Immunohistochemical and histochemical evidence for the presence of noradrenaline, serotonin and gamma-aminobutyric acid in chief cells of the mouse carotid body

1994 ◽  
Vol 278 (2) ◽  
pp. 249-254 ◽  
Author(s):  
Yukio Oomori ◽  
Kazuhiro Nakaya ◽  
Hiroshi Tanaka ◽  
Hiromichi Iuchi ◽  
Katsushi Ishikawa ◽  
...  
1994 ◽  
Vol 278 (2) ◽  
pp. 249-254 ◽  
Author(s):  
Yukio Oomori ◽  
Kazuhiro Nakaya ◽  
Hiroshi Tanaka ◽  
Hiromichi Iuchi ◽  
Katsushi Ishikawa ◽  
...  

2005 ◽  
Vol 102 (1) ◽  
pp. 110-116 ◽  
Author(s):  
Malin M. Jonsson ◽  
Sten G. E. Lindahl ◽  
Lars I. Eriksson

Background Propofol decreases the acute hypoxic ventilatory response in humans and depresses in vivo carotid body chemosensitivity. The mechanisms behind this impaired oxygen sensing and signaling are not understood. Cholinergic transmission is involved in oxygen signaling, and because general anesthetics such as propofol have affinity to neuronal nicotinic acetylcholine receptors, the authors hypothesized that propofol depresses carotid body chemosensitivity and cholinergic signaling. Methods An isolated rabbit carotid body preparation was used. Chemoreceptor activity was recorded from the whole carotid sinus nerve. The effect of propofol on carotid body chemosensitivity was tested at three different degrees of PO2 reduction. Nicotine-induced chemoreceptor response was evaluated using bolus doses of nicotine given before and after propofol 10-500 microM. The contribution of the gamma-aminobutyric acid A receptor complex was tested by addition of gamma-aminobutyric acid A receptor antagonists. Results Propofol reduced carotid body chemosensitivity; the magnitude of depression was dependent on the reduction in PO2. Furthermore, propofol caused a concentration-dependent (10-500 microM) depression of nicotine-induced chemoreceptor response, with a 50% inhibitory concentration (propofol) of 40 microM. Bicuculline in combination with propofol did not have any additional effect, whereas addition of picrotoxin gave a slightly more pronounced inhibition. Conclusions It is concluded that propofol impairs carotid body chemosensitivity, the magnitude of depression being dependent on the severity of PO2 reduction, and that propofol causes a concentration-dependent block of cholinergic chemotransduction via the carotid sinus nerve, whereas it seems unlikely that an activation of the gamma-aminobutyric acid A receptor complex is involved in this interaction.


1964 ◽  
Vol 11 (01) ◽  
pp. 064-074 ◽  
Author(s):  
Robert H Wagner ◽  
William D McLester ◽  
Marion Smith ◽  
K. M Brinkhous

Summary1. The use of several amino acids, glycine, alpha-aminobutyric acid, alanine, beta-alanine, and gamma-aminobutyric acid, as plasma protein precipitants is described.2. A specific procedure is detailed for the preparation of canine antihemophilic factor (AHF, Factor VIII) in which glycine, beta-alanine, and gammaaminobutyric acid serve as the protein precipitants.3. Preliminary results are reported for the precipitation of bovine and human AHF with amino acids.


1966 ◽  
Vol 16 (01/02) ◽  
pp. 198-206 ◽  
Author(s):  
W Straughn ◽  
R. H Wagner

SummaryA simple new procedure is reported for the isolation of canine, bovine, porcine, and human fibrinogen. Two molar β-alanine is used to precipitate fibrinogen from barium sulfate adsorbed plasma. The procedure is characterized by dependability and high yields. The material is 95% to 98% clottable protein but still contains impurities such as plasminogen and fibrin-stabilizing factor. Plasminogen may be removed by adsorption with charcoal. The fibrinogen preparations exhibit marked stability to freezing, lyophilization, and dialysis. Epsilon-amino-n-caproic acid and gamma-aminobutyric acid which were also studied have the property of precipitating proteins from plasma but lack the specificity for fibrinogen found with β-alanine.


2019 ◽  
Vol 1 (1) ◽  
pp. 6-12
Author(s):  
Fatima Javeria ◽  
Shazma Altaf ◽  
Alishah Zair ◽  
Rana Khalid Iqbal

Schizophrenia is a severe mental disease. The word schizophrenia literally means split mind. There are three major categories of symptoms which include positive, negative and cognitive symptoms. The disease is characterized by symptoms of hallucination, delusions, disorganized thinking and speech. Schizophrenia is related to many other mental and psychological problems like suicide, depression, hallucinations. Including these, it is also a problem for the patient’s family and the caregiver. There is no clear reason for the disease, but with the advances in molecular genetics; certain epigenetic mechanisms are involved in the pathophysiology of the disease. Epigenetic mechanisms that are mainly involved are the DNA methylation, copy number variants. With the advent of GWAS, a wide range of SNPs is found linked with the etiology of schizophrenia. These SNPs serve as ‘hubs’; because these all are integrating with each other in causing of schizophrenia risk. Until recently, there is no treatment available to cure the disease; but anti-psychotics can reduce the disease risk by minimizing its symptoms. Dopamine, serotonin, gamma-aminobutyric acid, are the neurotransmitters which serve as drug targets in the treatment of schizophrenia. Due to the involvement of genetic and epigenetic mechanisms, drugs available are already targeting certain genes involved in the etiology of the disease.


Diabetes ◽  
1979 ◽  
Vol 28 (7) ◽  
pp. 629-633 ◽  
Author(s):  
H. Taniguchi ◽  
Y. Okada ◽  
H. Seguchi ◽  
C. Shimada ◽  
M. Seki ◽  
...  

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