scholarly journals Short-term effect of adrenalin on S-100b and N-CAM level in the different rat brain areas

2015 ◽  
Vol 6 (2) ◽  
pp. 119-124
Author(s):  
Y. P. Kovalchuk ◽  
O. O. Dovban ◽  
A. M. Kanga ◽  
G. A. Ushakovа
Keyword(s):  
Rat Brain ◽  
Calcium Binding ◽  
Circulatory System ◽  
Protein S ◽  
Specific Protein ◽  
The Body ◽  
High Concentrations ◽  
Sense Of Danger ◽  
Almost All ◽  
The Brain

The level of adrenalin grows under stress conditions, sense of danger, anxiety, fear, trauma, burns and shock. In high concentrations adrenaline increases the speed of protein catabolism. Working through the circulatory system, adrenaline affects almost all the functions of organs, causing the body mobilization to counter stressful situations. Due to ELISA the astrocytes-specific protein (S-100b) and neural cell adhesion molecule (N-CAM) were studied. S-100b is produced mainly by astrocytes іn the brain and depending on the concentration it causes trophic or toxic effect on the neurons and glial cells.Strong stress and ischemia induce re-distribution of calcium-binding protein S-100b and elevation of its level. Quantitative changes of S-100b under the influence of various factors on the body which lead to the metabolic disorder in the brain are considered today as a sign of brain damage (cortical, ischemic one, etc.). Fluctuations in the concentration of S-100b in the brain are not always accompanied by marked deterioration of the physical condition of animals, but they can also lead to a number of violations of integrative functions of the brain depending on over-production of this protein. Most N-CAM are transmembrane proteins that cross the plasma membraneonce; intracellular domains have different size and it is thought they are involved in binding to cytoskeleton or cell signaling. Violation of N-CAM functions leads to disruption of nerve sprouts. Data obtained in our study showed no serious re-distribution of S-100b and N-CAM level in the different areas of rat brain (cerebral cortex, hippocampus and thalamus) under effect of adrenalin administered to the animals (under skin) in dosage of 0.45–0.60 mg per rat, 1 time per day during 10 days, probably because of the type of injection and/or short time of adrenalin action. Increased dosage of adrenaline 1 hour before decapitation leads to the decrease of level of total protein in membrane fraction extracted from brain tissue without changing the level of S-100b and N-CAM. 

*Grown MD CBD gummies Where To buy? Scam Pills | Alert* v1

2022 ◽  
Author(s):  
health not provided
Keyword(s):  
Circulatory System ◽  
Grape Seed ◽  
The Body ◽  
Secondary Effects ◽  
Psychological Issues ◽  
Primary Element ◽  
Grape Seed Oil ◽  
The Right ◽  
Sleeping Disorder ◽  
The Brain

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scholarly journals Vitamin C In Neuropsychiatry

2015 ◽  
Vol 16 (2) ◽  
pp. 157-161 ◽  
Author(s):  
Dragan M. Pavlović ◽  
Merdin Š. Markišić ◽  
Aleksandra M. Pavlović
Keyword(s):  
Ascorbic Acid ◽  
Vitamin C ◽  
The Body ◽  
Adult Brain ◽  
Normal Brain ◽  
Positive Effects ◽  
Normal Brain Function ◽  
High Concentrations ◽  
High Doses ◽  
The Brain

Abstract Vitamins are necessary factors in human development and normal brain function. Vitamin C is a hydrosoluble compound that humans cannot produce; therefore, we are completely dependent on food intake for vitamin C. Ascorbic acid is an important antioxidative agent and is present in high concentrations in neurons and is also crucial for collagen synthesis throughout the body. Ascorbic acid has a role in modulating many essential neurotransmitters, enables neurogenesis in adult brain and protects cells against infection. While SVCT1 enables the absorption of vitamin C in the intestine, SVCT2 is primarily located in the brain. Ascorbate deficiency is classically expressed as scurvy, which is lethal if not treated. However, subclinical deficiencies are probably much more frequent. Potential fields of vitamin C therapy are in neurodegenerative, cerebrovascular and affective diseases, cancer, brain trauma and others. For example, there is some data on its positive effects in Alzheimer’s disease. Various dosing regimes are used, but ascorbate is safe, even in high doses for protracted periods. Better designed studies are needed to elucidate all of the potential therapeutic roles of vitamin C.

Detection of adiponectin in cerebrospinal fluid in humans

2007 ◽  
Vol 293 (4) ◽  
pp. E965-E969 ◽  
Author(s):  
Markus Neumeier ◽  
Johanna Weigert ◽  
Roland Buettner ◽  
Josef Wanninger ◽  
Andreas Schäffler ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Serum Concentration ◽  
Physiological Function ◽  
The Body ◽  
Serum Adiponectin ◽  
Albumin Ratio ◽  
Adiponectin Mrna ◽  
Low Levels ◽  
High Concentrations ◽  
The Brain

Adiponectin circulates in the body in high concentrations, and 100-fold lower amounts were described in the cerebrospinal fluid (CSF) of mice, whereas in humans, contradictory results have been published. To clarify whether adiponectin is present in human CSF and is derived from the circulation, it was determined in human CSF and plasma of 52 nonselected patients. Adiponectin was detected by immunoblot in CSF and was quantified in CSF and serum by ELISA. CSF adiponectin was positively correlated to systemic levels, and the CSF/serum adiponectin ratio was correlated to the CSF/serum albumin ratio. Furthermore, disturbed function of the blood-brain barrier (BBB) was associated with an elevated CSF/serum adiponectin ratio. Adiponectin mRNA was not found in the brain, indicating that adiponectin crosses the BBB and/or the blood-cerebrospinal fluid barrier (BCB). Rat adiponectin with a COOH-terminal tag was injected into the tail vein of rats and was detected 3 h later in CSF. However, CSF adiponectin in humans and rats was ∼0.1% of the serum concentration and therefore was below the 0.5% expected in the CSF because of the residual leakage of an undisturbed BBB/BCB. Taken together, data from the present study show that adiponectin in human CSF is far below the level expected by the baseline BBB/BCB permeability, indicating that adiponectin enters the brain much less efficiently than albumin, thus supporting recent data that exclude adiponectin transport to the CSF. Additional studies are needed to reveal whether these low levels of adiponectin in CSF have a physiological function.

scholarly journals Regional distribution of SGLT activity in rat brain in vivo

2013 ◽  
Vol 304 (3) ◽  
pp. C240-C247 ◽  
Author(s):  
Amy S. Yu ◽  
Bruce A. Hirayama ◽  
Gerald Timbol ◽  
Jie Liu ◽  
Ana Diez-Sampedro ◽  
...  
Keyword(s):  
Rat Brain ◽  
Ex Vivo ◽  
Osmotic Shock ◽  
Regional Distribution ◽  
The Body ◽  
Specific Substrate ◽  
Ex Vivo Autoradiography ◽  
Molecular Imaging Probe ◽  
The Brain

Na+-glucose cotransporter (SGLT) mRNAs have been detected in many organs of the body, but, apart from kidney and intestine, transporter expression, localization, and functional activity, as well as physiological significance, remain elusive. Using a SGLT-specific molecular imaging probe, α-methyl-4-deoxy-4-[18F]fluoro-d-glucopyranoside (Me-4-FDG) with ex vivo autoradiography and immunohistochemistry, we mapped in vivo the regional distribution of functional SGLTs in rat brain. Since Me-4-FDG is not a substrate for GLUT1 at the blood-brain barrier (BBB), in vivo delivery of the probe into the brain was achieved after opening of the BBB by an established procedure, osmotic shock. Ex vivo autoradiography showed that Me-4-FDG accumulated in regions of the cerebellum, hippocampus, frontal cortex, caudate nucleus, putamen, amygdala, parietal cortex, and paraventricular nucleus of the hypothalamus. Little or no Me-4-FDG accumulated in the brain stem. The regional accumulation of Me-4-FDG overlapped the distribution of SGLT1 protein detected by immunohistochemistry. In summary, after the BBB is opened, the specific substrate for SGLTs, Me-4-FDG, enters the brain and accumulates in selected regions shown to express SGLT1 protein. This localization and the sensitivity of these neurons to anoxia prompt the speculation that SGLTs may play an essential role in glucose utilization under stress such as ischemia. The expression of SGLTs in the brain raises questions about the potential effects of SGLT inhibitors under development for the treatment of diabetes.

scholarly journals Pharmacokinetics of Leptin in Female Mice

2016 ◽  
pp. 311-320 ◽  
Author(s):  
R. A. HART ◽  
R. C. DOBOS ◽  
L. L. AGNEW ◽  
R. L. TELLAM ◽  
J. R. MCFARLANE
Keyword(s):  
Priming Effect ◽  
Time Course ◽  
The Body ◽  
Limited Attention ◽  
Gi Tract ◽  
Time Points ◽  
Female Mice ◽  
High Concentrations ◽  
The Brain ◽  
Major Target

Pharmacokinetics of leptin in mammals has received limited attention and only one study has examined more than two time points and this was in ob/ob mice. This study is the first to observe the distribution of leptin over a time course in female mice. A physiologic dose (12 ng) of radiolabelled leptin was injected in adult female mice via the lateral tail vein and tissues were dissected out and measured for radioactivity over a time course up to two hours. Major targets for administered leptin included the liver, kidneys, gastrointestinal tract and the skin while the lungs had high concentrations of administered leptin per gram of tissue. Leptin was also found to enter the lumen of the digestive tract intact from the plasma. Very little of the dose (<1 %) was recovered from the brain at any time. Consequently we confirm that the brain is not a major target for leptin from the periphery, although it may be very sensitive to leptin that does get to the hypothalamus. Several of the major targets (GI tract, skin and lungs) for leptin form the interface for the body with the environment, and given the ability of leptin to modulate immune function, this may represent a priming effect for tissues to respond to damage and infection.

scholarly journals Pathway in rat brains under experimental obesity caused long-term progesterone administration

2018 ◽  
Vol 75 (1) ◽  
pp. 59-63
Author(s):  
A. Aleksandrov ◽  
V. Konopelniuk ◽  
I. Kompanets ◽  
L. Ostapchenko
Keyword(s):  
Rat Brain ◽  
Tryptophan Hydroxylase ◽  
The Body ◽  
Control Group ◽  
Tryptophan Decarboxylase ◽  
Decarboxylase Activity ◽  
Prolonged Administration ◽  
Hydroxyindoleacetic Acid ◽  
The Brain

Obesity is one of the most common complex health problem. The pathway of serotonin synthesis takes part in neuroendocrine regulation, as well as in the regulation of a number of behavioral functions of the body and fat deposition. Serotonin is a mediator of the amine nature, which functions as a neurotransmitter and tissue hormone. The greatest amount of serotonin is synthesized in the brain and 12 duodenum. As a neurotransmitter, serotonin affects both directly and indirectly on the function of most brain cells. Female hormone progesterone influence on serotonin functions. One of the effect of progesterone is increasing of amount of fat tissue during the pregnancy. Long-term using of progesterone in hormone substitution therapy or as part of contraception also lead to fat accumulation effect. The levels of activity of serotonergic system enzymes, tryptophan hydroxylase, tryptophan decarboxylase and monoamine oxidase (MAO), and tryptophan, 5-hydroxytryptophan, serotonin and 5-hydroxyindoleacetic acid concentrations in the rat brain under obesity conditions caused by prolonged administration of progesterone were determined in this study. Studies have shown that the content of tryptophan, 5-hydroxytryptophan, serotonin and 5-hydroxyindoleacetic acid in the brain of rats under obesity caused by prolonged administration of progesterone increased in comparison with the rats of the control group. The levels of tryptophan hydroxylase and MAO activity decreased, and tryptophan decarboxylase activity levels increased in the rat brain under obesity conditions caused by prolonged administration of progesterone. Thus, as a result of our studies, we found an imbalance in the system of serotonin metabolism in the brain of rats with the development of hormonal obesity induced by prolonged administration of progesterone, which may indicate the involvement of the serotonergic neurotransmitter system in the mechanisms of the development of obesity and concomitant diseases.

BIOCHEMICAL STUDIES ON CHLORPROMAZINE: 2. EFFECTS OF CHLORPROMAZINE ON INCORPORATION INTO PROTEINS, AND BREAKDOWN OF GLYCINE-1-C14BY ISOLATED RAT BRAIN CORTEX

1957 ◽  
Vol 35 (1) ◽  
pp. 1145-1150 ◽  
Author(s):  
O. Lindan ◽  
J. H. Quastel ◽  
S. Sved
Keyword(s):  
Rat Brain ◽  
Brain Cortex ◽  
Experimental Conditions ◽  
Rat Brain Cortex ◽  
Brain Cortex Slices ◽  
High Concentrations ◽  
Cortex Slices ◽  
The Given ◽  
The Brain ◽  
Stimulation Of

Glycine is decomposed in rat brain cortex to yield carbon dioxide. This process, in which C14O2is formed from glycine-1-C14, is markedly stimulated by the presence of 10 mM glucose, the rate of production of C14O2being increased at least threefold. The presence of succinate exercises a much smaller stimulation of C14O2formation. The addition of KCl (0.1 M) or of 2,4-dmitrophenol (0.025 mM), whilst stimulating the rate of oxygen uptake, does not increase the rate of C14O2formation from glycine-1-C14. The addition of K+tends to diminish the rate. The process of glycine-1-C14breakdown to C14O2is almost insensitive to chlorpromazine, under the given experimental conditions, until relatively high concentrations (e.g. 0.6 mM) are used. The presence of chlorpromazine, however, brings about an inhibition of the rate of glycine-1-C14incorporation into rat brain cortex proteins, an inhibition of 20% being recorded at a concentration of the drug (0.2 mM) that has little or no effect on the respiration of the brain or on the rate of breakdown of glycine-1-C14into C14O2. Glycine incorporation into brain cortex proteins is a process relatively sensitive to chlorpromazine, the magnitude of inhibition being of the same order as that brought about by amytal at similar concentrations. It is suggested that chlorpromazine brings about its effects by an uncoupling of phosphorylation from oxidation in brain cortex slices.

scholarly journals Contractile pericytes determine the direction of blood flow at capillary junctions

2020 ◽  
Vol 117 (43) ◽  
pp. 27022-27033
Author(s):  
Albert L. Gonzales ◽  
Nicholas R. Klug ◽  
Arash Moshkforoush ◽  
Jane C. Lee ◽  
Frank K. Lee ◽  
...  
Keyword(s):  
Blood Flow ◽  
Circulatory System ◽  
The Body ◽  
Capillary Network ◽  
Transitional Region ◽  
Capillary Networks ◽  
Efficiency And Effectiveness ◽  
The Central Nervous System ◽  
Essential Function ◽  
The Brain

The essential function of the circulatory system is to continuously and efficiently supply the O2 and nutrients necessary to meet the metabolic demands of every cell in the body, a function in which vast capillary networks play a key role. Capillary networks serve an additional important function in the central nervous system: acting as a sensory network, they detect neuronal activity in the form of elevated extracellular K+ and initiate a retrograde, propagating, hyperpolarizing signal that dilates upstream arterioles to rapidly increase local blood flow. Yet, little is known about how blood entering this network is distributed on a branch-to-branch basis to reach specific neurons in need. Here, we demonstrate that capillary-enwrapping projections of junctional, contractile pericytes within a postarteriole transitional region differentially constrict to structurally and dynamically determine the morphology of capillary junctions and thereby regulate branch-specific blood flow. We further found that these contractile pericytes are capable of receiving propagating K+-induced hyperpolarizing signals propagating through the capillary network and dynamically channeling red blood cells toward the initiating signal. By controlling blood flow at junctions, contractile pericytes within a functionally distinct postarteriole transitional region maintain the efficiency and effectiveness of the capillary network, enabling optimal perfusion of the brain.

VASOACTIVE INTESTINAL PEPTIDE (VIP): TISSUE DISTRIBUTION IN THE RAT AS MEASURED BY RADIOIMMUNOASSAY AND BY RADIORECEPTORASSAY

1978 ◽  
Vol 87 (4) ◽  
pp. 799-810 ◽  
Author(s):  
J. Besson ◽  
M. Laburthe ◽  
D. Bataille ◽  
C. Dupont ◽  
G. Rosselin
Keyword(s):  
Digestive Tract ◽  
Plasma Membranes ◽  
Biologically Active ◽  
Muscular Tissue ◽  
Liver Plasma Membranes ◽  
Rat Liver Plasma Membranes ◽  
Brain Extracts ◽  
High Concentrations ◽  
Almost All ◽  
The Brain

ABSTRACT This work was undertaken to study the distribution of VIP in the digestive tract. VIP was measured both by radioimmunoassay and by radioreceptorassay in order to determine whether immunoreactive VIP is related to a biologically active component. The effect of digestive extracts in inhibiting the binding of porcine [125I]VIP to the antibody (RIA) and to the rat liver plasma membranes (RRA) paralleled that of porcine VIP used as the standard. VIP was found throughout the digestive tract with especially high concentrations between the duodenum (1676 ± 186 ng/g) and the colon (1214 ± 214 ng/g); the maximal quantity occurred in the jejuno-ileum (11 698 ± 687 ng/g). Less than 1 % of VIP was found in the epithelium whereas almost all VIP (> 99%) was localized in the mucosal muscular tissue of the jejunoileum. VIP concentration in the pancreas was 180 ± 26 ng/g of tissue. The VIP contents of the digestive tract were similar when measured either by radioimmunoassay or by radioreceptorassay. Immunoreactive VIP was found in the brain (155 ± 7 ng/g of tissue) and brain extracts competitively inhibited the binding of [125I]VIP (purified from gut) to liver plasma membranes. These results show that: 1) VIP from the overall gastrointestinal tract is a biological active molecule: 2) VIP from brain binds to receptors for intestinal VIP in liver.

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