scholarly journals Brain Eicosanoid Formation following Acute Penetration Injury as Studied by in vivo Microdialysis

1990 ◽  
Vol 10 (1) ◽  
pp. 143-146 ◽  
Author(s):  
James A. Yergey ◽  
Melvyn P. Heyes
Keyword(s):  
Time Course ◽  
Brain Injuries ◽  
Extracellular Fluid ◽  
Sampling Period ◽  
In Vivo Microdialysis ◽  
Rat Striatum ◽  
Microdialysis Probe ◽  
The Brain ◽  
Eicosanoid Formation

Formation of eicosanoids has been implicated in the pathological changes that follow brain injuries. In the present study, we used a microdialysis probe to both induce acute penetration injury and also sample extracellular fluid concentrations of eicosanoids. Formation of prostaglandin (PG) D2, PGF2 a, and thromboxane B2 was highest in the first hour following introduction of the probe into rat striatum. In contrast, the level of PGE2 was highest during the sixth hour of collection, while 6-keto-PGF1 a remained stable throughout the sampling period. We conclude that in vivo microdialysis may be useful in the evaluation of the time course of the effects of acute penetration injury of the brain on the local production of eicosanoids.

Modified microdialysis probe for sampling extracellular fluid and administering drugs in vivo

1993 ◽  
Vol 265 (5) ◽  
pp. R1205-R1211
Author(s):  
G. Yadid ◽  
K. Pacak ◽  
I. J. Kopin ◽  
D. S. Goldstein
Keyword(s):  
Extracellular Fluid ◽  
In Vivo Microdialysis ◽  
Microdialysis Probe ◽  
Simple Modification ◽  
Drug Concentrations ◽  
Catecholaminergic Cells ◽  
Fluid Levels ◽  
Local Release ◽  
In Vivo Delivery

In vivo microdialysis provides an important new tool for investigating changes in extracellular fluid levels of endogenous compounds in vivo. Delivery of drugs via the microdialysis probe can be used to study local release and metabolism of neurotransmitters, but the dialysis membrane limits diffusion of substances between the perfusate and the extracellular fluid. Thus there may be considerable delay in responses, drug concentrations at the effector sites are less than those in the probe, and high-molecular-weight substances cannot traverse the membrane at all. This report describes a simple modification of commercially available microdialysis probes. A cannula is glued to the external surface of the probe. When glycine was administered via the cannula into the striatum of conscious rats, increments in microdialysate concentrations of dopamine were at least 10 times greater than when glycine was administered via the dialysis fluid in the probe. The threshold glycine dose for behavioral (turning) effects was also decreased by approximately 60-fold, and the time to the peak neurochemical and behavioral effects was markedly decreased. The modified probe did not destroy local catecholaminergic cells, as indicated by tyrosine hydroxylase immunofluorescence. Use of the modified microdialysis probe should facilitate pharmacological and neuroendocrine studies in behaving animals.

Time course of exchanges between red cells and extracellular fluid during CO2 uptake

1975 ◽  
Vol 38 (4) ◽  
pp. 710-718 ◽  
Author(s):  
R. E. Forster ◽  
E. D. Crandall
Keyword(s):  
Carbonic Anhydrase ◽  
Time Course ◽  
Extracellular Fluid ◽  
Extracellular Ph ◽  
Co2 Uptake ◽  
Sudden Increase ◽  
Red Cell ◽  
Ph Change ◽  
Red Cell Membrane

A stopped-flow rapid-reaction apparatus was used to follow the time course of extracellular pH in a human red cell suspension following a sudden increase in PCO2. The extracellular pH change was slow (t1/2 similar to 3.5 s) considering the presence of carbonic anhydrase in the cells. When carbonic anhydrase was added to the extracellular fluid, the half-time was reduced to less than 20 ms. The explanation for these phenomena is that the equilibration of H+ across the red cell membrane is rate-limited by the uncatalyzed reaction CO2 plus H2O formed from H2CO3 outside the cells. A theoretical model was developed which successfully reproduced the experimental results. When the model was used to simulate CO2 exchange in vivo, it was determined that blood PCO2 and pH require long times (greater than 50 s) to approach equilibrium between cells and plasma after leaving an exchange capillary. We conclude that cell-plasma equilibrium may never be reached in vivo, and that in vitro measurements of these quantities may not represent their true values at the site of sampling.

scholarly journals Ferroptosis and Brain Injury

2018 ◽  
Vol 40 (5-6) ◽  
pp. 382-395 ◽  
Author(s):  
Leslie Magtanong ◽  
Scott J. Dixon
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Brain Injuries ◽  
Basic Problem ◽  
Oxygen Species ◽  
Brain Disorders ◽  
Small Molecule Screening ◽  
The Relationship ◽  
The Brain

Ferroptosis is a nonapoptotic form of cell death characterized by the iron-dependent accumulation of toxic lipid reactive oxygen species. Small-molecule screening and subsequent optimization have yielded potent and specific activators and inhibitors of this process. These compounds have been employed to dissect the lethal mechanism and implicate this process in pathological cell death events observed in many tissues, including the brain. Indeed, ferroptosis is emerging as an important mechanism of cell death during stroke, intracerebral hemorrhage, and other acute brain injuries, and may also play a role in certain degenerative brain disorders. Outstanding issues include the practical need to identify molecular markers of ferroptosis that can be used to detect and study this process in vivo, and the more basic problem of understanding the relationship between ferroptosis and other forms of cell death that can be triggered in the brain during injury.

scholarly journals Effect of AMPA receptors on dopamine release in the rat striatum studied by in vivo microdialysis.

1995 ◽  
Vol 67 ◽  
pp. 233
Author(s):  
Kumihiro Nakahara ◽  
Hidevasu Yokoo ◽  
Masami Yoshida ◽  
Takahiko Tanaka ◽  
Hiroyuki Emoto ◽  
...  
Keyword(s):  
Ampa Receptors ◽  
Dopamine Release ◽  
In Vivo Microdialysis ◽  
Rat Striatum

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.

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