Biomedical subjects

S Arancibia

Publications and source records attributed to S Arancibia.

At least 19 recordsLinked to original sources

PubMed2006

Cold stress induces metabolic activation of thyrotrophin-releasing hormone-synthesising neurones in the magnocellular division of the hypothalamic paraventricular nucleus and concomitantly changes ovarian sympathetic activity parameters.

Recent studies suggest thyrotrophin-releasing hormone (TRH) serves as a neurotransmitter and thereby provides a functional vegetative connection between the brain and the ovary. In the present study, magnocellular neurones of the paraventricular nucleus (PVN) in animals subjected to cold exposure were studied to determine the hypothalamic origin of the TRH involved in this pathway. In situ hybridisation analysis of hypothalamic tissue showed that cold exposure causes a two-fold increase in the total number of neurones expressing TRH mRNA in the PVN. Immunohistochemical studies showed that TRH peptide is localised to the magnocellular PVN and that the number of TRH immunoreactive cells increases two-fold following 64 h of cold exposure. Double-immunostaining for MAP-2 and TRH revealed that TRH peptide is localised in the perikarya of the magnocellular neurones. TRH release was measured in vivo from the magnocellular portion of the PVN using push-pull perfusion. Although controls exhibited a very low level of TRH release, animals subjected to cold showed a pulsatile-like TRH release profile with two different patterns of release: (i) low basal level with small bursts of TRH release and (ii) a profile with an up to seven-fold increase in TRH release compared to controls. The colocalisation of TRH with the specific somato-dendritic marker MAP-2 in processes of the magnocellular neurones suggested a local release of TRH. Additional studies demonstrated a reduction in ovarian noradrenaline content after 48 h of cold exposure, a feature indicative of nerve activation at the terminal organ. After 64 h of cold exposure, the ovarian noradrenaline returned to control values but the noradrenaline content of the coeliac ganglia was increased, suggesting a compensatory effect originating in the cell bodies of the sympathetic neurones that innervate the ovary. The correlation between the local release of TRH from dendrites within the magnocellular PVN in conditions of cold and the activation of the sympathetic nerves supplying the ovary raises the possibility that TRH contributes to the processing regulating sympathetic outflow and may thereby impact on the functional activity of the ovary.

Acclimatization↗

PubMed2003

Chronic intermittent cold stress activates ovarian sympathetic nerves and modifies ovarian follicular development in the rat.

We studied the effects of a chronic intermittent cold stress regime on sympathetic nerve activation and ovarian physiology. This paradigm (4 degrees C for 3 h/day, Monday-Friday, for 3 or 4 wk) does not affect basal plasma levels of corticosterone. After 3 wk of stress, we detected a decrease in noradrenaline (NA) in the ovary, but after 4 wk, this ovarian neurotransmitter concentration increased over that of unstressed control rats. To analyze whether this effect on NA is preceded by an activation of the neurotrophic factor system responsible for growth and survival of sympathetic neurons, we measured both nerve growth factor (NGF) (by enzyme immunoassay) and the intraovarian levels of its low affinity receptor mRNA (by reverse transcription-polymerase chain reaction). The activation of sympathetic nerves was followed by an increase in NGF concentration without affecting the ovarian levels of either NGF or the mRNA of its receptor. Interestingly, follicular development changed during the stress procedure; after 3 or 4 wk of stress, we found a decrease in preantral healthy follicles without a compensatory increase in atresia. Concomitantly with the increase in NA and NGF in the ovary, we observed that a new population of follicles with hypertrophied thecal cell layers appeared after 4 wk of stress. These results suggest that chronic stress, through an intraovarian neurotrophin-mediated sympathetic activation, produces changes in follicular development that could lead to an impairment of reproductive function.

Androstenedione↗

PubMed2003

Thyrotropin-releasing hormone as a mediator of the central autonomic pathway controlling ovarian function.

We studied the effect of thyrotropin-releasing hormone (TRH) applied centrally on the sympathetic activity of the ovary in female rats. Intracerebroventricular (i.c.v.) administration of a dose of 25 ng/kg weight produced an increase in noradrenaline (NA) content at the ovary after 5 days of hormone administration. However, higher doses in a range up to 500 ng/kg weight decreased NA content at the ovary. At the celiac ganglia (where the cell bodies of sympathetic neurons projecting to the ovary originate) there was an accumulation of NA in spite of a decrease in tyrosine hydroxylase activity (T-OH). After cold exposure, opposite effects on T-OH activity and no effects on NA in ganglia and in ovary were obtained. Besides, i.v. injection of TRH only induced a decrease in ovarian NA. In contrast to the increase in T(3) plasma levels obtained after the cold-stress procedure, none of the i.c.v. doses of TRH used produced changes in T(3) plasma levels, strongly suggesting that the effect on sympathetic activity is mediated by a central effect of TRH acting as a putative activator of ovarian sympathetic nerves.

Adrenal Glands↗

PubMed2002

Immobilization stress rapidly modulates BDNF mRNA expression in the hypothalamus of adult male rats.

We demonstrated that short times (15 min) of immobilization stress application induced a very rapid increase in brain-derived neurotrophic factor (BDNF) mRNA expression in rat hypothalamus followed by a BDNF protein increase. The early change in total BDNF mRNA level seems to reflect increased expression of the BDNF transcript containing exon III, which was also rapidly (15 min) modified. The paraventricular and supraoptic nuclei, two hypothalamic nuclei closely related to the stress response and known to express BDNF mRNA, were analyzed by in situ hybridization following immobilization stress. In the parvocellular region of the paraventricular nucleus, BDNF mRNA levels increased very quickly as early as 15 min. In contrast, in the two other regions examined, the lateral and ventral magnocellular regions of the paraventricular nucleus, as well as in the supraoptic nucleus, signals above control were increased later, at 60 min. After stress application, plasma adrenocorticotropic hormone and corticosterone levels were strongly and significantly increased at 15 min. These studies demonstrated that immobilization stress challenge very rapidly enhanced BDNF mRNA levels as well as the protein, suggesting that BDNF may play a role in plasticity processes related to the stress response.

Adrenocorticotropic Hormone↗

PubMed2002

Osmotic stress increases brain-derived neurotrophic factor messenger RNA expression in the hypothalamic supraoptic nucleus with differential regulation of its transcripts. Relation to arginine-vasopressin content.

We have shown that osmotic stress increases brain-derived neurotrophic factor (BDNF) mRNA in the supraoptic nucleus and that this increase seems to be determined by the high expression of transcripts containing exon I. The paraventricular nucleus is another hypothalamic neuronal subset where BDNF mRNA is also sensitive to osmotic stress stimulation. In this nucleus, transcripts containing exon I were not modified but only those containing exon II. By contrast, transcripts containing exon III did not exhibit any variation in our experimental conditions. The presence of BDNF mRNA in both paraventricular and supraoptic hypothalamic nuclei was recently reported. These nuclei are extremely sensitive to osmotic stimuli and their neurons secrete oxytocin and arginine-vasopressin in the posterior pituitary gland. This study was thus designed to investigate the possible involvement of BDNF in the response of supraoptic nucleus to osmotic stress stimulus. Osmotic stress was induced by hypertonic saline injection (1.35% NaCl) administered to animals 3 h before analysis. We used non-isotopic in situ hybridization to study the expression of BDNF mRNA and its transcripts with antisense riboprobes on histological brain sections, including paraventricular and supraoptic nuclei from control and osmotic stress-stimulated animals. To investigate a possible correlation between the expression of BDNF mRNA and arginine-vasopressin, the peptide content was analyzed by immunohistochemistry in both paraventricular and supraoptic nuclei at two different times after hyperosmotic injection. The results showed that BDNF mRNA expression preceded the arginine-vasopressin increase. In addition, on serial adjacent histological sections of supraoptic nucleus (10 microm), both BDNF and arginine-vasopressin mRNAs were visualized by isotopic in situ hybridization and the images were overlaid, showing that almost all of the hybridization signals were overlapped. Taken together our results are in keeping with the hypothesis that activation of the different BDNF promoters seems to be region-specific. Besides, the temporal correlation between both BDNF mRNA expression and arginine-vasopressin content, as well as the morphological vicinity between their respective producing cells in the supraoptic nucleus, suggest an autocrine or paracrine action for this neurotrophin in the regulation of arginine-vasopressin secretion.

Animals↗

PubMed2001

Effects of alcohol on brain-derived neurotrophic factor mRNA expression in discrete regions of the rat hippocampus and hypothalamus.

Chronic alcohol consumption has adverse effects on the central nervous system, affecting some hippocampal and hypothalamic functions. In this study we tempted to demonstrate that some of these modifications could involve impairment of neurotrophic factors. Three experimental groups of male Sprague Dawley rats were studied: one control group, one chronically treated with alcohol vapor according to a well-established model that induces behavioral dependence, and a third group treated similarly but killed 12 hr after alcohol withdrawal. In all groups, changes in brain-derived neurotrophic factor mRNA expression occurring in the hippocampus and supraoptic nucleus were first analyzed by reverse transcription-polymerase chain reaction and then by in situ hybridization. In parallel, we used ribonuclease protection assay to measure mRNA levels encoding trkB in the two central nervous system regions. We showed that chronic alcohol intoxication decreases brain-derived neurotrophic factor mRNA expression in discrete regions of the rat hippocampus (CA1 region and dentate gyrus) and in the supraoptic nucleus of the hypothalamus. We also showed a global up-regulation of trkB mRNA expression encoding the high-affinity brain-derived neurotrophic factor receptor (TrkB), after applying the same treatment. Following 12 hr of alcohol withdrawal, a significant increase in BDNF mRNA expression was observed in the dentate gyrus and CA3 region of hippocampus and in the hypothalamic supraoptic nucleus. These findings suggest that chronic alcohol intake may modify hippocampal and hypothalamic neuronal functions through modifications in growth factors and its receptors.

Alcohol-Induced Disorders, Nervous System↗

PubMed2001

Acute stress and dexamethasone rapidly increase hippocampal somatostatin synthesis and release from the dentate gyrus hilus.

Somatostatin is a neuropeptide whose facilitatory action in the generation of long-term potentiation (LTP) in the hippocampal dentate gyrus has been associated with memory processes. Since stress and memory seem to share some neural pathways, we studied somatostatin release from dentate gyrus hilar cells of the hippocampus in unanesthetized free-moving rats subjected to stress or dexamethasone treatments. In parallel, the number of dentate gyrus hilar cells expressing somatostatin mRNA was quantified by nonradioactive in situ hybridization in these two experimental conditions. Rats were stereotaxically implanted with a push-pull cannula in the dentate gyrus hilar region. Animals were perfused 1 week later in basal or stress (30 min immobilization stress) conditions. The other group was intraperitoneally injected with the synthetic glucocorticoid dexamethasone (3 mg/kg b.w.). Samples were collected every 15 min for somatostatin radioimmunoassay. In parallel, in other groups of animals undergoing the same treatments, brains were removed for in situ hybridization studies with an oligonucleotide labeled with digoxigenin that recognizes somatostatin-14. The results showed that stress induced a significant increase in somatostatin release from dentate gyrus hilar cells 30-45 min after immobilization stress application. Dexamethasone-injected animals exhibited a similar response 45 min after drug administration. In situ hybridization analysis revealed that the two treatments significantly increased the number of cells expressing somatostatin mRNA in the hilar region. In conclusion, somatostatin interneurons of the hippocampal hilar region appear to be a novel stress stimulus target. Their rapid reactivity, expressed as modifications of both somatostatin release and number of cells expressing somatostatin mRNA, provides an interesting model of neuronal plasticity.

Acute Disease↗

PubMed2001

Immobilization stress rapidly and differentially modulates BDNF and TrkB mRNA expression in the pituitary gland of adult male rats.

Brain-derived neurotrophic factor (BDNF) is a neurotrophin involved in neuronal survival and plasticity that binds to high-affinity receptors named TrkB. In the central nervous system, brain insults, including stress, induce modifications in BDNF messenger RNA (mRNA) expression. The present study attempted to determine in the adult rat pituitary, a peripheral structure relevant for the stress response: (1) whether BDNF and TrkB mRNA expression is influenced by different durations (15, 30, 60, 180 and 300 min) of single immobilization stress; (2) the expression of BDNF transcripts containing the different exons and their possible variations after stress exposure. Plasma corticotropin (ACTH) and corticosterone concentrations were strongly and significantly increased as early as 5 min after the stress stimulus. Using RNAse protection assay and in situ hybridization, a rapid increase in BDNF mRNA occurred at 15 min. This was accompanied by an increase in BDNF protein at 60 min, and by a rapid and significant decrease in TrkB mRNA expression observed at 15 and 30 min after stress application. RT-PCR analysis of BNDF transcripts showed strong basal expression of exons III and IV, whereas transcripts containing exons I and II seemed weakly expressed. After stress application, transcripts containing exons III and IV were rapidly and significantly increased at 30 min, whereas transcripts containing exons I and II remained unchanged. These results show that pituitary BDNF transcripts expression is differentially affected by immobilization stress.

Adrenocorticotropic Hormone↗

PubMed2000

Rapid reduction in somatostatin mRNA expression by hypothalamic neurons induced by dexamethasone.

We have previously reported that peripherally administered dexamethasone induces a rapid increase in hypothalamic somatostatin release. Here we investigated whether somatostatin synthesis could also be affected by this treatment and the potential involvement of glutamate in this effect. Male rats received a saline or a dexamethasone injection (300 microg/100 g body weight) and were killed 30 min later. Thirty minutes prior to dexamethasone treatment, another group received an i.p. injection of MK-801, a NMDA receptor antagonist. Cells expressing somatostatin mRNA in the periventricular nucleus were analyzed by in situ hybridization using digoxigenin-labeled somatostatin oligonucleotide probe. Dexamethasone decreased the number of digoxigenin-labeled cells expressing somatostatin mRNA in the periventricular nucleus as compared to the same histological sections from control rats. The dexamethasone effect was reversed by pretreatment with MK-801, which alone also decreased the number of cells expressing somatostatin mRNA. In summary, dexamethasone administration induces a significant rapid decrease in periventricular cells expressing somatostatin mRNA and this effect is partly abolished by MK-801.

Animals↗

PubMed2000

Concomitant changes in CRH mRNA levels in rat hippocampus and hypothalamus following immobilization stress.

By using in situ hybridization, we have demonstrated an increased expression of corticotropin-releasing hormone (CRH) mRNA in the hippocampus following immobilization stress (3 h) in rats. It paralleled that measured in the hypothalamic paraventricular nucleus (PVN). Pretreatment of control and stressed rats with MK-801 (a NMDA receptor antagonist) further increased CRH mRNA expression, in the two structures. The concomitant up-regulation of CRH mRNA expression in these structures suggests a common regulatory finality for a single molecule at two different loci.

Animals↗

PubMed2000

Rapid modifications of somatostatin neuron activity in the periventricular nucleus after acute stress.

We have previously reported that stress induces a rapid increase in hypothalamic somatostatin (SS) release. In the present work, we investigated whether SS synthesis is also affected by this treatment. Male rats were subjected to 15-min immobilization (IMO) stress, and measurements of both SS mRNA levels and SS mRNA-containing cells were analyzed in the periventricular nucleus (PeV) by radioactive and nonradioactive in situ hybridization (ISH), respectively. In addition, SS content and total SS mRNA were measured in the whole hypothalamus by radioimmunoassay (RIA) and northern blot analysis, respectively. ISH was conducted by applying either a radioactive-labeled (35S) or a digoxigenin (DIG)-labeled oligonucleotide probe on histological sections containing the periventricular region of the anterior hypothalamic area (AHA). ISH analysis using radioactive label showed a significant increase in SS mRNA levels in stressed rats. In contrast, stress treatment decreased the number of DIG-labeled cells expressing SS mRNA in this region by 35% as compared to the same histological sections from naive control rats. In addition, a significant decrease in the total SS mRNA DIG-labeled area was observed. Finally, SS content and SS mRNA measured in the whole hypothalamus of stressed rats were markedly inhibited as compared to control rats. Our data show that IMO stress induces a significant and rapid increase in SS mRNA level accompanied by a decrease in the number of cells expressing SS mRNA in the PeV-AHA. The present results suggest that a subset of PeV SS neurons, which became silent at the onset of stress, are regulated independently of the remaining whole mass of PeV neurons. This differential control is in line with the cellular heterogeneity described in periventricular SS-producing neurons and with the multiple hypothalamic and pituitary functions assigned to SS.

Acute Disease↗

PubMed1998

Expression of mRNAs encoding BDNF and its receptor in adult rat hypothalamus.

We used a digoxigenin-UTP-labeled cRNA probe with in situ hybridization and Northern blot analysis to investigate the localization of brain derived neurotrophic factor (BDNF) mRNA and expression of its different transcripts in adult rat hypothalamus. As the BDNF gene is under the control of alternative multiple promoters, which provide tissue-specific gene expression, we studied whether these transcripts were expressed in adult hypothalamus. Our data revealed two novel sources of hypothalamic BDNF mRNA: the supraoptic and periventricular nuclei. In addition, we observed the expression of transcripts from exons, I, II and III as well as the presence of 1.6 and 4.2 kb BDNF mRNAs. Finally, our findings confirmed expression of mRNA encoding neurotrophins receptors in the hypothalamus.

Animals↗

PubMed1998

Effect of acute, but not chronic ethanol treatment on somatostatin secretion in rat hypothalamic neurons.

To examine the possible involvement of somatostatin in growth hormone modifications induced by ethanol, we examined: (1) the effects of chronic ethanol exposure of cultured hypothalamic neurons on somatostatin content and mRNA levels; (2) the acute effect of ethanol on somatostatin release stimulated by N-methyl-D-aspartate (NMDA). The results showed that 8 days of ethanol exposure (10-100 mM) did not decrease somatostatin content or somatostatin mRNA levels. Ethanol treatment alone had no significant effect on cell morphology or on protein content. In contrast, acute application of ethanol in 8 day-old cultures significantly reduced (50 mM) or completely blocked (100 mM) somatostatin release elicited by 50 microM NMDA without modifying basal release. We conclude that chronic ethanol treatment to concentrations up to 100 mM has no effect on somatostatin biosynthesis in fetal rat hypothalamic neurons, while weaker concentrations decrease NMDA-induced somatostatin release.

Animals↗

PubMed1998

Allopregnanolone-induced modification of presynaptic basal and K+-induced [3H]-norepinephrine efflux from rat cortical slices during the estrous cycle.

Superfused frontal slices of cerebral cortex were preloaded with [3H]-norepinephrine ([3H]NE). Basal [3H]NE efflux and K+-induced [3H]NE release were studied during the estrous cycle and in the presence of neurosteroids. Basal [3H]NE efflux showed estrous cycle-related variations, with lowest values found during estrus and diestrus II. Allopregnanolone (10(-9) M) potentiated basal [3H]NE efflux from the 1st minute of its application; the effect of the steroid was still present after 20 min. This effect was also dependent upon the estrous cycle, since basal [3H]NE efflux was mainly increased during estrus diestrus I, and to a lesser degree only during proestrus. During diestrus II and after ovariectomy, basal [3H]NE efflux was no longer affected by the neurosteroid. In the presence of yohimbine (10(-6) M), the effect of allopregnanolone on basal efflux was potentiated only during the first 3 min but vanished thereafter. Allopregnanolone (10(-9) M) potentiated the K+-induced [3H]NE release during estrus, but pregnenolone (10(-9) M) was ineffective, suggesting specificity of the neurosteroid. Yohimbine (10(-6) M) also potentiated K+-induced [3H]NE release. When applied simultaneously with allopregnanolone (10(-9) M), a potentiating effect on [3H]NE release was observed. The present results suggest that allopregnanolone is a neurosteroid able to modulate norepinephrine release in the cerebral cortex in an estrous cycle-dependent manner, and that the effect could involve noradrenergic alpha-2 receptors.

Adrenergic alpha-2 Receptor Antagonists↗

PubMed1997

Responsiveness to depolarization of hypothalamic neurons secreting somatostatin under stress and estrous cycle conditions: involvement of GABAergic and steroidal interactions.

We studied the sensitivity to a depolarizing stimulus of hypothalamic fragments dissected from cycling female donor rats exposed or not to 30-min stress at 4 degrees C. The neuronal response was estimated in terms of the ability of tissue to release somatostatin when stimulated with 40 mM K+. The data showed no differences in response to K+, regardless of the ovarian cycle of the female donors, whereas tissues dissected from ovariectomized or pregnant rats responded significantly to K+. However, when donors underwent previous cold stress, significant differences were noted at all stages of the cycle, except diestrus-1, compared with control rats. We tested whether GABA and/or neuroactive steroids could be involved in this phenomenon and observed no GABA inhibition of somatostatin release in vitro, but inhibition occurred in the presence of a neuroactive steroid, THDOC. The effect of GABA in vivo on somatostatin release was estrogen dependent because bicuculline modified the total amount of somatostatin secreted in estrus but not in diestrus II. Finally, in hypothalamic primary cultures, GABA inhibition of somatostatin release was only detected when steroids were present in the media throughout culture. Our results suggest that steroid-GABA-somatostatin interactions could explain the different responses of neurons to depolarization.

Animals↗

PubMed1997

Rapid and opposite effects of dexamethasone on in vivo and in vitro hypothalamic somatostatin release.

We have previously reported the rapid response of hypothalamic somatostatin (SS) neurons to acute stress. Since it is well known that glucocorticoids (GC) are involved in neuroendocrinal stress regulation, we investigate in this study the effects of acute administration of dexamethasone (Dex) on both in vivo and in vitro SS release. Freely moving animals received stereotaxic implant of a push-pull cannula into the median eminence for 10 days, and then they were perfused with artificial cerebrospinal fluid for 120-150 min. An i.p. injection of Dex (200 or 300 micrograms/100 g) induced, 15-30 min later, a mean increase in SS hypothalamic output of 62.6 +/- 6.2% of basal secretion. By contrast, after 15 min incubation of hypothalamic fragments with either 10(-7) or 10(-6) M Dex, SS release decreased abruptly to 57.3 +/- 3.3% (n = 16; P < 0.001 compared with basal release) and 78.0 +/- 9.5% (n = 13; P < 0.05 compared with basal release) of basal release, respectively. Other Dex concentrations induced no variations, giving the dose-effect curve an abrupt "on-off" effect. The inhibitory effect was blocked by picrotoxin (10(-4) M) and was immediately reversed when Dex was removed from the medium. Specificity was tested by using another steroid, estradiol, and another tissue, cortex. The rapid action of GC whatever the model used and in particular the blocking in vitro effect of picrotoxin could suggest that GCs act at the level of the membrane and could operate physiologically in response to stress. In addition, the opposite in vivo and in vitro effects on SS release would indicate that GCs exert two different controls on SS neurons.

Animals↗

PubMed1996

N-methyl-D-aspartate receptor involvement in dexamethasone and stress-induced hypothalamic somatostatin release in rats.

The median eminence (ME) push-pull perfusion technique was used in this work and the results clearly showed that i.p. administration of MK-801 (4 mg/kg), a specific N-methyl-D-aspartate (NMDA) receptor antagonist, totally abolished dexamethasone (Dex) (300 micrograms/ 100 g i.p. injected) and immobilization stress-induced hypothalamic somatostatin release in adult male rats. We also observed that glutamate from median eminence-hypothalamic medio basal (ME-MBH) complex, measured by high performance liquid chromatography (HPLC), exhibited a conspicuous secretory pattern, with the total amount released not modified by Dex administration. This indicates that Dex and stress-induced somatostatin (SS) secretion is not mediated by endogenous glutamate variations but likely by activation of NMDA receptors.

Animals↗

PubMed1996

Variations in hypothalamic somatostatin release and content during the estrous cycle in the rat. Effects of ovariectomy and estrogen supplementation.

To investigate the secretory pattern of somatostatin (SS) from the median eminence (ME) in the female rat, as well as estrogenic influence on this secretion, we measured both SS release and hypothalamic content in cycling, 10-day ovariectomized, and ovariectomized rats treated with estradiol for 3 days before. Animals were stereotaxically implanted with a push-pull cannula into the ME, and 10 days later the hypothalamic structure was perfused with artificial cerebrospinal fluid for 120-150 min at a regular flow rate of 17 mu l/min. Secretion peaks were observed in the pattern of SS release, whatever the stage of the estrous cycle. The mean amplitude of SS peaks was similar throughout the cycle: 11.7 +/- 4.0, 8.6 +/- 1.5 and 10.5 +/- 1.3 pg at proestrus, estrus and diestrus, respectively, and it was affected neither by ovariectomy (7.4 +/- 1.3 pg) nor by estrogen replacement (5.5 +/- 1.0 pg). By contrast, mean SS release levels in the proestrus phase were significantly higher than those measured in the other phases: 21.6 +/- 2.1 vs. 17.7 +/- 1.2 pg/15 min in diestrus (p < 0.05) and vs. 12.0 +/- 0.7 pg/15 min in estrus (p < 0.001). Hypothalamic SS content showed variations quite similar to those observed during its release, i.e. with the highest values corresponding to the proestrus phase (1,170.5 +/- 224.9 pg/mg of tissue) and to the diestrus (1,156.5 +/- 332.1 pg/mg of tissue) and the lowest values in the estrus (511.5 +/- 52.9 pg/mg of tissue; p < 0.05 vs. proestrus and diestrus). In addition, the lowest SS content and secretion values were found in ovariectomized animals: 95.5 +/- 5.1 pg/mg of tissue (p < 0.001 compared to the values obtained for each stage of the estrous cycle) and 10.0 +/- 0.9 pg/15 min (p < 0.001 vs. proestrus and diestrus), respectively. Patterns of SS release and SS hypothalamic content were not modified by estradiol treatment in ovariectomized animals. Our results suggest that (1) whatever the stage of the estrous cycle, SS release from the ME is not uniform and exhibits irregular peaks; (2) mean SS release levels were subjected to gonadal influence; (3) the occurrence of SS peaks seems to be estrogen-independent, and (4) variations in hypothalamic SS content were generally in good agreement with those of neurohormone release.

Animals↗