[Waking effect in the rat of semi-chronic treatment with oxolinic acid].
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Animals↗
Biomedical subjects
V Guillaume
Publications and source records attributed to V Guillaume.
[Effects of adrenal medullectomy and passive immunization with an anti-CRF antiserum on the corticotropin secretion in response to stress in Long-Evans rats].
Ether stress-induced ACTH and corticosterone secretion is similar in 60 days adrenal medullectomized and intact Long-Evans Rats. Passive immunisation with a 41-CRF antiserum impairs corticotropic function after stress. This decrease is more pronounced in adrenal medullectomized than in intact animals. These results suggest that epinephrine plays a minor role on the stress induced ACTH secretion. This role can be demonstrated only after immunoneutralisation of endogenous 41-CRF.
Adrenal Medulla↗
[The periodic hypersomnia and megaphagia syndrome in a young female, correlated with menstrual cycle (author's transl)].
A 21-year-old female was first seen in 1974 for periodic hypersomnia. It had started at 13 years of age and was characterized by 4-6 days of drowsiness with megaphagia and some light psychic disorders. The attacks usually occurred at approximately 5-6 days after menstruation. Later, after an interval of oral contraception, they appeared during ovulation and increased in duration. During the periods of contraception, these attacks disappeared completely. At present (1980), the episodes are characterized by periodic hypersomnia, seen in a nocturnal polygraphic study; megaphagia has decreased, but the patient appears uncommunicative, sub-active and inexpressive when awaking in the course of the periods of somnolence. Several EEG recordings were made between 1974 and 1980, which showed few or no abnormalities during the attacks and which were normal with in the inter-ictal periods. Hormonal investigations failed to show any striking abnormality or correlation with continuous polygraphic studies. Similarity of this syndrome with the 'periodic hypersomnia and megaphagia in adolescent males' syndrome (Kleine-Levin) is discussed.
Adult↗
[A safe technic for anesthesia of the rabbit].
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Anesthesia↗
Influence of endogenous growth hormone-releasing factor (GRF) on the secretion of GH during the perinatal period in the rat.
Passive immunization of pregnant rats with a specific antiserum to rat GRF (GRF-AS) is followed by a decrease in fetal serum GH on the 19th day of gestation. A significant reduction in serum GH is still observed in older fetuses and newborn rats. Pituitary GH content increases in 19- and 20-day-old fetuses after GRF-AS administration to their mothers. These results suggest that endogenous fetal hypothalamic GRF (or placenta GRF) play a physiological role in the secretion of pituitary GH as early as the 19th day of fetal life and may be responsible for the peak of GH release that occurs in fetuses at the end of gestation.
Aging↗
Topographical distribution of CRF immunoreactivity in the pigeon brain.
The distribution of corticotropin-releasing factor (CRF) immunoreactivity was demonstrated by immunocytochemistry in intact and colchicine-treated pigeons. Colchicine injections were administered at different times related to the circadian activity of the CRF-adrenocorticotropin (ACTH)-corticosterone axis. Three CRF antisera were used, two directed against synthetic rat CRF and one directed against synthetic ovine CRF. No fundamental differences appeared in the pigeon brain with respect to the specific CRF antiserum used. The most effective colchicine injection times corresponded to hypersecretion in the corticotropic axis. CRF-immunopositive neurons were scattered throughout the pigeon brain. In addition to the paraventricular hypothalamic system, which is involved in adenohypophysial ACTH regulation, several other hypothalamic and extrahypothalamic areas showed CRF neurons. The distribution suggests that CRF may also act as a modulator and a neurotransmitter. Two hypothalamic paraventricular nucleus-median eminence CRF pathways are described here. Moreover, CRF-immunopositive reactions were observed in specific areas of cerebral ventricle walls, suggesting that CRF may be released into the cerebral fluid.
Animals↗