A new metabolic pathway of L-threo-3,4-dihydroxyphenylserine, a precursor amino acid of norepinephrine, in the brain Studies by in vivo microdialysis

1994 ◽  
Vol 7 (1) ◽  
pp. 21-33 ◽  
Author(s):  
W. Maruyama ◽  
D. Nakahara ◽  
M. Naoi
Keyword(s):  
Amino Acid ◽  
Metabolic Pathway ◽  
In Vivo Microdialysis ◽  
Precursor Amino Acid ◽  
The Brain

Monitoring Amino Acid Neurotransmitter Release in the Brain by In Vivo Microdialysis

2003 ◽  
pp. 239-250
Author(s):  
Mark Zuiderwijk ◽  
Wim E. J. M. Ghijsen
Keyword(s):  
Amino Acid ◽  
Neurotransmitter Release ◽  
In Vivo Microdialysis ◽  
The Brain

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.

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.

Presynaptic modulation of excitatory amino acid release: An in vivo microdialysis study

1996 ◽  
Vol 35 (6) ◽  
pp. A2
Author(s):  
G. Battaglia ◽  
J.A. Monn ◽  
K. Perry ◽  
D.D. Schoepp
Keyword(s):  
Amino Acid ◽  
Excitatory Amino Acid ◽  
In Vivo Microdialysis ◽  
Presynaptic Modulation ◽  
Amino Acid Release ◽  
Acid Release ◽  
Microdialysis Study

Acute administration of a tryptophan-free amino acid mixture decreases 5-HT release in rat hippocampus in vivo

1997 ◽  
Vol 272 (3) ◽  
pp. R991-R994 ◽  
Author(s):  
R. Stancampiano ◽  
F. Melis ◽  
L. Sarais ◽  
S. Cocco ◽  
C. Cugusi ◽  
...  
Keyword(s):  
Amino Acid ◽  
Oral Administration ◽  
Free Amino Acid ◽  
Free Amino ◽  
Dorsal Hippocampus ◽  
Amino Acid Mixture ◽  
Acid Mixture ◽  
Acute Administration ◽  
The Brain

The effect of oral administration of a tryptophan-free amino acid mixture or the same mixture containing tryptophan (Trp) on hippocampal serotonin (5-HT) extracellular levels was studied using in vivo brain microdialysis of freely moving rats. During chloral hydrate anesthesia rats were implanted with dialysis probes in the dorsal hippocampus, and experiments were performed 24 h later. In vehicle-treated rats, the extracellular levels of 5-hydroxyindolacetic acid (5-HIAA) and 5-HT did not change during 240 min after ingestion. Oral administration of the Trp-free amino acid mixture significantly decreased basal 5-HT and 5-HIAA output 100 min after ingestion (65 and 81% of basal value, respectively) and remained at this level for another 140 min. The amino acid mixture containing Trp failed to significantly change basal extracellular levels of 5-HT, but enhanced that of 5-HIAA by approximately 134%. Moreover, in rats receiving the Trp-free amino acid mixture, the increase of hippocampal 5-HT release induced by d-fenfluramine (206%) was smaller than that released by the same drug in rats receiving the nutritionally balanced amino acid mixture (271%). Thus these results show that removal of Trp from the balanced amino acid mixture decreases spontaneous and d-fenfluramine-induced release of 5-HT in the hippocampus. In conclusion, our study supports the hypothesis that the mood-lowering effect observed in man after ingestion of a Trp-free amino acid mixture is associated with diminished 5-HT release in the brain.

Increased Noradrenergic Neurotransmission to a Pain Facilitatory Area of the Brain Is Implicated in Facilitation of Chronic Pain

2015 ◽  
Vol 123 (3) ◽  
pp. 642-653 ◽  
Author(s):  
Isabel Martins ◽  
Paulina Carvalho ◽  
Martin G. de Vries ◽  
Armando Teixeira-Pinto ◽  
Steven P. Wilson ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Locus Coeruleus ◽  
Camp Response Element Binding ◽  
In Vivo Microdialysis ◽  
Reticular Nucleus ◽  
Analgesic Effects ◽  
Inhibitory Function ◽  
Noradrenaline Reuptake ◽  
The Brain

Abstract Background: Noradrenaline reuptake inhibitors are known to produce analgesia through a spinal action but they also act in the brain. However, the action of noradrenaline on supraspinal pain control regions is understudied. The authors addressed the noradrenergic modulation of the dorsal reticular nucleus (DRt), a medullary pronociceptive area, in the spared nerve injury (SNI) model of neuropathic pain. Methods: The expression of the phosphorylated cAMP response element-binding protein (pCREB), a marker of neuronal activation, was evaluated in the locus coeruleus and A5 noradrenergic neurons (n = 6 rats/group). pCREB was studied in noradrenergic DRt-projecting neurons retrogradely labeled in SNI animals (n = 3). In vivo microdialysis was used to measure noradrenaline release in the DRt on nociceptive stimulation or after DRt infusion of clonidine (n = 5 to 6 per group). Pharmacology, immunohistochemistry, and western blot were used to study α-adrenoreceptors in the DRt (n = 4 to 6 per group). Results: pCREB expression significantly increased in the locus coeruleus and A5 of SNI animals, and most noradrenergic DRt-projecting neurons expressed pCREB. In SNI animals, noradrenaline levels significantly increased on pinprick (mean ± SD, 126 ± 14%; P = 0.025 vs. baseline) and acetone stimulation (mean ± SD, 151 ± 12%; P < 0.001 vs. baseline), and clonidine infusion showed decreased α2-mediated inhibitory function. α1-adrenoreceptor blockade decreased nociceptive behavioral responses in SNI animals. α2-adrenoreceptor expression was not altered. Conclusions: Chronic pain induces brainstem noradrenergic activation that enhances descending facilitation from the DRt. This suggests that antidepressants inhibiting noradrenaline reuptake may enhance pain facilitation from the brain, counteracting their analgesic effects at the spinal cord.

scholarly journals Hypoglycemia alters striatal amino acid efflux in perinatal rats: An in vivo microdialysis study

1990 ◽  
Vol 28 (4) ◽  
pp. 516-521 ◽  
Author(s):  
Faye S. Silverstein ◽  
Jennifer Simpson ◽  
Kevin E. Gordon
Keyword(s):  
Amino Acid ◽  
In Vivo Microdialysis ◽  
Microdialysis Study ◽  
Amino Acid Efflux
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