neurons, as well as neural injury in CUMS-induced rats. Downregulation of miR-383 ameliorated the behavioral and neurochemical changes induced by chronic stress in rats by directly targeting Wnt2, indicating that the miR-383/Wnt2 axis might be a potential therapeutic target for MDD.

Photoperiodically Induced Changes in Glutamatergic Stimulation of LH Secretion in Male Syrian Hamsters: Role of Circulating Testosterone and Endogenous Opioids

1994 ◽  
Vol 96 (1) ◽  
pp. 50-62 ◽  
Author(s):  
Francis J.P. Ebling ◽  
Anju Mirakhur ◽  
Elizabeth S. Maywood ◽  
Michael H. Hastings
Keyword(s):  
Endogenous Opioids ◽  
Syrian Hamsters ◽  
Induced Changes ◽  
Lh Secretion ◽  
Stimulation Of

scholarly journals Deletion of the Actin-Associated Tropomyosin Tpm3 Leads to Reduced Cell Complexity in Cultured Hippocampal Neurons—New Insights into the Role of the C-Terminal Region of Tpm3.1

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 715
Author(s):  
Tamara Tomanić ◽  
Claire Martin ◽  
Holly Stefen ◽  
Esmeralda Parić ◽  
Peter Gunning ◽  
...  
Keyword(s):  
Amino Acid ◽  
Hippocampal Neurons ◽  
Molecular Mechanisms ◽  
Growth Cones ◽  
Amino Acid Residues ◽  
Terminal Amino Acid ◽  
C Terminus ◽  
Primary Mouse ◽  
Terminal Amino

Tropomyosins (Tpms) have been described as master regulators of actin, with Tpm3 products shown to be involved in early developmental processes, and the Tpm3 isoform Tpm3.1 controlling changes in the size of neuronal growth cones and neurite growth. Here, we used primary mouse hippocampal neurons of C57/Bl6 wild type and Bl6Tpm3flox transgenic mice to carry out morphometric analyses in response to the absence of Tpm3 products, as well as to investigate the effect of C-terminal truncation on the ability of Tpm3.1 to modulate neuronal morphogenesis. We found that the knock-out of Tpm3 leads to decreased neurite length and complexity, and that the deletion of two amino acid residues at the C-terminus of Tpm3.1 leads to more detrimental changes in neurite morphology than the deletion of six amino acid residues. We also found that Tpm3.1 that lacks the 6 C-terminal amino acid residues does not associate with stress fibres, does not segregate to the tips of neurites, and does not impact the amount of the filamentous actin pool at the axonal growth cones, as opposed to Tpm3.1, which lacks the two C-terminal amino acid residues. Our study provides further insight into the role of both Tpm3 products and the C-terminus of Tpm3.1, and it forms the basis for future studies that aim to identify the molecular mechanisms underlying Tpm3.1 targeting to different subcellular compartments.

scholarly journals A continuum hypothesis of psychotomimetic rapid antidepressants

2021 ◽  
Vol 5 ◽  
pp. 239821282110077
Author(s):  
Joost Haarsma ◽  
Catherine J Harmer ◽  
Sandra Tamm
Keyword(s):  
Continuum Hypothesis ◽  
Sense Of Self ◽  
Predictive Coding ◽  
Common Mechanism ◽  
Symptoms Of Depression ◽  
Research Areas ◽  
Sensory Evidence ◽  
Perceptual Distortions ◽  
Psychotomimetic Effects

Ketamine, classical psychedelics and sleep deprivation are associated with rapid effects on depression. Interestingly, these interventions also have common psychotomimetic actions, mirroring aspects of psychosis such as an altered sense of self, perceptual distortions and distorted thinking. This raises the question whether these interventions might be acute antidepressants through the same mechanisms that underlie some of their psychotomimetic effects. That is, perhaps some symptoms of depression can be understood as occupying the opposite end of a spectrum where elements of psychosis can be found on the other side. This review aims at reviewing the evidence underlying a proposed continuum hypothesis of psychotomimetic rapid antidepressants, suggesting that a range of psychotomimetic interventions are also acute antidepressants as well as trying to explain these common features in a hierarchical predictive coding framework, where we hypothesise that these interventions share a common mechanism by increasing the flexibility of prior expectations. Neurobiological mechanisms at play and the role of different neuromodulatory systems affected by these interventions and their role in controlling the precision of prior expectations and new sensory evidence will be reviewed. The proposed hypothesis will also be discussed in relation to other existing theories of antidepressants. We also suggest a number of novel experiments to test the hypothesis and highlight research areas that could provide further insights, in the hope to better understand the acute antidepressant properties of these interventions.

The role of chloride transport in postsynaptic inhibition of hippocampal neurons

Science ◽  
1986 ◽  
Vol 232 (4756) ◽  
pp. 1413-1415 ◽  
Author(s):  
U Misgeld ◽  
R. Deisz ◽  
H. Dodt ◽  
H. Lux
Keyword(s):  
Hippocampal Neurons ◽  
Chloride Transport ◽  
Postsynaptic Inhibition

The role of blood platelets in nucleoside metabolism: regulation of platelet thymidine phosphorylase

1988 ◽  
Vol 200 (1-2) ◽  
pp. 117-131 ◽  
Author(s):  
T. Shaw ◽  
R.H. Smillie ◽  
A.E. Miller ◽  
D.G. MacPhee
Keyword(s):  
Thymidine Phosphorylase ◽  
Blood Platelets ◽  
Metabolism Regulation ◽  
Nucleoside Metabolism

A meta-analysis and review examining a possible role for oxidative stress and singlet oxygen in diverse diseases

2017 ◽  
Vol 474 (16) ◽  
pp. 2713-2731 ◽  
Author(s):  
Athinoula L. Petrou ◽  
Athina Terzidaki
Keyword(s):  
Oxidative Stress ◽  
Excited State ◽  
Singlet Oxygen ◽  
Ground State ◽  
Meta Analysis ◽  
Common Mechanism ◽  
High Electron ◽  
A Value ◽  
First Excited State

From kinetic data (k, T) we calculated the thermodynamic parameters for various processes (nucleation, elongation, fibrillization, etc.) of proteinaceous diseases that are related to the β-amyloid protein (Alzheimer's), to tau protein (Alzheimer's, Pick's), to α-synuclein (Parkinson's), prion, amylin (type II diabetes), and to α-crystallin (cataract). Our calculations led to ΔG≠ values that vary in the range 92.8–127 kJ mol−1 at 310 K. A value of ∼10–30 kJ mol−1 is the activation energy for the diffusion of reactants, depending on the reaction and the medium. The energy needed for the excitation of O2 from the ground to the first excited state (1Δg, singlet oxygen) is equal to 92 kJ mol−1. So, the ΔG≠ is equal to the energy needed for the excitation of ground state oxygen to the singlet oxygen (1Δg first excited) state. The similarity of the ΔG≠ values is an indication that a common mechanism in the above disorders may be taking place. We attribute this common mechanism to the (same) role of the oxidative stress and specifically of singlet oxygen, (1Δg), to the above-mentioned processes: excitation of ground state oxygen to the singlet oxygen, 1Δg, state (92 kJ mol−1), and reaction of the empty π* orbital with high electron density regions of biomolecules (∼10–30 kJ mol−1 for their diffusion). The ΔG≠ for cases of heat-induced cell killing (cancer) lie also in the above range at 310 K. The present paper is a review and meta-analysis of literature data referring to neurodegenerative and other disorders.

Suppressed hypothalamo–pituitary–adrenal (HPA) responses to central neuropeptide Y (NPY) in late pregnancy and the role of endogenous opioids

2006 ◽  
Vol 27 (1) ◽  
pp. 55 ◽  
Author(s):  
Juliana Bales ◽  
Paula J. Brunton ◽  
John A. Russell
Keyword(s):  
Neuropeptide Y ◽  
Late Pregnancy ◽  
Endogenous Opioids

Neurobiology of Anxiety Disorders

2020 ◽  
Author(s):  
Pooja Palkar ◽  
Eric Hollander
Keyword(s):  
Anxiety Disorders ◽  
Fear Conditioning ◽  
Endogenous Opioids ◽  
Aminobutyric Acid ◽  
Nmda Antagonists ◽  
Important Goal ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
New Learning

In recent years, advances in the fields of neuroimaging and experimental psychology increased our understanding of the basic mechanisms of classical conditioning and learning, contributing to our knowledge of the neurobiology of anxiety disorders. Research has shown that the amygdala is the cornerstone of fear circuitry and that abnormalities in amygdala pathways can affect the acquisition and expression of fear conditioning. Activation of the amygdala in response to disorder-relevant stimuli has been observed in anxiety disorders. The roles of the hippocampus, nucleus accumbens, periaqueductal gray, and insular and medial prefrontal cortices in response to fear have been identified as well. Neurotransmitters such as serotonin, dopamine, γ-aminobutyric acid, glutamate, and some neurosteroids play an important part in the neurobiology of anxiety disorders. Neuropeptides such as oxytocin, neuropeptide Y, galanin, and cholecystokinin have been shown to modulate stress response. Drugs such as N-methyl-d-aspartate (NMDA) antagonists and blockers of voltage-gated calcium channels in the amygdala are anxiolytic. Fear extinction, which entails new learning of fear inhibition, is the mechanism of effective antianxiety treatments such as d-cycloserine, a partial NMDA agonist. Extinction is thought to occur by the medial prefrontal cortex, which inhibits the lateral amygdala under hippocampal modulation. Harnessing extinction to delink neutral stimuli from aversive responses is an important goal of the psychotherapy and pharmacotherapy of anxiety disorders. Discovery of the role of microRNAs in the etiology of anxiety disorders and their possible utility as targets to treat these disorders is fascinating. In this review, we discuss the neurobiology of anxiety disorders, which will help us better manage them clinically. This review contains 5 figures, 6 tables, and 39 references. Key words: Amygdala, anxiety disorders, neurobiology, fear conditioning, neurocircuitry, neurotransmitters, neuropeptides, neurosteroids, endogenous opioids.

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