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J F Rodriguez-Sierra

Publications and source records attributed to J F Rodriguez-Sierra.

At least 55 records · Page 3Linked to original sources
PubMed1981

Intrinsic neurons of the septal area are involved in reproductive development of the female rat. Alterations after kainic acid lesioning.

Three experiments were conducted using intracranial infusion of kainic acid (KA) to lesion the medial septal (MS) neurons and dorsal hippocampal (DH) neurons in 25-day-old female rats. Rats of experiment 1 were allowed to develop until vaginal opening (VO) after which vaginal lavages were taken to monitor the vaginal cycle. Rats of experiment 2 received estradiol benzoate (EB) subcutaneously immediately after KA infusion. Blood was obtained at 11.00 and 16.00 h, 2 days after EB and measured for luteinizing hormone (LH) by radioimmunoassay. Rats of experiment 3 received MS KA lesions and 2 days later tested for pituitary responsiveness to LHRH-induced LH release. In experiment 1, MS KA-lesioned rats exhibited a significant delay in VO when compared to the sham-lesioned or the unoperated control groups. Hippocampal KA-lesioned rats in contrast, showed no difference in the age of VO from the control groups. Septal KA-lesioned rats also showed disrupted vaginal cycles after the onset of puberty. In experiment 2, all the EB-treated animals exhibited the expected rise in serum LH on the afternoon 2 days following EB with the exception of the septal KA-lesioned rats. In every case, KA infusion into the medial septum abolished the ability of EB to induce an LH increase at 16.00 h 2 days after EB administration. DH KA lesion on the other hand had no effect on the EB-induced LH increase. The block of LH secretion by MS KA infusion shown in experiment 2 is not a result of decreased pituitary gland sensitivity to LH-releasing hormone (LHRH) as shown in experiment 3. These results indicate that MS neurons play a vital role in the feedback mechanism whereby EB induces an LH increase in the prepuberal female rat, and that they play a role in the timing of VO.

Animals↗
PubMed1981

Effects of hypothalamic arcuate nucleus lesions on pulsatile luteinizing hormone concentration in ovariectomized rats.

We investigated the effects of hypothalamic arcuate nuclei destruction on the postovariectomy rise in plasma luteinizing hormone (LH) concentration and the pulsatile LH release mechanism in ovariectomized rats. Rats were injected with 1, 2, or 4 mg/g body wt of L-monosodium glutamate (MSG) on Days 1, 3, 5, 7, and 9 of life to lesion the arcuate nuclei. They were then ovariectomized as adults and used 2 or 4-8 weeks later. Serial blood sampling at 10-min intervals and measurement of plasma LH concentration revealed elevated plasma LH levels which fluctuated in a pulsatile fashion in all control and 1 and 2 mg/g/MSG-treated rats. In 4 mg/g MSG-treated rats, plasma LH levels were lower than in controls of both time periods after ovariectomy due to a decrease in the amplitude and/or frequency of LH pulses. Phenobarbital was administered to all 4- to 8-week ovariectomized rats to block endogenous pulsatile LH release. In phenobarbital-blocked rats, three sequential iv injections of LH releasing hormone (LHRH) caused substantial elevations in plasma LH concentrations even in the 4 mg/g MSG-treated animals which had low plasma LH concentrations during control bleedings prior to the injection of phenobarbital. The results indicate that the postovariectomy rise in plasma LH concentration and the associated pulsatile LH release mechanism are functional in rats with extensive arcuate nucleus lesions. The diminution in the rise in plasma LH levels and the decreased amplitude and/or frequency of LH pulses in the MSG-treated rats is likely due to a diminution in hypothalamic LHRH release.

Animals↗
PubMed1980

Monosodium glutamate disruption of behavioral and endocrine function in the female rat.

Experiments were conducted to determine the effects of neonatal administration of L-monosodium glutamate (MSG) on behavioral and endocrine function in the female rat. Administration of MSG (4 mg/kg body weight) at days 1, 3, 5, 7 and 9 in neonates results in a delay of vaginal opening (VO) and the absence of ovulation at the time of VO. However, some rats were observed to ovulate after VO if they were subjected to sequential laparotomies. MSG-treated rats also fail to exhibit compensatory ovarian hypertrophy. Ovariectomized MSG-treated rats injected with estradiol benzoate (EB) followed by a progesterone injected 2 days later did not exhibit sexual beahvior to male rats, while all the control rats displayed lordosis. Chronic treatment with EB for 12 days, followed by a progesterone injection on the 12th day, resulted in a marked improvement of the sexual receptivity of the MSG-treated rats. The body weight of the MSG-treated animals was lower than that of the controls during development although the MSG animals looked obese. Food intake is normal in the MSG-treated rats, but when expressed as intake/100 g body weight, the MSG-treated rats appeared slightly hyperphagic, MSG-treated rats respond with increased food intake after ovariectomy and EB treatment suppresses the increased food intake. Thus, the control of food intake by estrogen does not seem to be affected by the MSG treatment; in fact, these animals seem to be more sensitive than control rats to the anorectic effects of EB. Neonatal MSG treatment appears to affect the neural control for the tonic secretion of gonadotropins by destroying arcuate nuclei. This undoubtedly reduces the reproductive capacity of the animals by impeding the growth and secretions of their ovaries. The findings that chronic estrogen followed by progesterone treatment can reinstate sexual receptivity in MSG-treated animals suggests that the arcuate nuclei are not needed for the expression of sexual behavior and that estrogens might remedy the fertility problems of MSG-treated animals.

Animals↗
PubMed1979

Intrahypothalamic implants of progesterone inhibit lordosis behavior in ovariectomized, estrogen-treated rats.

Intracranial implants of crystalline progesterone (P) were used to examine in site of action of P's facilitatory and inhibitory effects on lordosis behavior in the ovariectomized, estradiol-benzoate (EB)-primed RAT. P implanted in the medial basal hypothalamus (MBH) 1 h prior to subcutaneous (s.c.) EB injection inhibited lordosis in response to a systemic P injection 44 h after EB (concurrent inhibition). P implanted in the MBH did not facilitate lordosis when implanted 44 h after EB injection, but this same implant of P inhibited lordosis in response to P injection 68 h after EB (sequential inhibition). Cholesterol (Chol) implants in the MBH did not inhibit lordosis behavior in either the concurrent or the sequential inhibition experimental paradigms. The results indicate that the MBH is an important site of P inhibition of sexual receptivity in the rat.

Animals↗
PubMed1978

Lordosis induction in the rat by prostaglandin E2 systemically or intracranially in the absence of ovarian hormones.

Within 20 minutes of an intraperitoneal injection, PGE2 induced lordosis responding to manual stimulation in 6 of 9 rats that were ovariectomized-hysterectomized and hormonally untreated. Similarly, intracranial application of PGE2, through guide cannulae that were chronically-implanted in the basal hypothalamus, induced lordosis responding to manual stimulation within 10 minutes in ovariectomized, hormonally-untreated rats.

Animals↗
PubMed1977

Analgesia induced by vaginal stimulation in rats is apparently independent of a morphine-sensitive process.

Previous studies have suggested that in rats probing against the vaginal cervix with a glass of is analgesic, for this stimulus elevates the threshold for eliciting vocalization in response to tail shock. In the present studies pretreatment with naloxone HCl (1 or 10 mg/kg), a potent narcotic antagonist did not antagonize this vaginal stimulation-induced analgesia. Furthermore, vaginal stimulation was found to exert its analgesic effect even in rats made tolerant to, and dependent upon, morphine sulfate. These results suggest that the analgesic effect of vaginal stimulation is not necessarily mediated by an opiate-sensitive neural system. However, we hypothesize that even though vaginal stimulation and other analgesic manipulations may act via different neural substrates, they may nevertheless converge onto a final common mechanism for pain suppression.

Analgesia↗