The effect of taurine on kindled seizures in the rat

1978 ◽  
Vol 56 (3) ◽  
pp. 497-500 ◽  
Author(s):  
W. M. Burnham ◽  
P. Albright ◽  
R. J. Racine
Keyword(s):  
Amino Acid ◽  
Anticonvulsant Drugs ◽  
Threshold Levels ◽  
Kindled Seizures ◽  
The Brain ◽  
Anticonvulsant Effects ◽  
Near Threshold

Recently, it has been reported that taurine, an amino acid with anticonvulsant properties, does not suppress experimental seizures generated by the 'kindling' technique. This finding seems somewhat paradoxical since taurine antagonizes other sorts of experimental convulsion and since kindled seizures are easily suppressed by other anticonvulsant drugs. Further tests were therefore conducted during which taurine's anticonvulsant effects were assessed: (1) when kindling stimulation was dropped to near-threshold levels; (2) when cortical as well as limbic kindled foci were stimulated; (3) when developing as well as fully kindled seizures were involved; and (4) when taurine was introduced directly into the ventricles of the brain. Even in these tests which were specifically designed to favour the appearance of anticonvulsant effects, no taurine antagonism of kindled seizures was found.

Immunoelectron microscope detection of C-type natriuretic peptide in normal human atrial tissue

1993 ◽  
Vol 51 ◽  
pp. 388-389
Author(s):  
Chi-Ming Wei ◽  
Margaret Hukee ◽  
Christopher G.A. McGregor ◽  
John C. Burnett
Keyword(s):  
Amino Acid ◽  
Natriuretic Peptide ◽  
Vascular Tone ◽  
Cardiac Tissue ◽  
Ring Structure ◽  
Terminal Amino Acid ◽  
Amino Acid Peptide ◽  
Normal Human ◽  
Terminal Amino ◽  
The Brain

C-type natriuretic peptide (CNP) is a newly identified peptide that is structurally related to atrial (ANP) and brain natriuretic peptide (BNP). CNP exists as a 22-amino acid peptide and like ANP and BNP has a 17-amino acid ring formed by a disulfide bond. Unlike these two previously identified cardiac peptides, CNP lacks the COOH-terminal amino acid extension from the ring structure. ANP, BNP and CNP decrease cardiac preload, but unlike ANP and BNP, CNP is not natriuretic. While ANP and BNP have been localized to the heart, recent investigations have failed to detect CNP mRNA in the myocardium although small concentrations of CNP are detectable in the porcine myocardium. While originally localized to the brain, recent investigations have localized CNP to endothelial cells consistent with a paracrine role for CNP in the control of vascular tone. While CNP has been detected in cardiac tissue by radioimmunoassay, no studies have demonstrated CNP localization in normal human heart by immunoelectron microscopy.

Association of the brain anion exchanger, AE3, with the repeat domain of ankyrin

1993 ◽  
Vol 105 (4) ◽  
pp. 1137-1142 ◽  
Author(s):  
C.W. Morgans ◽  
R.R. Kopito
Keyword(s):  
Amino Acid ◽  
Amino Acid Sequence ◽  
Anion Exchanger ◽  
Deletion Mutant ◽  
Tandem Repeats ◽  
Structural Homology ◽  
Terminal Domain ◽  
Repeat Domain ◽  
The Brain

The 89 kDa NH2-terminal domain of erythrocyte ankyrin is composed almost entirely of 22 tandem repeats of a 33 amino acid sequence and constitutes the binding site for the cytoplasmic NH2-terminal domain of the erythrocyte anion exchanger, AE1. We have developed an assay to evaluate the in vivo interaction between a fragment of ankyrin corresponding to this domain (ANK90) and two non-erythroid anion exchangers, AE2 and AE3, that share considerable structural homology with AE1. Association was assessed by co-immunoprecipitation of ANK90-anion exchanger complexes from detergent extracts of cells cotransfected with plasmids encoding the ankyrin fragment and the anion exchanger or mutants thereof. ANK90 was co-immunoprecipitated with AE1 but not with an AE1 deletion mutant lacking the cytoplasmic NH2-terminal domain. Using this assay, we show that the brain anion exchanger AE3, but not the closely related homologue, AE2, is capable of binding to ankyrin.

The anticonvulsant effects of progesterone and its metabolites on amygdala-kindled seizures in male rats

2006 ◽  
Vol 1101 (1) ◽  
pp. 110-116 ◽  
Author(s):  
Deborah Lonsdale ◽  
Kirk Nylen ◽  
W. McIntyre Burnham
Keyword(s):  
Male Rats ◽  
Kindled Seizures ◽  
Anticonvulsant Effects

scholarly journals A novel antioxidant ergothioneine PET radioligand for in vivo imaging applications

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
William J. Behof ◽  
Clayton A. Whitmore ◽  
Justin R. Haynes ◽  
Adam J. Rosenberg ◽  
Mohammed N. Tantawy ◽  
...  
Keyword(s):  
Amino Acid ◽  
Mouse Model ◽  
Peripheral Tissues ◽  
Molar Activity ◽  
Model Of Alzheimer’S Disease ◽  
Specific Retention ◽  
5Xfad Mice ◽  
The Brain

AbstractErgothioneine (ERGO) is a rare amino acid mostly found in fungi, including mushrooms, with recognized antioxidant activity to protect tissues from damage by reactive oxygen species (ROS) components. Prior to this publication, the biodistribution of ERGO has been performed solely in vitro using extracted tissues. The aim of this study was to develop a feasible chemistry for the synthesis of an ERGO PET radioligand, [11C]ERGO, to facilitate in vivo study. The radioligand probe was synthesized with identical structure to ERGO by employing an orthogonal protection/deprotection approach. [11C]methylation of the precursor was performed via [11C]CH3OTf to provide [11C]ERGO radioligand. The [11C]ERGO was isolated by RP-HPLC with a molar activity of 690 TBq/mmol. To demonstrate the biodistribution of the radioligand, we administered approximately 37 MBq/0.1 mL in 5XFAD mice, a mouse model of Alzheimer’s disease via the tail vein. The distribution of ERGO in the brain was monitored using 90-min dynamic PET scans. The delivery and specific retention of [11C]ERGO in an LPS-mediated neuroinflammation mouse model was also demonstrated. For the pharmacokinetic study, the concentration of the compound in the serum started to decrease 10 min after injection while starting to distribute in other peripheral tissues. In particular, a significant amount of the compound was found in the eyes and small intestine. The radioligand was also distributed in several regions of the brain of 5XFAD mice, and the signal remained strong 30 min post-injection. This is the first time the biodistribution of this antioxidant and rare amino acid has been demonstrated in a preclinical mouse model in a highly sensitive and non-invasive manner.

scholarly journals Phenylalanine and Tryptophan Intake of Hyperactive Children with Autism

2017 ◽  
Vol 3 (2) ◽  
pp. 34
Author(s):  
Puspito Arum ◽  
Dahlia Indah Amareta ◽  
Faridlotul Zannah
Keyword(s):  
Amino Acid ◽  
Children With Autism ◽  
The Body ◽  
Cross Sectional ◽  
Food Frequency ◽  
Hyperactivity Disorder ◽  
Normal Behavior ◽  
Hyperactive Children ◽  
Dsm Iv ◽  
The Brain

Background: Hyperactive is behavior which demonstrates the attitude of more energy than normal behavior. Level of neurotransmitter dopamine and serotonin in the body may be the factor of this disorder behavior.  Level of phenylalanine and serotonin were found high in hyperactive children with autism. Level phenylalanine in the brain shows that it is not changed into tyrosine so dopamine can not be form. Serotonin derived from an amino acid tryptophan.Objective: To understand the association between phenylalanine and tryptophan intake to hyperactivity of  children with autism.Methods: A survey analytic research with cross sectional approach involving 20 subjects. Phenylalanine and tryptophan intake data was collected by Semi Quantitative-Food Frequency Questionnaire (SQ-FFQ), and hyperactivity disorder of children with autism was measured based on DSM-IV guidelines. Results: Eight (40%) children had low hyperactivity, 9 (45%) children had moderate hyperactivity, 2 (10%) children had severe hyperactivity, and 1 (5%) child had very severe hyperactivity. Mean phenylalanine intake was 4899.74mg (±1543.42) with maximum and minimum intake respectively 7735.42mg and 1843.88mg. Tryptophan intake was 1153.91mg (±384.99) with maximum and minimum intake respectively 1953.89mg and 367.69mg. There was significant association between phenylalanine intake (p=0,034; r=0,477) and tryptophan intake and hyperactivity (p=0,026; r=0,492).Conclusion: There is an association between intakes of amino acid phenylalanine and amino acid tryptophan with hyperactivity of autistic children

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