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J F Rodriguez-Sierra

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

At least 37 records · Page 2Linked to original sources
PubMed1987

Incorporation of amino acids into proteins of the hypothalamus of prepuberal female rats after estradiol treatment.

The arcuate nucleus-median eminence complex (AM) undergoes major structural and functional changes during normal puberty or if exposed to a pulse of estradiol in the prepuberal period. Those changes are expressed by increased synaptogenesis and by a drastic alteration in the feedback control of anterior pituitary gland hormone release. In this study we investigated the effects of estradiol benzoate (EB) on specific proteins in this hypothalamic area. Prepuberal, 25-day-old female rats were administered 10 micrograms of EB s.c. in oil or sesame oil vehicle. The animals were decapitated either 17 or 42 h after treatment. The brains were removed, blocked and serially sections at 300 micron using a Vibratome. The AM was dissected out and incubated for 6 h in a medium containing 35S-methionine and 35S-cysteine. Proteins from the AM were separated by two-dimensional gel electrophoresis, and the gels were exposed to X-ray film. The resulting autofluorographs were analyzed by scanning densitometry. The results show that the incorporation of labeled amino acids was increased in 10 proteins and decreased in 2 proteins in rats killed 17 h after EB. At 42 h after EB, 6 proteins showed an increased incorporation of amino acids and two proteins showed a decrease. Our results suggest that one or several of these proteins might be involved in the neuroendocrine and structural changes observed in the AM during puberty.

Animals↗
PubMed1986

Isolation of specific proteins affected by estradiol in the arcuate-median eminence of prepuberal female rats.

Prepuberal female rats (25 days of age) were injected with estradiol benzoate (EB 10 micrograms/rat, s.c. in oil) or oil vehicle. Forty-eight hours after treatment, all animals were decapitated, their brains removed and sectioned. The arcuate nucleus of the hypothalamus and median eminence were microdissected and processed for isoelectric focusing followed by slab gel electrophoresis. The resulting two-dimensional electrophoretic gels were analyzed to quantitate the specific proteins resolved using a scanning microdensitometric method. Out of 235 proteins measured, 8 proteins were found to be significantly increased and 4 were decreased by EB treatment. The proteins which increased in concentration ranged in molecular weight from 15 to 43 kDa and isoelectric points (pI) of 4.9 to 7.0. The 4 proteins decreased by the EB treatment were 44, 67, 74 and 80 kDa in molecular weight and their pI's ranged from 6.5 to 7.1. It is suggested that these proteins might be involved in some of the neuroendocrine effects that are induced by estradiol in this region of the brain.

Animals↗
PubMed1986

Anxiolytic effects of progesterone are sexually dimorphic.

We evaluated the effects of progesterone administration to estrogen-primed rats on licking behavior during a lick suppression test. This test assesses the behavior of water-deprived rats to lick a drinking tube for water reinforcement that is paired to electric shock. Chlordiazepoxide (a commonly used tranquilizer) is very effective in increasing licking during this test. Normal females and neonatally castrated males displayed an increase in shock-punished responses in tests conducted after hormone injections. Normal males and neonatally androgenized females were unaffected. Our results suggest that ovarian steroids, and particularly progesterone, can modulate anxiety in females and feminized males. In addition, the anxiolytic effect of progesterone appears to be mediated by a mechanism different from that of Chlordiazepoxide.

Animals↗
PubMed1986

Kainic acid lesioning of the preoptic area alters positive feedback of estrogen in prepubertal female rats.

Stereotaxic infusion of kainic acid (KA) was performed to induce intrinsic neural lesions of the preoptic area (POA) in 25-day-old female rats. After KA infusion, rats in Experiment 1 received 10 micrograms of estradiol benzoate (EB) administered subcutaneously to assess positive feedback of EB on release of luteinizing hormone (LH) from the pituitary gland. Rats were perfused for light microscopic (LM) or electron microscopic (EM) evaluation of the lesion site. Rats of Experiment 2 were allowed to develop until the appearance of vaginal opening (VO) after which time vaginal lavages were taken to monitor the cyclicity of the vaginal epithelium. At 50 days of age, the right ovary from each rat was removed, trimmed of fat, and weighed. At 60 days of age, the remaining ovary was removed to assess compensatory ovarian hypertrophy (COH). In Experiment 3, we investigated the effects of POA/KA-infusion on sexual behavior. Sex behavior tests were conducted at 48 h after EB during the dark phase of the light cycle. In Experiment 1, all the control and saline-infused rats exhibited the expected rise of plasma LH two days after estrogen injection while the POA/KA-infusion abolished the positive feedback effect of EB on LH release. Ultrastructural examination of the lesion site revealed that neurons were undergoing acute degeneration while axons and afferent terminals seen in the same fields of analysis were morphologically intact. Preoptic area/KA lesions caused a marked delay in the appearance of VO. Duration of this temporal delay in POA/KA-lesioned rats was approximately 4 days, or one vaginal cycle. The lesioned animals showed normal compensatory hypertrophy after unilateral ovariectomy.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Evidence that cell bodies in the arcuate nucleus of the hypothalamus are not cholinergic.

Central cholinergic pathways have been implicated in the control of pituitary hormone release. Based on studies using acetylcholinesterase (AChE) histochemistry, it has been proposed that the cholinergic neurons controlling hormone release originate in neurons of the arcuate nucleus (AH). Although AChE histochemistry has been widely utilized to map central cholinergic pathways, AChE is not an unequivocal marker for cholinergic neurons. A more precise method for determining that neurons are cholinergic is the immunocytochemical labeling of choline acetyltransferase (CAT). In order to determine if the AChE-positive neurons in the AH are cholinergic, we double-labeled tissue sections for CAT and AChE using a combined immunocytochemical and AChE-histochemical method. Although neurons in several areas of the brain could be labeled for both CAT and AChE, neurons in the AH were only AChE-positive. We concluded that the AChE-positive neurons in the AH may be cholinoceptive but are not likely to be the source of cholinergic neurons controlling hormone release from the pituitary gland.

Acetylcholinesterase↗
PubMed1985

Monosodium glutamate and pituitary gland luteinizing hormone (LH) release in response to LH-releasing hormone: an in vitro study.

We studied whether an increase in the basal LH release rate and/or the anterior pituitary gland (APG) LH response to LHRH is involved in maintaining normal or near-normal serum LH levels in monosodium L-glutamate (MSG)-treated rats which have small APGs for their body weight. Female rats were injected with MSG (4 mg/g BW) or saline on days 1, 3, 5, 7, and 9 after birth (day of birth = 0). At 8-9 weeks of age, saline-treated and MSG-treated rats were ovariectomized, and 7 days later, they were decapitated. Trunk blood was collected from 18 controls and 19 MSG-treated rats, and serum LH concentrations were measured by RIA. APGs were bisected and each hemi-APG was placed in culture medium for a 30-min preincubation period, followed by two 30-min incubation periods during which water or 10 or 30 ng LHRH were added to the medium. Despite the fact that the APGs of the MSG-treated rats were half the size of those of the saline-treated rats, the serum LH levels in the 2 groups were not different. Basal LH release rates (the response to water) and LHRH-induced LH release per mg APG were increased in MSG-treated rats. Calculation of the basal LH release rates and LHRH-induced LH release on the basis of the entire weights of the APGs showed no differences between the MSG-treated rats and the controls. In 6 additional control and 6 additional MSG-treated rats, the APG LH concentration was measured and was not different between the 2 groups. The results suggest that increases in both the basal LH release rate per mg APG and the amount of LH released per mg APG in response to LHRH are of importance in the maintenance of normal or near-normal serum LH concentrations in MSG-treated rats with small APGs.

Animals↗
PubMed1984

A decrease in thymus-mediated immune responses as a result of treatment of neonatal rats with glutamate.

We investigated whether administration of monosodium 1-glutamate (MSG) to neonatal rats would disrupt immune responses in intact and orchidectomized adult male rats. Neonatal male rats were treated with saline or MSG which causes severe endocrine abnormalities. Half of each group of animals were orchidectomized as adults and killed one week later along with intact rats. MSG treatment resulted in suppressed serum LH levels in intact rats. Thymus weight and spleen cellularity in intact animals were not affected by MSG treatment, but thymus weight increased within one week after orchidectomy in both saline- and MSG-treated groups. In intact rats, lymphocyte stimulation by the T cell specific mitogens (concanavalin A or phytohemagglutinin) or the B cell specific mitogen (lipopolysaccharide) was unaffected by prior treatment with MSG. However, MSG treatment blocked the decrease attributable to orchidectomy in concanavalin A and phytohemagglutinin stimulation of lymphocyte blastogenesis. The results suggest that administration of MSG to neonatal male rats can alter some immune responses in the adult animal.

Animals↗
PubMed1984

Effect of ovarian hormones on conflict behavior.

We injected ovariectomized female rats with estrogen and progesterone. Some of the injection regimens used are known to induce estrus, while other do not. The effects of these treatments on operant behavior were evaluated. Operant behavior was maintained under a reinforcement schedule, one segment of which involved experimentally induced conflict. Such behaviors previously have been shown to be modified by anti-anxiety drugs. Those hormone treatments effective in inducing estrus had behavioral effects similar to the effects observed for established anti-anxiety agents. Hormone-injection regimens not capable of inducing estrus were without effect on operant behavior. Our findings suggest that the reproductive cycles of female rats are associated with behavioral changes which may be indicative of changing anxiety levels mediated in part by changing titers of ovarian hormones. We suggest that the evaluation of hormonal influences on operant behaviors sensitive to tranquilizers should be a useful model system for studying possible mechanisms underlying emotional changes associated with reproductive cycles.

Animals↗
PubMed1983

Increase in hypothalamic nicotinic acetylcholine receptors in prepuberal female rats administered estrogen.

In previous studies, it has been reported that the administration of estrogen to prepuberal female rats produces precocious surges in the serum concentrations of luteinizing hormone (LH) and prolactin and the number of synaptic contacts in the arcuate nucleus. In the study reported here, we tested the hypothesis that the concentration of hypothalamic nicotinic acetylcholine receptors is the synaptic event initiating the precocious hormonal surges. A single injection of estrogen was administered to prepuberal female rats on day 25 and the serum concentrations of LH and prolactin and the concentration of the binding sites for alpha-bungarotoxin (BuTX), a putative nicotinic acetylcholine receptor ligand, were measured on day 27. The concentration of hypothalamic BuTX binding sites was increased by the estrogen treatment, but we found no evidence that this increase in receptors precedes or initiates the serum hormonal surges.

Animals↗
PubMed1983

Dissociation between increased growth hormone and prolactin secretion during the morning hours of early pregnancy in the rat.

We investigated whether serum growth hormone (GH) concentration changes in association with the rise in serum prolactin (PRL) concentration known to occur during the early morning hours in the pregnant rat. Animals were kept in a room with the lights on from 0500 to 1900 hours (hr) daily and decapitated for the collection of trunk blood at 2200 or 2400 hr on Day 6 of pregnancy or at 0200, 0400, 0800 or 1000 hr on Day 7 of pregnancy. Serum GH concentration rose more than 4-fold from low levels at 2200 and 2400 hr to higher levels at 0400 and 0800 hr and then declined by 1000 hr. Serum prolactin (PRL) concentration followed a similar pattern except that it returned to low levels earlier, by 0800 hr. Serum luteinizing hormone, follicle-stimulating hormone and thyroid-stimulating hormone concentrations showed no significant changes. Serum GH levels at 0800 hr in pregnant rats were higher than those observed in cyclic rats (13 time periods sampled). The results demonstrate that serum GH concentration is elevated during a circumscribed period in the 6- to 7-day pregnant rat. The time of onset of the rise is similar to that for serum PRL but the elevation in GH levels persists longer than that for PRL.

Animals↗
PubMed1983

Synaptic changes in the hypothalamus of the prepuberal female rat administered estrogen.

Subcutaneous administration of estradiol benzoate (EB) to prepuberal female rats can advance vaginal opening, phasic pituitary gland luteinizing hormone (LH) secretion, and ovulation, presumably through a neural mechanism. This study investigated whether these effects are associated with changes in synaptic profiles in the arcuate nucleus of the hypothalamus (ARC) and the preoptic area (POA). Twenty-five-day-old female rats were administered EB, EB followed by progesterone on day 27, or oil vehicle alone; or they received no treatment. Blood was collected by jugular venipuncture at 1600 hr, on day 27, and plasma was assayed for LH by radioimmunoassay. Rat brains were immediately perfused for electron microscopy, and the ARC and POA were dissected out. Tissue blocks from these areas were processed with phosphotungstic acid for selective staining of neural synapses. Serum LH was markedly elevated in the EB-treated rats compared with controls. In the treated groups, LH values in serum were above 1,000 ng/ml, whereas the control values were less than 50. This acute rise of serum LH was accompanied by an acute increase of synaptic volume percent, area density, and numerical density in the ARC of EB-treated rats. The numerical density of the control groups was approximately 800 million observed synapses per cubic millimeter, whereas in the EB-treated groups, there were approximately 1.8 billion synapses per cubic millimeter. We found no differences in synaptic profiles of the POA in EB-treated animals as compared to the controls. We conclude from this study that estrogens act through neural mechanisms to accelerate maturation of neuroendocrine processes that govern phasic pituitary gland LH release and that this maturation process entails synaptogenesis in the ARC.

Animals↗
PubMed1983

Estrogen accelerates the recovery of the lordosis response after its exhaustion induced by cervical probing.

Repetitive flank-perineum palpation combined with probing the vaginal cervix in ovariectomized hormonally untreated rats elicited a mean of 4.2 +/- 0.2 (SEM) successive lordosis responses before the response was exhausted. Two days after a single injection of estradiol benzoate (100 micrograms/kg body wt) in ovariectomized rats, a significantly greater number (7.8 +/- 0.2) of lordosis responses could be elicited before the response was exhausted (P less than 0.01). After this exhaustion, recovery of lordosis responsiveness to this stimulation occurred significantly earlier in the estrogen-treated rats (6 hr) than in the oil-treated rats (60 hr) (P less than 0.01). Several possible mechanisms mediating these effects are proposed.

Animals↗
PubMed1982

A decrease of cytosol estrogen receptors in the hypothalamus as a result of treatment of neonatal rats with glutamate.

Experiments were performed to determine whether the neuroendocrine dysfunctions of rats treated neonatally with monosodium glutamate (MSG) could be related to a loss of cytoplasmic estrogen receptors. Female rats treated with MSG as neonates were ovariectomized as adults and killed by decapitation 2 or 3 weeks after ovariectomy. Body, gonadal and anterior pituitary gland weights in MSG-treated rats were depressed when compared to that seen in their littermate controls. Serum prolactin concentration was elevated in the MSG-treated rats. Serum luteinizing hormone (LH) concentration was significantly lower in MSG-treated rats than in controls at 2 weeks, but not at 3 weeks after ovariectomy, suggesting a sluggish postovariectomy rise of serum LH concentration. Serum follicle-stimulating hormone (FSH) concentration was not altered by the MSG treatment. The concentration of cytosol estrogen receptors in the anterior pituitary gland was similar to that of controls, but hypothalamic concentration of estrogen receptors decreased as a result of the MSG treatment. After dissection of different hypothalamic regions, it was found that the greatest depletion of the cytosol estrogen receptors occurred in the arcuate-median eminence region. The results raise the possibility that some reproductive impairments of MSG-treated rats could stem from a decrease in cytosol estrogen receptors in the arcuate-median eminence region.

Animals↗
PubMed1982

Catecholestrogens and release of anterior pituitary gland hormones. I. Luteinizing hormone.

We investigated the effects of peripheral administration of 17 beta-estradiol (E2), estrone (E1), and the catecholestrogens, 2-hydroxyestradiol (2-OHE2) and 2-hydroxyestrone (2-OHE1), on anterior pituitary gland LH release in the prepuberal rat. Steroids in oil were injected sc into 25-day-old female and 35- to 40-day-old male rats. The injection of E2, E1, or 2-OHE2 caused a surge in serum LH levels in female rats 48 h later, during the after hours. Only E1 induced a LH surge 24 h after injection. The positive effects of 2-OHE2 in the females were only observed if a massive dose was administered, the steroid was injected on 2 consecutive days, or E2 or progesterone was given to 2-OHE2-primed rats. The 2-OHE1 was totally ineffective in causing a serum LH surge under a variety of experimental protocols. In male rats, the injection of any one of the four steroids decreased serum LH levels. Even the injection of E2 or 2-OHE2 for 2 days or the injection of E2 in 2-OHE2-primed rats failed to elevate the serum LH concentration in male rats. The results suggest that 2-OHE2 and E1 could play a role in the preovulatory release of LH in the female; 2-OHE2 and 2-OHE1 could play a role in the negative feedback control of LH release in the male.

Animals↗
PubMed1982

Catecholestrogens and release of anterior pituitary gland hormones. II. Prolactin.

We investigated the effects of the peripheral administration of 17 beta-estradiol (E2), estrone (E1), and the catecholestrogens, 2-hydroxyestradiol (2-OHE2) and 2-hydroxyestrone, (2-OHE1), on anterior pituitary gland PRL release in the prepuberal rat. Steroids in oil were injected sc into 25-day-old female and 35- to 40-day-old male rats. The injection of E2, E1, or 2-OHE2, but not of 2-OHE, caused a surge in serum PRL levels in female rats 48 h later, during the afternoon hours. Only E1 induced a PRL surge 24 h after injection. In male rats, the injection of E1 or 2-OHE2, but not of 2-OHE1, elevated serum PRL levels on a chronic basis. The results suggest that 2-OHE1 plays no discernible role in PRL release in either sex, but that 2-OHE2 might play a role in the tonic release of PRL in the male and in the preovulatory release of PRL in the female.

Animals↗