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G Ixart

Publications and source records attributed to G Ixart.

At least 37 records · Page 2Linked to original sources
PubMed1993

Circadian variations in the amplitude of corticotropin-releasing hormone 41 (CRH41) episodic release measured in vivo in male rats: correlations with diurnal fluctuations in hypothalamic and median eminence CRH41 contents.

The possible correlation between the circadian and episodic release of corticotropin-releasing hormone 41 (CRH41) in male rats was explored in a comparative study, including the measurement at 0700 hr and 1700 hr of (1) the quantitative parameters of the episodic release pattern of CRH41 into the push-pull-cannulated median eminence (ME); (2) CRH41 content measured by radioimmunoassay in the hypothalamus, and immunocytochemically in the ME; and (3) plasma adrenocorticotropic hormone (ACTH). The data showed that in early evening, the 3.4-fold rise in plasma ACTH coincided with a doubling of CRH41 content in the hypothalamus and in the ME, and of the CRH41 release from the perfused ME. The immunocytochemical data further indicated that the ME area labeled with CRH41 immunoreactivity, rather than the labeling intensity of CRH41-stained neurons, increased in the evening, which may point to an evening recruitment of additional CRH41-producing neurons as the origin of the evening increment in CRH41 and ACTH releases. Finally, the computerized analysis of the CRH41-releasing pattern with three different algorithms (Pulsar, Ultra, and the Santen and Bardin algorithm) showed for the first time that the evening rise in CRH41 output was associated with correlative increases of three parameters of the episodic pattern--peak amplitude (+55% to +80%), peak duration (+20%), and mean absolute peak values (+73%)--while the pulse frequency remained at the baseline level of 3 cycles.hr-1. The data suggest the occurrence of a connection between the circadian pacemaker and the machinery generating the episodic release of CRH41.

Adrenocorticotropic Hormone↗
PubMed1993

[Stress. Neurophysiologic studies].

The hypothalamic-pituitary-adrenocortical (HPA) axis knowingly plays a key role in the physiological response to various stressing situations, owing to its gluconeogenetic function, and also, possibly, to its large range of modulating effects on a series of more specific defense mechanisms including the immune system, the latter effect serving to protect the organism against overactive defense reactions. It has long been accepted that under most aggressive conditions the CNS is an essential part of the mechanism controlling the subsequent acute stimulation of the HPA axis. In this line of research, the HPA axis reacts within a few minutes after a standard ether-stress, with a 6 fold increase over the baseline of CRH41 secretion, and at the periphery with 20-fold and 14-fold increases, respectively, in plasma concentrations of ACTH and corticosterone in unanesthetized free-moving rats. From a series of additional experiments a few selected brain structures emerged as basic components of the CNS control involved in the HPA axis stress responses: 1) The catecholamine (CA) producing neurons of the medulla oblongata (A1/C1 and A2/C2 nuclei) which directly innervate the CRH41-secreting neurons in the paraventricular nuclei (PVN) via the ventral noradrenergic bundle (VNAB), yield the major stimulatory pathway to the stress-induced CRH-ACTH surge. Not only was this surge dramatically obliterated by a neurotoxic deletion of the VNAB, with a local microinfusion of 6-hydroxydopamine (6-OHDA) but it was restored by intra-cerebroventricular (icv) microinfusions of adrenaline (AD) or noradrenaline (NA).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

A quantitative study of the pulsatile parameters of CRH-41 secretion in unanesthetized free-moving rats.

Having recently improved the sensitivity of the RIA CRH-41 measurements in perfusates from push-pull cannulas implanted in the rat median eminence, we explored quantitatively the pulsatile parameters of the CRH-41 measured with this technique at 2.5 or 5 min intervals in a series of unanesthetized male rats under basal conditions. The data were analysed by computer using 4 algorithms, i.e. Santen & Bardin, Ultra, Pulsar and Periodogram. Under a basal mean secretion rate of 15.5 pg CRH-41/15 min, the pulsatile pattern of CRH-41 release was statistically assessed with the 4 methods, with a mean pulse frequency of 3.1 c/h, pulse length of 11.6 min and a peak amplitude above mean levels of 4 pg. The respective advantages of the 4 algorithms and the physiological relevance of the neurohormone's pulsatility are discussed.

Activity Cycles↗
PubMed1990

Intrahypothalamic infusion of interleukin-1 beta increases the release of corticotropin-releasing hormone (CRH 41) and adrenocorticotropic hormone (ACTH) in free-moving rats bearing a push-pull cannula in the median eminence.

In two simultaneous studies on unanesthetized rats implanted 1 week earlier with either an intracerebral (i.c.) cannula adjacent to the paraventricular nucleus of the hypothalamus and an intracarotid cannula, or the same i.c. cannula together with a push-pull cannula in the median eminence (ME), we explored the effect of i.c. infused interleukin-1 beta (IL 1 beta, 5 ng in 0.25 microliter of vehicle within 2 min) on the release of corticotropin-releasing hormone (CRH) 41 and adrenocorticotropic hormone (ACTH). Intracerebral infusion of the vehicle alone had no significant effect on either the pulsatility or the level of CRH 41 release and only a short-lived minor effect on plasma ACTH, whereas i.c. IL 1 beta injection led to a significant and long lasting (1-2 h) rise in CRH 41 release peaking 3 times higher than the mean peaks of basal pulsatility (26.1 +/- 3.5 pg/5 min vs 9.5 +/- 0.7 pg/5 min), and in plasma ACTH culminating 15-20 times higher than basal levels. Simultaneously, body temperature was increased by 2.3 +/- 0.3 degrees C. In another experiment, i.c.v. infusion of IL 1 beta produced a similar increase in plasma ACTH in rats whose catecholaminergic innervation to the hypothalamus had been obliterated by a bilateral injection of 6-hydroxydopamine into the ventral noradrenergic bundle, which appears to rule out modulation of this innervation in the stimulatory effect of IL 1 beta. The precise cellular site of action of IL 1 beta on CRH 41 secreting neurons and the physiological relevance of the study are discussed within the framework of functional interactions between the neuroendocrine and immune systems.

Adrenocorticotropic Hormone↗
PubMed1988

Evaluation by push-pull cannulation of ACTH in the cerebrospinal fluid of intact and hypophysectomized rats.

Adrenocorticotropin (ACTH) was measured in the cerebrospinal fluid (CSF) of male rats implanted with a push-pull cannula in the 3rd ventricle (ICV) and perfused for 3-6 hr. In 5 conscious sham-lesioned controls studied one week after cannulation, CSF ACTH displayed a pulsatile circhoral pattern with a mean concentration of 10.3 +/- 1.1 pg ACTH/15 min, and a peak/trough ratio of about 2. This pattern was not affected by 2 min of ether vapor inhalation or by pentobarbital anesthesia. The high mortality rate following ICV push-pull cannulation in rats hypophysectomized for 2 weeks led us to perform the ICV perfusion just after cannulation in 5 hypophysectomized rats when they were still under pentobarbital anesthesia. Even so the levels and pulsatile pattern of ACTH release into the CSF were unchanged despite the complete disappearance of any detectable amount of ACTH from the plasma. In two of the latter specimens perfused again one week later but without anesthesia, CSF ACTH levels still were indistinguishable from controls. It can thus be concluded that the ACTH detected in the 3rd ventricle CSF is of neuronal origin.

Adrenocorticotropic Hormone↗
PubMed1987

Evidence for basal and stress-induced release of corticotropin releasing factor in the push-pull cannulated median eminence of conscious free-moving rats.

Fourteen adult male rats were successfully implanted in their median eminence with a push-pull cannula perfusing an artificial fluid at a rate of 13 microliters/min, to measure the release of corticotropin releasing factor (rCRF-41) under physiological conditions assessed by baseline plasma adrenocorticotropic hormone (ACTH) levels. In the basal conscious free-moving state, rCRF-41 release displayed a fluctuating pattern, with peaks about every 45 min at a mean value of 9.0 +/- 0.7 pg/15 min sample (n = 42) vs a mean trough value of 4.1 +/- 0.3 pg/sample (n = 44). Ether stress was followed by a striking rise in rCRF-41 release which generally lasted about 45 min and reached mean peak values of 54.3 +/- 3.2 pg/15 min sample (n = 7). These data constitute the first direct measurements of basal and stress-induced CRF releases in conscious unrestrained rats.

Adrenocorticotropic Hormone↗
PubMed1987

[Adrenergic activation of the liberation of corticotropin-releasing hormone (CRH41) in the median eminence of unanesthetized rats].

To shed light on the persistent controversy concerning the role of central adrenergic systems in the corticotropic axis, we measured the effects of adrenaline on the release of IR-rCRH41 into a push-pull cannula stereotaxically implanted in the median eminence. Eight days before experimentation, the cannula was implanted, under deep anesthesia, at which time a standard cannula was additionally placed in the lateral ventricle (i.c.v.). The rats were not anesthetized during the main experiment. An i.c.v. injection of 5 microliter of solvent only slightly affected the release of CRH41, whereas an i.c.v. infusion of 1.4 micrograms adrenaline bitartrate under the same conditions led to an instantaneous, but short-lived, 8-fold rise in the CRH41 release above baseline. The data provide the first demonstration of a central stimulatory effect of adrenaline on the secretory activity of CRH41 producing neurons, in unanesthetized, free-moving rats.

Animals↗
PubMed1986

Plasma ACTH and corticosterone responses to limbic kindling in the rat.

Changes in plasma ACTH and corticosterone concentrations were measured in individual cannulated rats at stages 1 and 5 of limbic kindling induced by electrical stimulation of the basolateral amygdala or the dorsal hippocampus. At both stages, a stimulation of either structure produced swift surges, first of ACTH and then of corticosterone. At stage 5 of hippocampal stimulation, ACTH baseline concentrations were four times higher than in the controls. The results are discussed in relation to the central control of the adrenocorticotropic system and to the neuroendocrine correlates of the kindling process.

Adrenocorticotropic Hormone↗
PubMed1986

Probable extrapituitary source of the immunoreactive prolactin measured in the cerebrospinal fluid of unanesthetized rats by push-pull cannulation of the 3rd ventricle.

The dynamic pattern of the immunoreactive prolactin (PRL) concentrations in the cerebrospinal fluid (CSF) of the 3rd ventricle was explored by push-pull cannulation during either stimulation or blocking of PRL production in the plasma, which itself was sampled by chronic cannulation of the carotid. Some of the results were compared to the PRL concentrations in CSF samples obtained by 3rd-ventricle puncture. Ether stress, which induced a 4- to 6-fold rise in plasma PRL, altered neither the pulsatile circhoral pattern of PRL in the CSF nor the mean level and amplitude of its pulses. However, the sustained intense hyperprolactinemia induced by haloperidol increased the mean PRL level in the CSF and possibly its pulse rate. Surprisingly, hypophysectomy, which suppressed production of PRL in the plasma, did not alter its baseline level or cycling pattern in the CSF. The possibility that tuberal adenohypophysial cells and/or CNS prolactinergic neurons supply the CSF with PRL is discussed.

Animals↗
PubMed1985

Diurnal-stimulated and stress-induced ACTH release in rats is mediated by ventral noradrenergic bundle.

Female rats were bilaterally injected with 3 micrograms of 6-hydroxydopamine (6-OHDA) dissolved in 0.2 microliter saline, via a glass micropipet stereotaxically implanted into the ventral noradrenergic-ascending bundle (VNAB). This bundle conveys most of the catecholaminergic innervation to the paraventricular nuclei and originates from the locus coeruleus and from two medullary groups of neurons (A1 and A2). Two weeks after injection, and 1 wk after the subsequent implantation of an arterial cannula, serial blood samples were taken from each rat over a 36-h period for assay of basal secretion patterns of ACTH and corticosterone (C) by radioimmunoassay and radiocompetition, respectively. Other blood samples were collected at short intervals over a 2-h period to explore the stress-ether responses of both hormones. Effects of 6-OHDA injections on catecholaminergic innervation were attested by the striking decrease in the histofluorescence of hypothalamic catecholamines and by the 86% drop in the hypothalamic noradrenaline concentrations measured by high-performance liquid chromatography at constant dopamine titers. Compared with control, sham-lesioned rats, pharmacological destruction of the VNAB by 6-OHDA led to 1) obliteration of the circadian patterns for ACTH and C and the emergence in their place of ultradian fluctuations of reduced amplitude above base-line levels and 2) 80% inhibition of the ACTH stress response which correlated with a short-lived, depressed C response. These results are discussed within the framework of the controversial literature on the mechanisms by which catecholamines may control corticotropic function.

Adrenocorticotropic Hormone↗
PubMed1985

[Passive immunization with an anti-oCRF41 immune serum inhibits the circadian increase of plasma ACTH in rats].

For 24 hrs. after i.v. injection of 1 ml of an undiluted immune serum raised against oCRF41, the diurnal surge of plasma ACTH dropped to a short-lived limited rise above baseline level. On the second day after injection, the ACTH level in treated rats rose to a subnormal level, although both plasma dilution of the immune serum and its binding capacity in the plasma remained unchanged throughout the experiment. Plasma corticosterone, on the contrary, displayed a normal circadian rhythm during the entire experiment. However, in animals given a second injection of 0.5 ml oCRF41 immune serum 32 hrs. after the first, both ACTH and corticosterone titers fell rapidly below their circadian minimal levels in controls. Concomitantly, the concentration of immune serum in the peripheral plasma, and its capacity to bind to oCRF, rose by 50%. The major role of CRF41 as a diurnal trigger of the circadian rhythm of ACTH is discussed, as well as the limits of passive immunization.

Adrenocorticotropic Hormone↗
PubMed1985

[Evaluation of the inhibitory effect of circulating corticosteroids on circadian stimulated and stress induced secretion of ACTH in rats].

Male rats were bilaterally adrenalectomized in order to measure the extent of inhibition exerted by endogenous corticosteroids on both basal ACTH secretion along its circadian rhythm and ether-stress induced ACTH secretion. In intact controls, plasma ACTH levels at the circadian maximum exceeded by 4 times the circadian minimum, and ACTH response 15 min after ether-stress surpassed the circadian minimum by 20 times. In adrenalectomized rats, the daily minimum was 8 times that of the controls. Nevertheless the circadian maximum was 3 times above the rhythm's minimum, while the maximal stress response (15 min) surpassed the circadian minimum by 8 times. In adrenalectomized rats supplemented with a solid source of corticosterone inducing a stable plasma corticosterone level equivalent to the controls' circadian minimum (3 micrograms/100 ml), the ACTH rhythm still fluctuated twice as high as in intact controls. The tonic feed-back inhibition exerted by endogenous corticosteroids on ACTH secretion appeared thus significantly stronger than the GABAergic inhibition to the corticotropic system which was previously studied under similar standard conditions.

Adrenalectomy↗
PubMed1985

[Demonstration of prolactin flow into the cerebrospinal fluid of the alert rat in a pulsatile circhoral manner by push-pull cannulation of the 3d ventricle].

In 8 male unanesthetized rats, sequential sampling of cerebrospinal fluid (CSF) from a push-pull cannula implanted into the 3rd ventricle revealed that prolactin was present in this fluid, where it displayed circhoral pulsatility resembling the temporal variations in plasma prolactin observed in the same animals. Although basal prolactin levels were lower in the CSF than in the plasma, the amplitude of the circhoral prolactin pulses was twice as great in the CSF as in the plasma compartment. The possible origin and role of CSF prolactin are discussed.

Animals↗
PubMed1983

Acute and delayed effects of picrotoxin on the adrenocorticotropic system of rats.

To investigate the possible effect of GABA on the corticotropic system, the potent GABA antagonist picrotoxin was injected into two groups of 14 female rats at 07.00 h and 19.00 h, respectively. A single subconvulsive I.p. injection dramatically raised plasma ACTH and corticosterone, and thereafter suppressed the circadian rhythm of ACTH, but not of corticosterone, for 24 h in the group injected at 07.00 h and for 48 h in the one injected at 19.00 h and increased mean hormonal levels. Results are discussed in the light of the possibility that inhibition by the GABAergic system and stimulation by the serotoninergic system might be components of the mechanism controlling the circadian rhythm of ACTH.

Adrenocorticotropic Hormone↗
PubMed1983

CNS control of the circadian adrenocortical rhythm.

The effects of various CNS impairments on the circadian rhythm of plasma ACTH and Corticosterone (C) were studied in individual cannulated female Sprague-Dawley rats. Pinealectomy had no effect whatever the light perception (intact or blinded rats). Bilateral ablation of paraventricular nuclei did not obliterate the hormonal rhythms, although the rhythms' amplitude were markedly depressed. On the other hand, destruction of suprachiasmatic nuclei (SCN) or systemic blockade of the serotoninergic (5-HT) system by pCPA blocked ACTH rhythm at baseline levels, although circadian or ultradian fluctuations with normal amplitudes persisted for C. Similar effect was observed in several blinded rats with raphe lesions suppressing 5-HT innervation of SCN. Daily 5-HTP injections, if given 4 h after dawn restored normal ACTH rhythm. The respective role of related structures in the rhythms' control will be discussed.

Adrenal Cortex↗
PubMed1983

[Persistance of phase-coupling between the circadian rhythms of hypophyseal hormones in free-running rats].

The circadian rhythms in plasma ACTH, TSH, LH and PRL were explored in sighted or blind, spayed and estrogen-implanted rats. A marked endogenous circadian rhythmicity was shown to persist in the blind animals for the 4 endocrine rhythms. The endogenous rhythms also kept very close reciprocal phase relationship as in the synchronized state, and they were peaking almost simultaneously, after 60 d. of free-running. Finally the endogenous hormonal rhythm maintained their usual phase relationships with the endogenous activity rhythm, so that the circadian phase of increased hormonal secretion coincided with the circadian resting phase of the sleep/wake rhythm. These results are discussed in the light of the alternate theory of one vs multiple but phase-locked circadian pacemakers driving endocrine and behavioral circadian rhythms.

Adrenocorticotropic Hormone↗
PubMed1983

[Persistence of circadian rhythms of plasma ACTH and corticosterone after pinealectomy in sighted or blind rats].

The possible effects of pinealectomy on the corticotropic system was studied in either sighted or ocular enucleated adult female Rats. Individual ACTH and corticosterone measurements were performed on sequential plasma samples obtained over a 48 hrs period from a carotid implanted cannula. Compared with their respective sighted or blind controls, pinealectomized Rats displayed no alteration in the hormonal rhythms' periodicity, phase, mean level and amplitude. On the other hand, ocular enucleation, whether or not associated with pinealectomy depressed the amplitude and to a lesser extent the mean level of the ACTH rhythm, and paradoxically increased the corticosterone rhythm's mean level. While no pineal factors appear therefore required for a normal corticotropic rhythmicity, the possible regulating role of retinal melatonin may be discussed.

Adrenocorticotropic Hormone↗