scholarly journals Hormonal imprinting in the central nervous system: causes and consequences

2013 ◽  
Vol 154 (4) ◽  
pp. 128-135 ◽  
Author(s):  
György Csaba
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Binding Capacity ◽  
Animal Experiments ◽  
Environmental Pollutants ◽  
Methylation Pattern ◽  
Critical Periods ◽  
Hormonal Imprinting ◽  
Modern Age ◽  
The Central Nervous System

The notion of the perinatal „hormonal imprinting” has been published at first in 1980 and since that time it spred expansively. The imprintig develops at the first encounter between the developing receptor and the target hormone – possibly by the alteration of the methylation pattern of DNA – and it is transmitted to the progeny generations of the cell. This is needed for the complete development of the receptor’s binding capacity. However, molecules similar to the target hormone (hormone-analogues, drugs, chemicals, environmental pollutants) can also bind to the developing receptor, causing faulty imprinting with life-long consequences. This can promote pathological conditions. Later it was cleared that in other critical periods such as puberty, imprinting also can be provoked, even in any age in differentiating cells. The central nervous system (brain) also can be mistakenly imprinted, which durably influences the dopaminergic, serotonergic and noradrenergic system and this can be manifested – in animal experiments – in alterations of the sexual and social behavior. In our modern age the faulty hormonal imprintig is inavoidable because of the mass of medicaments, chemicals, the presence of hormone-like materials (e.g. soya phytosteroids) in the food, and environmental pollutants. The author especially emphasizes the danger of oxytocin, as a perinatal imprinter, as it is used very broadly and can basically influence the emotional and social spheres and the appearance of certain diseases such as auitism, schizophrenia and parkinsonism. The danger of perinatal imprinters is growing, considering their effects on the human evolution. Orv. Hetil., 2013, 154, 128–135.

scholarly journals Environmental Pollution and Non-Perinatal Faulty Hormonal Imprinting: A Critical Review

2018 ◽  
Vol 1 (1) ◽  
pp. 54-62
Author(s):  
Csaba G
Keyword(s):  
Hormone Receptors ◽  
Binding Capacity ◽  
Animal Experiments ◽  
Critical Periods ◽  
Hormone Production ◽  
Hormonal Imprinting ◽  
Functional Changes ◽  
Dividing Cells ◽  
Synthetic Hormones ◽  
Survivors Of Childhood Cancer

The perinatal hormonal imprinting takes place perinatally, when the developing hormone receptors meet the hormones of the newborn and this suits the normal receptor-hormone connections for life. In this period the developmental window for imprinting is open and the receptors can be cheated by hormone-related exogeneous molecules, provoking faulty hormonal imprinting with lifelong consequences, as alteration of receptor binding capacity and hormone production, functional changes, altered sexual behavior, immunological alterations and inclination to or manifestation of diseases. However, there are other critical periods of life, when the window is open, as weaning, adolescence, regeneration in adults as well, as in continously dividing cells. The most sensitive non-perinatal critical period is the adolescence. In these periods hormone-like endocrine disruptors (e.g. bisphenol A, benzpyrene, pesticides and herbicides, soy isoflavones, medically used synthetic hormones etc) are provoking faulty hormonal imprinting with lifelong consequences. The hormonal imprinting is an epigenetic process, which is inherited to the progeny cells of the organism and to the offspring of the organism, by which it can chip in the evolution. The non-perinatal faulty hormonal imprinting is justified in animal experiments and seems to be likely in case of survivors of childhood cancer treatment. Similar to the faulty perinatal hormonal imprinting, the late (non-perinatal) faulty imprinting can participate in the provocation of later manifested diseases.

scholarly journals THE ROLE OF MAGNESIUM DEFICIENCY AND ITS SUPPLEMATION IN DISEASES OF CENTRAL NERVOUS SYSTEM. REVIEW

2018 ◽  
Vol 13 (3-4) ◽  
pp. 70-75
Author(s):  
M.V. Khaitovych
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Magnesium Deficiency ◽  
Close Association ◽  
Animal Experiments ◽  
Depression And Anxiety ◽  
Literary Sources ◽  
The Central Nervous System ◽  
System Review

Relevance. Anti-depressant effects of NMDA receptor antagonists have been proven, a close association between low levels of magnesium in the blood and depression. Therefore, in recent years, antidepressant properties of magnesium are actively studied in animal experiments. Objective: To review modern literary sources about the role of magnesium deficiency in the pathogenesis of diseases of the central nervous system. Materials and methods. Searching for a depth of 12 years at Scopus, Google Scholar. Results. The results of experimental and clinical researches pointed out on association between low level of magnesium in hair, liquor, brain with higher risk of development dementia, depression and anxiety. An additional supplementation with magnesium in patients associates with decreasing risk of ischemic stroke and dementia, in pregnancy – provides neuroprotection of fetus, in case of depression increases effectiveness of antidepressants, in brain injury associates with faster recovery of cognitive functions, in migraines - with decreasing in the frequency of attacks and improvement of the quality patients’ lives, in case of neuroleptic therapy - with the possibility of delayed appearance or absence of manifestations of drug parkinsonism. These changes are explained by antagonistic effects of magnesium on glutamate receptors, decreasing oxidative stress intensity as well as neural cell  apoptosis. Conclusion. Magnesium plays an important neuroprotective role.

A Clinical Trial with a New Anticonvulsant Drug, α-(P-Aminophenyl)-α-Ethyl Glutarimide Preparation 16038 (Ciba)

1959 ◽  
Vol 105 (439) ◽  
pp. 448-456 ◽  
Author(s):  
Walter Fabisch
Keyword(s):  
Clinical Trial ◽  
Central Nervous System ◽  
Nervous System ◽  
Animal Experiments ◽  
Anticonvulsant Drug ◽  
The Central Nervous System ◽  
Derivatives Of

Derivatives of glutarimide are known to exert an effect upon the central nervous system. To name only two which are widely used for clinical purposes: Glutethimide (“Doriden”) is a sedative, Bemigride (“Megimide”) a stimulant. Preparation 16038 (Ciba) α-(p-aminophenyl)-α-ethyl glutarimide, in animal experiments had shown properties which suggested its use as an anticonvulsant, and this paper is an account of a clinical trial with the substance on in- and out-patients suffering from epilepsy.

Oxidative Stress and Accelerated Aging in Neurodegenerative and Neuropsychiatric Disorder

2019 ◽  
Vol 24 (40) ◽  
pp. 4711-4725 ◽  
Author(s):  
Ridhima Wadhwa ◽  
Riya Gupta ◽  
Pawan K. Maurya
Keyword(s):  
Oxidative Stress ◽  
Central Nervous System ◽  
Nervous System ◽  
Oxidative Damage ◽  
Neurodegenerative Diseases ◽  
Bipolar Depression ◽  
Environmental Pollutants ◽  
X Rays ◽  
Neuropsychiatric Diseases ◽  
The Central Nervous System

Background: Neurodegenerative diseases are becoming more and more common in today’s world. As people are continuously being exposed to exogenous factors like UV radiations, gamma rays, X-Rays, environmental pollutants and heavy metals, the cases of increased oxidative damage are increasing. Even though some amount of oxidative damage occurs in all metabolic reactions but their increase from the normal level in organisms causes neurodegenerative diseases. These neurodegenerative disorders like Alzeimers, Parkinsons disease and neuropsychiatric disorders such as schizophrenia, bipolar, depression are caused due to the decline in physiological and psychological functions caused by ROS and RNS. These ROS and RNS are formed as the result of excess oxidative damage in the system. Methods: The following article goes into detail explaining all the effects caused by excess oxidative damage like ROS/RNS formation and telomere shortening. Further, it explains the pathways of neurodegenerative diseases and neuropsychiatric diseases. This article also sheds light on the effective treatments of such disorders by changing lifestyle and activating antioxidant pathways. Conclusion: It is clear that neurodegenerative diseases are caused due to excess oxidative stress and alter the functioning of the central nervous system. The central nervous system undergoes neurodegenerative or neuropsychiatric changes.

Effects of Hyperoxia on Lung Utrastructure

1970 ◽  
Vol 28 ◽  
pp. 26-27
Author(s):  
Gladys Harrison
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Light Microscopy ◽  
Oxygen Effects ◽  
Age Dependent ◽  
The Central Nervous System ◽  
The Subject ◽  
Space Age ◽  
Alveolar Septa ◽  
Extensive Damage

With the advent of the space age and the need to determine the requirements for a space cabin atmosphere, oxygen effects came into increased importance, even though these effects have been the subject of continuous research for many years. In fact, Priestly initiated oxygen research when in 1775 he published his results of isolating oxygen and described the effects of breathing it on himself and two mice, the only creatures to have had the “privilege” of breathing this “pure air”.Early studies had demonstrated the central nervous system effects at pressures above one atmosphere. Light microscopy revealed extensive damage to the lungs at one atmosphere. These changes which included perivascular and peribronchial edema, focal hemorrhage, rupture of the alveolar septa, and widespread edema, resulted in death of the animal in less than one week. The severity of the symptoms differed between species and was age dependent, with young animals being more resistant.

Emigration of neutrophils in the central nervous system

1983 ◽  
Vol 41 ◽  
pp. 788-789
Author(s):  
John L.Beggs ◽  
John D. Waggener ◽  
Wanda Miller ◽  
Jane Watkins
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Osmium Tetroxide ◽  
White Blood Cells ◽  
Arterial Perfusion ◽  
E Coli ◽  
Intracisternal Injection ◽  
The Central Nervous System ◽  
Brain And Spinal Cord ◽  
Interendothelial Junctions

Studies using mesenteric and ear chamber preparations have shown that interendothelial junctions provide the route for neutrophil emigration during inflammation. The term emigration refers to the passage of white blood cells across the endothelium from the vascular lumen. Although the precise pathway of transendo- thelial emigration in the central nervous system (CNS) has not been resolved, the presence of different physiological and morphological (tight junctions) properties of CNS endothelium may dictate alternate emigration pathways.To study neutrophil emigration in the CNS, we induced meningitis in guinea pigs by intracisternal injection of E. coli bacteria.In this model, leptomeningeal inflammation is well developed by 3 hr. After 3 1/2 hr, animals were sacrificed by arterial perfusion with 3% phosphate buffered glutaraldehyde. Tissues from brain and spinal cord were post-fixed in 1% osmium tetroxide, dehydrated in alcohols and propylene oxide, and embedded in Epon. Thin serial sections were cut with diamond knives and examined in a Philips 300 electron microscope.

Mammalian Bone Marrow Acetylcholinesterase

1982 ◽  
Vol 40 ◽  
pp. 44-45
Author(s):  
Ezzatollah Keyhani
Keyword(s):  
Central Nervous System ◽  
Bone Marrow ◽  
Nervous System ◽  
Common Property ◽  
Extracellular Medium ◽  
The Central Nervous System ◽  
The Common ◽  
Mammalian Bone

Acetylcholinesterase (EC 3.1.1.7) (ACHE) has been localized at cholinergic junctions both in the central nervous system and at the periphery and it functions in neurotransmission. ACHE was also found in other tissues without involvement in neurotransmission, but exhibiting the common property of transporting water and ions. This communication describes intracellular ACHE in mammalian bone marrow and its secretion into the extracellular medium.

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