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S Arancibia

Publications and source records attributed to S Arancibia.

At least 37 records · Page 2Linked to original sources

Neuroendocrine and autonomous mechanisms underlying thermoregulation in cold environment.

This review focuses on the central regulation of thermoregulatory responses with special attention to the participation of thyrotropin-releasing hormone (TRH) in both autonomous and endocrine responses to a cold environment. Besides a direct projection of TRH neurons from paraventricular nuclei (PVN) to the median eminence, and the subsequent activation of the thyroid axis, there are direct projections from the PVN to the autonomic preganglionic neurons controlling autonomous responses. There projections convey information to peripheral targets involved in thermogenesis through the dorsal vagal complex and the spinal cord, for parasympathetic and sympathetic neurotransmissions respectively. Furthermore, cold exposure increases TRH mRNA levels in the PVN but also in dorsal motor and caudal raphe nuclei, thus providing strong evidence for a functional link between autonomous and neuroendocrine systems involved in thermoregulation. The review also focuses on neuroendocrine regulation of cold-induced TRH/TSH release associated with modifications in somatostatin release, with special reference to the participation of several central neurotransmitters (catecholamines, serotonin or GABA) or the influence of sex steroids.

Animals↗

Neuroactive steroids modulate GABA inhibition of hypothalamic somatostatin release.

The reduced steroids 3 alpha-hydroxy-5 alpha-pregnan-20-one (allopregnanolone) and 3 alpha,21-di-hydroxy-5 alpha-pregnan-20-one (allotetrahydroDOC) are potent ligands of GABAA receptors. This study examined the possible modulatory effect of these metabolites on GABA inhibition of somatostatin release in cultured hypothalamic neurones. Allopregnanolone potentiates GABA inhibition, and reversed picrotoxin and bicuculline-induced augmentation of somatostatin release in a dose-dependent manner. AllotetrahydroDOC also inhibits the stimulated release induced by the antagonists, but did not modify that induced by depolarizing concentrations of K+. Pregnenolone sulphate had no effect on picrotoxin-induced somatostatin release. These findings clearly establish that 3 alpha-hydroxysteroids modulate GABA inhibition of hypothalamic somatostatin release.

Animals↗

The inhibitory effect of picrotoxin on basal and cold-induced thyrotropin secretion involves somatostatin mediation.

This work was undertaken to investigate whether the inhibitory tone exerted by GABA on somatostatin (SRIH) release operates in the control of thyrotropin (TSH) secretion in both basal and cold-stimulated conditions. In a first group of animals (G1) undergoing both carotid and third ventricle push-pull cannulation, i.vt. injection of picrotoxin (10(-5) M) induces a significant decrease in plasma TSH level under basal conditions (0.09 +/- 0.02 versus 0.27 +/- 0.4 ng/100 microliters; P < 0.03, n = 5). In a median eminence (ME) push-pull cannulated group of rats (G2), picrotoxin, peripherally administered, blocks cold-induced inhibition of SRIH release (35.0 +/- 1.8 versus 7.4 +/- 3.3 pg/15 min; P < 0.005; n = 5). In a third group of intact rats (G3), peripheral administration of picrotoxin (2 mg/kg i.p.) blunts the cold-induced TSH release (0.17 +/- 0.03 versus 0.46 +/- 0.04 ng/100 microliters; P < 0.001; n = 5). Our results strongly suggest that a decrease in SRIH release is involved in the GABAergic control of basal and cold-induced TSH secretion.

Animals↗

Rapid changes in somatostatin and TRH mRNA in whole rat hypothalamus in response to acute cold exposure.

Acute cold stimulus induces activation of the thyreotropic axis characterized by a rapid increase in plasma thyrotropin (TSH). Since pituitary TSH release is mainly regulated by two hypothalamic hormones: thyrotropin-releasing hormone (TRH) and somatostatin, the aim of this study was to analyse whether changes in the steady state mRNA levels and peptide content of these neurohormones occur under acute cold stimulation in rats. Northern blot analysis of hypothalamic somatostatin mRNA levels after 15, 30, 60 or 180 min of cold exposure revealed a 2.0-fold increase after 15 min at 4 degrees C. This augmentation was followed by a return to control values at 30 min. However, the hypothalamic content of somatostatin was not significantly modified at any cold exposure time. TRH mRNA showed a similar pattern to somatostatin, with a 2.5-fold increase after 15 min at 4 degrees C. In contrast, hypothalamic TRH content was significantly decreased after 15 min cold exposure, returning to control values at 30 min. The increase in mRNA levels was specific for the two hypothalamic hormones, since there was no concomitant variation in GAPDH mRNA used as negative control. These results suggest that the organism is quickly aroused by cold stimulus, triggering rapid activation in transcription of the two neurohormones involved in the regulation of the thyreotrope axis. Since the peptide contents did not show the same pattern, a quantitative change in transcription or in mRNA stability does not appear to be a prerequisite for increased peptide expression, suggesting that somatostatin and TRH gene expressions could be regulated at translational or post-translational steps.

Animals↗

Chronic stress affects in vivo hypothalamic somatostatin release but not in vitro GH responsiveness to somatostatin in rats.

One week after stereotaxical implantation of a push-pull cannula into the median eminence (ME), rats were stressed by immobilization for 2 h daily for 7 days. Thereafter, ME was perfused for 1 h in basal, stress and recovery conditions, respectively, and somatostatin (SRIH) was measured in perfusate fractions. Pituitaries were in vitro perifused to assess GH responsiveness to SRIH. In the stressed group, basal SRIH release was significantly higher than in the control group and stress caused a significant sharp peak in neurohormone release. GH responsiveness to SRIH was not affected in pituitaries obtained from stressed donors. High SRIH levels secreted under chronic stress thus did not impair the GH pituitary response to SRIH.

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Antidepressant/anxiolytic ipsapirone inhibits cold-induced hypothalamic TRH release.

Acute administration of the serotonin (5-HT)1A receptor agonist ipsapirone has been previously shown to elicit a dose-dependent decrease of cold-elicited thyrotropin (TSH) secretion. Therefore, the aim of the present study was to evaluate, by means of a push-pull cannula implanted in the median eminence (ME), whether ipsapirone acts primarily through an inhibition of cold-elicited thyrotropin-releasing hormone (TRH) release. Ipsapirone administration (10 mg kg-1 i.p., 30 min before cold) prevented cold-elicited TRH release, thereby confirming the above hypothesis. In addition, this study further validates push-pull perfusion in the ME as a key tool for measuring TRH secretion in vivo.

Animals↗

Presence but not synthesis of thyrotrophin-releasing hormone in rat salivary glands detected by radioimmunoassay and northern blot analysis.

Thyrotrophin-releasing hormone (TRH) is one of the ubiquitous peptides first isolated from hypothalamus. This study sought to examine if it could also be detected in rat submandibular salivary glands, as can other neurogastrointestinal peptides. Radioimmunoassay of submandibular gland homogenates revealed TRH-like immunoreactivity in all samples from male rats (637.34 pg/gland +/- 166.17, n = 15). In contrast, Northern blot analysis to determine whether the peptide was locally synthesized in the glands failed to detect TRH mRNA. Consequently, the presence of TRH in the glands (as revealed by radioimmunoassay) could be associated with binding to presumptive TRH receptors in the mediation of physiological activities.

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Role of somatostatin in the acute immobilization stress-induced GH decrease in rat.

In the present work we have investigated to what extent somatostatin (SRIF) release from median eminence (ME) is affected by stress immobilization (IMO) in unanesthetized rats stereotaxically implanted with a push-pull cannula (PPC). One week after implantation, the ME was perfused with artificial cerebrospinal fluid for 1 hour in basal, stress and recovery conditions respectively. Samples were collected every 15 min and SRIF was measured by RIA. In another group of animals, a jugular cannula was inserted the day before and plasma samples were taken off simultaneously with the ME perfusate for GH and SRIF analysis respectively. SRIF release from the ME is rapidly (15 min) and significantly increased (58 +/- 11 vs 28 +/- 5 pg/15 min; n = 7; P < 0.01) in rats bearing only PPC. Intriguingly, animals bearing a jugular catheter plus a PPC showed no increase in SRIF release during the first 15 min of IMO in spite of a striking decrease of plasma GH (27.2 +/- 3.8 vs 3.6 +/- 1.3 ng/ml; n = 6; P < 0.001) observed at this time. However, in spite that the animals responded with a significant increase in SRIF, the response was later and more reduced than in animals without jugular cannula. Since our two rat groups--as result of jugular cannula surgery 24 hours before--showed differences such as a food intake, body weight gain, plasma GH levels and basal SRIF release, we think that these differences could explain the modifications in the regulatory mechanisms involved in GH control under acute stress.

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Chronic but not acute exposure to stress is associated with hypothalamic vasoactive intestinal polypeptide (VIP) release into median eminence.

The influence of stress on hypothalamic VIP release into the pituitary portal blood has not been assessed at present despite the fact that this peptide has been implicated in the control of several pituitary hormones and especially in the release of prolactin (PRL) caused by stress. In the present work the effect of stress on the in vivo release of VIP into the pituitary portal blood of male rats was evaluated by means of push-pull perfusion (PPP) of median eminence (EM). VIP content in the PPP liquid was successfully measured and their levels agree well with pituitary portal blood levels measured by other authors. Whereas plasma PRL levels strongly increased during acute immobilization (IMO), no changes in VIP secretion into the ME were observed. VIP release into the ME was also unaffected by exposure to ether. In contrast, in chronically immobilized rats a significant increase in VIP release into the ME was obtained in response to acute IMO. The present data argue against a major role of hypothalamic VIP in PRL release caused by acute stress and show that chronic stress qualitatively alters the signal of hypothalamic VIP to the pituitary.

Animals↗

Gamma-aminobutyric acid-glutamate interaction in the control of somatostatin release from hypothalamic neurons in primary culture: in vivo corroboration.

Recent studies have provided new data on the neuroendocrine role of glutamate (the major excitatory neurotransmitter) on somatostatin release. The neuroendocrine role of gamma-aminobutyric acid (GABA) (the major inhibitory neurotransmitter) on this same secretion, is also well established. Our objective was thus to investigate whether GABA and glutamate, which have opposite neurotransmission signals, could interact in the control of hypothalamic somatostatin release. Pharmacological manipulations of the two types of receptors were performed in vitro on primary cultures of hypothalamic neurons secreting somatostatin. We found that tonic release of somatostatin was reduced by 76% in the presence of tetrodotoxin (TTX) and was regulated by endogenous secretion of glutamate and GABA. CGS 19755, a highly selective N-methyl-D-aspartate (NMDA) receptor antagonist, significantly reduced tonic somatostatin secretion whereas it was strongly increased by picrotoxin and bicuculline, two GABAA antagonists. When CGS 19755 was applied with picrotoxin, somatostatin release was the same as levels obtained in the control group with TTX. GABA reduced tonic somatostatin release (in the presence or absence of TTX), and glutamate-stimulated secretion in a dose-dependent manner. Picrotoxin stimulation of tonic somatostatin release was additive with that obtained after glutamate stimulation and was also dose-dependent. This interaction was also studied in vivo in unanesthetized rats bearing a push-pull cannula stereotaxically implanted into the median eminence. Ip injected CGS 19755 (an antagonist that can freely permeate the blood-brain barrier) completely blocked the peak secretion of somatostatin observed after ip picrotoxin administration, whereas there was no significant effect when it was injected alone. These findings corroborated our in vitro data and allow us to postulate that GABA and glutamate interact in the control of somatostatin.

Animals↗

[Decrease of pineal AMPc and TOH activity in the superior cervical ganglia after ablation of submaxillary glands in rats].

In order to investigate a possible functional relationship between the submandibular salivary gland (SSG) and the central nervous system (CNS), we have extirpated the salivary organs from thirty male rats. Twenty days after ablation both the pineal glands and the cervical superior ganglions (CSG) were dissected, homogenized and frozen until AMPc and TOH were assayed respectively. We observed a significant decrease in pineal AMPc (53.9 +/- 6.2 vs 76.1 +/- 7.6% of maximum value; p less than 0.02) which seems to be linked with a significant drop in TOH activity measured at CSG level (1.5 +/- 0.6 vs 3.7 +/- 0.9 nmoles of DOPA/h/pair GCS; p less than 0.03). Our results suggest that both findings might be due to the lack of NGF normally reaching the CSG from SSG. This data reinforces the idea of a functional link between SSG and CNS via the pineal gland.

Animals↗

[A non-exocrine function of the submaxillary gland].

Emphasizing on the concept of "banalization" and multifactoriality of the signal molecules of the cellular communication, the authors review data of the literature which allow to attribute to some substances synthetized by the submandibular salivary glands (SSG), mainly growth factors as EGF and NGF, an endocrine role. Because of their direct secretion in the oral cavity or their overflow into bloodstream the consequences of the deficit of these growth factors could be correlated with some oral pathologies such as aphthous lesions, puberty and pregnancy gingivitis, which endocrine etiology is often assumed, as well as autoimmune salivary pathologies. Thus, the results obtained after SSG removal furnish a support for envisaging a link between the submandibular salivary glands and the reproductive function (decrease in plasma LH level, ultrastructural changes of the Leydig cells, spontaneous abortion) and with some structures of the central nervous system such as hypothalamus (variation in hypothalamic TRH content) or pineal gland (decrease in pineal cyclic AMP content). Particularly interesting is the possibility that NGF secreted in blood by the SSG during a stress may represent the signal able to stimulate the peripheral immunity cells as well as to inform the central nervous system through a neuronal pathway via the superior cervical ganglia and the pineal gland. This brain afferent information could be associated with an increased hypothalamic NGF synthesis, also observed during stress, whose finality might be to stimulate the secretion of hypophyseal ACTH, the main hormone involved in the interrelationship between endocrine and immune response.

Animals↗

Peripheral administration of picrotoxin and bicuculline stimulates in vivo somatostatin release from rat median eminence.

The gamma-Aminobutyric acid-A (GABAA) antagonist picrotoxin and bicuculline were administered to male rats to determine their effects on somatostatin (SRIF) release, measured in unanesthetized animals stereotaxically implanted with push-pull cannula in the median eminence (ME). I.p. injection (3 mg/kg) of picrotoxin (n = 5) or bicuculline (n = 6) significantly increased (35.4 +/- 10.8 vs 13.7 +/- 4.3 pg/15 min; P less than 0.03 and 38 +/- 3.5 vs 14 +/- 1.8 pg/15 min; P less than 0.001, respectively) SRIF release from the ME compared to baseline levels measured in the same animals. In contrast, with local perfusion of picrotoxin, (10(-4) to 10(-6) M) SRIF release from the ME was not affected. These data suggest a physiological endogenous inhibitory tone of GABA on SRIF release.

Animals↗

Ablation of submandibular salivary glands in rats provokes a decrease in plasma luteinizing hormone levels correlated with morphological changes in Leydig cells.

This work was designed to determine whether changes in plasma and hypophyseal levels of LH are the source of the previously reported atrophy of testicular interstitial tissue following ablation of submandibular salivary glands. The plasma and hypophyseal levels of LH were assayed, and testicular sections examined by electron microscopy in rats, weighing 230-260 g, whose submandibular glands had been removed. Twenty days after sialectomy, the rats were killed, and the pituitary glands removed, homogenized and frozen until used in LH-RIA like the blood samples. Testes were removed and fixed in osmic acid. There was a significant decrease in plasma LH levels in operated animals when compared with sham-operated controls (47.28 +/- 7 ng/ml versus 70.42 +/- 8; p less than 0.02), but the hypophyseal LH content was not significantly modified. Electron microscopy mainly showed important changes in the morphology of the Leydig cells, with a distinct reduction in the number of mitochondria and elements of the smooth endoplasmic reticulum. These findings suggest a physiological involvement of submandibular glands in a possible endocrinological link with the gonadotropic axis.

Animals↗

["Push-pull" perfusion technic, a new approach applied to the study of transdentinal fluid].

The flux through the dentin tubuli is at the origin of the hydrodynamic theory of tooth sensitivity. After a review of the various in vivo techniques reported in the literature, this study describes an original method of dentin perfusion--so called "push-pull" and specific to this topic. With this technique, the authors have demonstrated the kinetics of this flux, as well as the effect of some factors (age, colchicine, ouabain), on transdentinal fluid exchanges. The analysis of all these results suggests that a combination of active and passive movements could be at the origin of this flux, the temporary inhibition of which could present major advantages in current Periodontics practice.

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Physiological evidence for alpha 1-adrenergic facilitatory control of the cold-induced TRH release in the rat, obtained by push-pull cannulation of the median eminence.

The alpha-adrenergic antagonists phentolamine and prazosin were administered to male rats to explore their effects on cold-induced TRH release, measured by a chronic push-pull cannula stereotaxically implanted in the median eminence (ME). Phentolamine was given either i.p. (24 or 40 mg/kg), or locally (10(-5) M) in the ME, whereas prazosin was only applied locally (10(-5) M). Phentolamine significantly decreased the cold response (5 +/- 1 pg/15 min vs 21 +/- 5 pg/15 min; P less than 0.02), whatever the administration mode. Moreover, the blocking effect of prazosin directly perfused into the ME (11 +/- 3 pg/15 min vs 26 +/- 9 pg/15 min; P less than 0.05), indicates the specific involvement of alpha 1-adrenergic receptors in the cold-induced TRH response, and points to the ME as a possible site of facilitatory adrenergic control.

Animals↗

Increases in concentrations of somatostatin- and insulin-like immunoreactivities in submandibular salivary gland of diabetic rats: effect of insulin treatment.

To investigate whether systemic insulin levels can influence somatostatin-like immunoreactivity and insulin-like immunoreactivity concentrations in the rat submandibular salivary glands, we measured the concentrations of the two peptides in an experimental group rendered diabetic by streptozotocin administration. The diabetic group showed a low plasma level of insulin compared with the control group: 0.5 +/- 0.1 vs 3.5 +/- 0.8 micrograms/l, (P less than 0.01). Concomitantly, they exhibited clear glucosuria and a blood glucose level which was four times higher than in normal animals: 35.5 +/- 1.4 vs 8.8 +/- 0.8 mmol/l, (P less than 0.001). The two peptide concentrations in the submandibular glands of diabetic rats showed an increase compared with controls: 42.9 +/- 4.7 protein vs 24.7 +/- 3.1 pg/mg protein (P less than 0.001) and 34.9 +/- 4.9 protein vs 18.4 +/- 4.0 pg/mg protein (P less than 0.01), for insulin-like immunoreactivity concentration and somatostatin-like immunoreactivity concentration, respectively. Chronic insulin treatment of diabetic rats reversed the increase in somatostatin, but had no effect on the increase in insulin-like immunoreactivity concentration. A negative correlation (r = 0.24, P less than 0.05) was found between the plasma insulin level and the somatostatin concentration of the submandibular glands. Our results suggest that the submandibular glands of rats may participate in the peripheral regulation of glucose homeostasis.

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[Changes induced by ouabain and colchicine in the transdentinal flow estimated in vivo by perfusion: the "push-pull" of the incisors of rats].

The active or passive mechanisms regulating the various movements of dentinal fluid have not yet been sufficiently studied. For this reason different "in vivo" factors that may modulate the kinetics of transdentinal flow were investigated. After systemic administration of a radiotracer in rats, the kinetics were examined with a push-pull perfusion device fixed to the incisor dentin. The drugs chosen, i.e. ouabain and colchicine, were for their respective effects on microtubules and on the ATPase-dependent Na+ K+ pump, since these two factors are involved in the transport process. Anesthetized animals were prepared to allow intravenous injection of iodine 125 (0,5 to 0,7 mCi), carotid sampling, and perfusion of upper incisors. Ouabain induced a very significant decrease in transdentinal flow, which was particularly evident in younger animals (2,81 x 10(-2) % vs 0,04 x 10(-2)%, p less than 0,05). However, colchicine produced two different kinds of results : at low doses (3,5 to 5 mg/100 g) the pulsatile pattern of the curves was partially inhibited, whereas, at higher doses (6 to 7 mg/100 g), the transdentinal flow of radioactivity increased. These results suggest that a combination of active and passive transport may be involved in the various movements of this fluid.

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