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Your search keyword '"Domoki, F."' showing total 7 results
Start Over Author "Domoki, F." Journal neuroscience letters
7 results on '"Domoki, F."'

1. Post-ischemic administration of diazoxide attenuates long-term microglial activation in the rat brain after permanent carotid artery occlusion

Author

Farkas, E, Timmer, NM, Domoki, F, Mihaly, A, Luiten, PGM, Bari, F, and Timmer, Nienke M.

Subjects
Male, Vasodilator Agents, Hippocampus, Morris water navigation task, Pharmacology, DEPENDENT POTASSIUM CHANNELS, MITOCHONDRIAL, Brain Ischemia, PROTECTS, Medicine, Carotid Stenosis, Drug Interactions, Gliosis, OXIDATIVE STRESS, cerebral hypoperfusion, NEURONS, DAMAGE, Learning Disabilities, General Neuroscience, spatial learning, DEATH, medicine.anatomical_structure, Neuroprotective Agents, Treatment Outcome, Anesthesia, Cerebrovascular Circulation, Circulatory system, Encephalitis, Potassium channel opener, Microglia, medicine.drug, Brain Infarction, Central nervous system, Ischemia, ischemia, Neuroprotection, Diazoxide, Animals, Sodium Hydroxide, Dimethyl Sulfoxide, Rats, Wistar, Maze Learning, Memory Disorders, business.industry, CD11 Antigens, EXPERIMENTAL CEREBRAL HYPOPERFUSION, medicine.disease, Rats, Disease Models, Animal, business
Abstract

Diazoxide is a putative mitochondrial, ATP-sensitive potassium channel opener that has been implicated in neuroprotection in cerebral ischemia. Administered as pretreatment, diazoxide can attenuate ischemia-related neuronal injury, but little is known about the potential neuroprotective properties of the drug when it is given after the onset of an ischemic insult. In a previous study, we applied diazoxide after imposing chronic cerebral hypoperfusion by means of permanent, bilateral occlusion of the common carotid arteries (2VO) in rats. We observed that ischemia-induced learning impairment assessed in the Morris water maze, and microglial activation visualized by immunocytochemistry, were prevented by diazoxide as determined at 13 weeks after 2VO. However, dimethyl sulfoxide, the organic solvent of diazoxide also prevented memory deficits, without any effect on microglial activity. Therefore, we have repeated our experiments with the use of an inorganic solvent, aqueous NaOH solution in order to clarify the effect of diazoxide independent of dimethyl sulfoxide. The present results demonstrated that diazoxide alone did not improve learning performance, but it prevented microglial activation in the hippocampus 13 weeks after the onset of 2VO. These data provide evidence that post-treatment with diazoxide is not effective in impeding a long-term memory deficiency, but it can attenuate ischemia-induced microglial activation, independently of the solvent used. (C) 2005 Elsevier Ireland Ltd. All rights reserved.

Published
2005

6. Perineural capsaicin treatment attenuates reactive hyperaemia in the rat skin.

Author

Domoki F, Sántha P, Bari F, and Jancsó G

Subjects
Animals, Capsaicin administration & dosage, Femoral Artery physiology, Hyperemia physiopathology, Laser-Doppler Flowmetry methods, Male, Rats, Rats, Wistar, Regional Blood Flow, Skin Diseases physiopathology, Time Factors, Capsaicin therapeutic use, Coronary Circulation drug effects, Hyperemia drug therapy, Skin Diseases drug therapy
Abstract

The neural mechanisms of reactive cutaneous hyperaemia were studied by using a novel experimental approach: the simultaneous measurement of cutaneous blood flow by laser-Doppler flowmetry in adjacent innervated and chemodenervated skin regions of the rat hindpaw served by the same artery. Transient occlusion of the femoral artery (0.5-6 min) resulted in reactive hyperaemia that was greatly reduced in the chemodenervated region. After 3 min arterial occlusion, peak cutaneous blood flow was 109+/-13% vs. 53+/-7%* (% change from baseline, n=11, *P<0.05), and the total hyperaemic response was 110+/-21 vs. 52+/-12* (arbitrary perfusion units) in intact vs. chemodenervated skin regions, respectively. The findings provide clear evidence for the involvement of peptidergic capsaicin-sensitive afferent nerves in the mechanism of reactive cutaneous hyperaemia.

Published
2003
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7. Beta-amyloid (1-42) peptide impairs blood-brain barrier function after intracarotid infusion in rats.

Author

Jancsó G, Domoki F, Sántha P, Varga J, Fischer J, Orosz K, Penke B, Becskei A, Dux M, and Tóth L

Subjects
Amyloid beta-Peptides administration & dosage, Animals, Brain blood supply, Brain drug effects, Brain pathology, Capillary Permeability drug effects, Dose-Response Relationship, Drug, Endothelium, Vascular drug effects, Evans Blue administration & dosage, Evans Blue analysis, Extravasation of Diagnostic and Therapeutic Materials, Infusions, Intra-Arterial, Injections, Intravenous, Lectins metabolism, Male, Parietal Lobe chemistry, Peptide Fragments administration & dosage, Rats, Rats, Wistar, Serum Albumin analysis, Serum Albumin metabolism, Amyloid beta-Peptides pharmacology, Blood-Brain Barrier drug effects, Carotid Arteries, Peptide Fragments pharmacology
Abstract

The effects of intracarotid infusions of beta-amyloid (1-42) peptide was studied on the permeability of brain vessels. Using a quantitative Evans blue method a dose-dependent increase of brain tissue albumin content was established following intracarotid injections of the peptide. Cerebral vessels of increased permeability were also demonstrated with a vital 'staining' technique. Lectin histochemistry revealed an almost complete abolition of specific lectin binding sites of affected endothelial cells. The findings indicate a significant deterioration by beta-amyloid (1-42) peptide of blood-brain barrier function and suggest that this may result from endothelial damage. It is assumed that altered permeability of cerebral vessels may be involved in the development of brain pathologies associated with Alzheimer's disease.

Published
1998
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