Search PubMed⌕ Search

Biomedical subjects

S R Ojeda

Publications and source records attributed to S R Ojeda.

At least 163 records · Page 9Linked to original sources
PubMed1980

Neuroendocrine control of the onset of puberty in the rat.

In the female rat, the onset of reproductive capacity is signaled by the first ovulation, an event usually associated with vaginal opening. First ovulation is induced by an abrupt, proestrous-type surge of gonadotropins which in all probability results from the expression of estrogen positive feedback. Central nervous system--pituitary sensitivity to the feedback develops gradually and quantitatively as the animal matures. By contrast, sensitivity to estrogen negative feedback appears to decrease (abruptly) only after first ovulation has occurred. Instrumental in the process of maturation of estrogen positive feedback are an enhanced capability of the hypothalamus to release LHRH (luteinizing hormone-releasing hormone) and an increase in responsiveness of the ovaries to gonadotropins. While serum gonadotropins seem to change very little during the days antecedent to the first preovulatory surge, the somatomamotrophic hormones prolactin (PRL) and growth hormone (GH) become unambiguously elevated. One of the mechanisms by which PRL (and perhaps GH) appears to participate in the maturational process that leads to puberty is by enhancing ovarian responsiveness to gonadotropins. Prolactin exerts part of this effect by increasing luteinizing hormone (LH) receptor content of granulosa cells. In addition, PRL can also act centrally to advance puberty by a mechanism still poorly understood.

Animals↗
PubMed1979

Cyclic GMP and cyclic AMP levels in median eminence, hypothalamus and pituitary gland of the rat after decapitation or microwave irradiation.

Cyclic AMP and cyclic GMP content of the median eminence (ME), medial basal hypothalamus (MBH), posterior pituitary (PP) and anterior pituitary (AP) of inact male rats was measured by radioimmunoassay following decapitation or exposure to microwave irradiation (MW). Levels of both nucleotides in MW irradiated animals were higher in all three nervous tissues studied than in the AP. Following decapitation cyclic AMP levels increased strikingly in the MBH and ME, slightly in the AP, but remained unchanged in the PP. Cyclic GMP levels increased more markedly in the ME than in the MBH, slightly in the PP and did not change in the AP. The distinct synthesizing capability of the cyclic AMP and cyclic GMP generating systems in the ME, a region rich in neurohormones known to control anterior pituitary function, raises the possibility that these nucleotides are involved in the process of neurohormone secretion by the ME.

Animals↗
PubMed1979

Effects of central administation of probenecid on fevers produced by leukocytic pyrogen and PGE2 in the rabbit.

1. Single intracerebroventricular (I.C.V.) injections of probenecid (PBCD, 0.125--0.5 mg) enhanced and prolonged fever caused by I.V. administration of leukocytic pyrogen (LP) in rabbits resting in neutral (23 degrees C), cold (10 degrees C) and hot (30 degrees C) environments. Similar effects were produced by single I.C.V. injections of PBCD given before PGE2 (0.5 microgram) was injected I.C.V. in the three ambient temperatures. 2. Fever produced by IV. LP was also prolonged by infusion and by multiple injections of PBCD. 3. PBCD given I.P. (100 mg/kg) enhanced and prolonged fever caused by I.V. injection of Salmonella typhosa endotoxin. 4. Hyperthermia produced by I.C.V. PGE2 was not augmented by subsequent PBCD infusion. However, pre-treatment with PBCD followed by PGE2 injection and PBCD infusion caused hyperthermia that was very high and prolonged, and, in some cases, lethal. 5. Acetaminophen (2 mg, I.C.V.) and indomethacin (10 mg/kg, I.V.) lowered body temperature when given during fever induced by LP and prolonged by PBCD infusion. 6. The concentration of PGE in cerebrospinal fluid (c.s.f.) samples taken from the third or lateral ventricles rose or stabilized during PBCD infusions made during LP fever. However, similar changes in PGE concentration also occurred during control infusions when body temperature was low. 7. We conclude that termination of the actions of both central endogenous pyrogen and centrally administered PGE2, and the subsequent reduction of fevers produced by them, require a PBCD-sensitive facilitated transport system. The reduction of PBCD-prolonged PL fevers by antipyretics which block PGE synthesis suggests that prolongation by PBCD of LP fever is not due to blockade of PGE transport in a subsequent step in fever mediation per se, but is due to inhibition of transport of LP itself, or of other mediators associated with it.

Animals↗