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Biomedical subjects

C Debray

Publications and source records attributed to C Debray.

At least 19 recordsLinked to original sources

Contributions of AMPA and GABA(A) receptors to the induction of NMDAR-dependent LTP in CA1.

The contributions of (+/-)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) and gamma-aminobutyric acid (GABA[A]) receptors in the induction of long-term potentiation (LTP) have been studied in the CA1 region of the rat hippocampus. The results suggest that: (1) in physiological conditions, AMPARs are necessary for the induction of N-methyl-D-aspartate receptor (NMDAR)-dependent LTP since LTP cannot be elicited in the presence of the AMPAR antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). Although a NMDAR-dependent LTP occurs in the presence of a GABA(A) antagonist and high concentrations of divalents cations, blockade of AMPARs leads to a voltage-dependent calcium channels (VDCC)-dependent LTP since its induction is blocked by nifedipine and not by APV. (2) The bicarbonate-induced GABA(A) receptor-mediated depolarizing response is not necessary in the induction of NMDAR-dependent or VDCC-dependent LTP since induction of these two types of LTP were not blocked by acetazolamide or in a nominally bicarbonate-free solution.

2-Amino-5-phosphonovalerate↗

[Primary exocrine pancreatic insufficiency in the adult. Presentation of a case].

The authors report the case of a 37-year-old female complaining of chronic diarrhea since childhood. She had gross steatorrhea and azotorrhea . Pancreatic function tests using secretin and cholecystokinin-pancreozymin stimulation, and analysis of pure pancreatic juice collected under secretin stimulation proved exocrine pancreatic insufficiency. Oral glucose tolerance test was normal. Intestinal absorption tests, small bowel X-ray films and jejunal histology were normal. Brush-border specific enzyme activities were increased. In vitro palmitic acid uptake and esterification in the jejunal mucosa were decreased. There was no pancreatic calcification. Biliary tract was normal. Retrograde pancreatography, pancreatic ultrasonography and tomodensitometry showed no morphologic abnormality. No cause of exocrine pancreatic insufficiency could be detected. A son and a niece of the proband had chronic diarrhea and growth failure. The relationship of the described case with primary lipomatosis of the pancreas in childhood and hereditary exocrine pancreatic insufficiency in CBA/J epi mice is discussed.

Adult↗

[Upper gastrointestinal bleeding: comparison between the diagnostic conclusions of emergency fibroscopy and those of surgery (author's transl)].

Amongst 1035 patients who underwent oesophago-gastro-duodenal fibroscopy as an emergency for an upper gastrointestinal haemorrhage between January 1973 and May 1977, 100 required surgery. The operative findings were compared with those of endoscopy. In 92 cases, surgical exploration found the same lesions that the endoscopist had reported as being responsible for the haemorrhage. In 14 of these patients, surgical exploration provided complementary data to the endoscopic findings. In the other 8 patients, there was disagreement between the surgical and endoscopic findings. In particular, there were 5 diagnostic errors: 2 false negatives, 1 error of localisation of the lesion and 2 errors of interpretation. The earlier endoscopy is performed, the better are the results: discovery of the bleeding lesion and elimination of other non-haemorrhagic lesions.

Diagnostic Errors↗

Methadone blockade of 2-deoxyglucose-induced pancreatic secretion in the rat.

The effects of methadone on pancreatic exocrine secretions in the rat were tested under basal conditions and after hormonal stimulation by secretin and caerulein or after stimulation of the differentially acting cholinergic agents acetylcholine, 2-deoxyglucose, and electrical stimulation of the vagus. Methadone had no effect on basal hydroelectrolytic secretion. It decreased basal enzyme secretion very slightly under our experimental conditions. The stimulatory effects of 75 mg of 2-deoxyglucose per kg were completely blocked by methadone at 5 mg per kg and this blockade was reversed by nalorphine at 6 to 9 mg per kg. It was found that there are doses of methadone (100 microgram) which block 2-deoxyglucose effects when injected into brain ventricles but are ineffective when systemically introduced. The effects of secretin, caerulein, acetylcholine, and electrical stimulation of the vagus were not depressed by methadone. These results strongly suggest that the methadone blockade of 2-deoxyglucose effects occurs at a central level and is mediated by narcotic drug receptors.

Acetylcholine↗