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Biomedical subjects

G Barbanel

Publications and source records attributed to G Barbanel.

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

K(+)-stimulated neuropeptide Y release into the paraventricular nucleus and relation to feeding behavior in free-moving rats.

Neuropeptide Y (NPY) strongly stimulates food intake when it is injected in the central nervous system and especially in the hypothalamus. The major site of NPY synthesis in the hypothalamus is the arcuate nucleus which projects to the paraventricular nucleus. These two nuclei form the arcuate-paraventricular axis, a local circuit in the control of food intake. It was demonstrated that neuropeptide Y concentration in the paraventricular nucleus can be modified by ingestive or metabolic factors. Actually, these modifications cannot be associated with the existence of a release of neuropeptide Y in this nucleus. That is why we used push-pull perfusion during the light phase in freely-behaving rats with food and water available. Perfusates were collected with standard artificial cerebrospinal fluid (CSF) as medium and hyperosmotic CSF obtained by addition of potassium chloride (55 mM). Hyperosmotic perfusion was repeated a second time for some animals. Results clearly demonstrated that neuropeptide Y is released into the paraventricular nucleus during normal perfusion with a mean value of 35.5 +/- 1.5 pg/tube. The potassium perfusion produced an increase in the release of neuropeptide Y (peak at 71.4 +/- 7.1 pg/tube; p < 0.01), and this phenomenon was reproduced with the second potassium stimulation (peak at 47.7 +/- 2.3 vs pg/tube; p < 0.05). Neuropeptide Y release returned to normal values after or between stimulations. Behavioral analysis showed that these stimulations were associated with an increase in food intake. Neuropeptide Y is therefore physiologically released into the paraventricular nucleus of the hypothalamus.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Endogenous dopamine differently affects N-[1-(2-benzo(b)thiophenyl)cyclohexyl]piperidine and cocaine binding to the dopamine uptake complex.

1. [3H]N-[1-(2-Benzo(b)thiophenyl)cyclohexyl]piperidine ([3H]BTCP) labels in vivo the dopamine uptake complex in the mouse striatum. 2. In mice treated with gamma-butyrolactone (GBL, 400 mg/kg), [3H]BTCP specific binding was increased and ID50 values of BTCP and cocaine for the prevention of [3H]BTCP binding were significantly lowered. 3. In GBL-treated mice, cocaine (5 mg/kg, s.c.) had no effect on the BTCP ID50 value, whereas GBR 12783 (2 mg/kg, s.c.) increased it significantly. 4. Thus in vivo, endogenous dopamine and cocaine are competitive and non-competitive inhibitors, respectively, of the binding of [3H]BTCP.

4-Butyrolactone↗
PubMed1993

Evidence for an age-dependent decrease in the immunoreactive prolactin-containing terminals of the median eminence of male rats.

Labelling patterns of immunoreactive prolactin (IR-PRL)-containing and tyrosine hydroxylase (TH)-containing nerve terminals of the median eminence (ME) were compared in young adult (aged 3 months) and old (aged 24 months) male Wistar rats. In the young rats, IR-PRL- and TH-immunostained fibres extended throughout the external most layer of the ME. In the old rats, a significant decrease in the intensity of labelling of IR-PRL terminals was observed in this layer, with a slight reduction in the extent of labelling. As far as TH terminals were concerned, no difference could be detected between young and old animals.

Aging↗
PubMed1993

Effects of discrete lesions in the ventral noradrenergic ascending bundle on the corticotropic stress response depend on the site of the lesion and on the plasma levels of adrenal steroids.

Stereotaxic deletion of selected areas of the ventral noradrenergic ascending bundle (VNAB-X) by discrete bilateral injections of 6-hydroxydopamine (6-OHDA; 4 micrograms in 0.2 microliter saline) was used to explore the role of brain catecholamines (CA) and their interaction with corticosteroid feedback in stress responses of the ACTH-corticosterone (CORT) axis. The stereotaxic coordinates used for 6-OHDA lesions and the optimization of postlesion delays were determined by (a) radioautographic labeling of the VNAB axons after tracer injections into the dorsal A2/C2, or the ventral A1/C1 medullary areas, (b) histofluorescence and immunocytochemical location of interrupted CA pathways versus the postlesional scar, and (c) postlesional noradrenaline and adrenaline concentrations in whole hypothalami and paraventricular nuclei (PVN) punch samples. Two sites of 6-OHDA lesions were selected; both led to striking falls in PVN concentrations of both CA. The more dorsal lesion (dVNAB-X) was the same as that of our earlier studies and interrupted pathways originating predominantly in the A2/C2 area; the second more ventral lesion (vVNAB-X) interrupted axons stemming preferentially from the A1/C1 area. Both VNAB lesions inhibited the ether stress-induced ACTH and CORT surges in rats with intact adrenals. But the blockade (overall poststress release, amplitude and swiftness of hormonal responses) by dVNAB-X was greater than by vVNAB-X. The basal ACTH level in adrenalectomized rats (ADX) was elevated 20-fold and ether stress induced a 4-fold ACTH surge. As in sham-ADX rats, vVNAB-X in ADX rats induced only moderate inhibition of the ACTH response versus ADX + sham-vVNAB-X controls. On the other hand ADX + dVNAB-X rats showed a greatly amplified ACTH stress response over the ADX-sham dVNAB-X controls. This amplification was reversed by oral CORT supplementation. The data suggest that the CA pathways of the VNAB participating, directly or indirectly, in the poststress corticotropic activation may include subsets of CA axons of different origins, whose functional roles in stress are modulated in opposite directions by the plasma corticosteroid level.

Adrenal Cortex Hormones↗
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

Inhibitory interactions between alpha 2-adrenergic and opoid but not NPY mechanisms controlling the CRF-ACTH axis in the rat.

Following a series of investigations supporting the concept that the brain stem catecholaminergic (CA) system played a major stimulatory role on both basal and stress-triggered states of the hypothalamic-pituitary-adrenocortical (HPA) axis, across alpha 1 and beta receptors and also via alpha 2 receptors, the present study was designed to gain a deeper insight into the fine mechanism of functional interactions between the alpha 2 receptors mediated CA system and two peptidergic mechanisms, both shown to take part in the stimulatory control of the HPA axis: beta-endorphin and NPY. All experiments were conducted on rats whose noradrenergic bundles, which directly innervate the CRF neurons and are strongly implicated in the ether stress-induced corticotropic response, had been bilaterally obliterated by an intracerebral (i.c.) injection of 6-OHDA (NAB-X). Results showed that: (1) the blockade of the ether-stress induced ACTH response resulting from NAB-X was entirely reversed by an intraventricular (i.c.v.) infusion of the alpha 2 antagonist idazoxan (10 nmol), which appeared ineffective under basal conditions; (2) the restoration of a normal post-stress ACTH surge by i.c.v. idazoxan was itself blunted by an i.c.v. pretreatment with naloxone (10 nmol), whereas an i.c. pretreatment with an anti-NPY serum appeared ineffective. These data suggest that, in addition to a stimulatory control exerted by postsynaptic alpha 2 receptors directly on CRF neurons, other alpha 2 receptors participate, exclusively under the stress conditions above, in a tonic inhibitory control, indirectly mediated to the HPA axis across a stimulatory opioid, but not NPY regulatory component.

Adrenal Cortex↗
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↗
PubMed1991

Modulation by dopamine of [3H]N-[1-(2-benzo(b)thiophenyl)cyclohexyl]piperidine ([3H]BTCP, a phencyclidine derivative) binding to the dopamine uptake complex.

The modulation by dopamine of the binding of [3H]BTCP to the dopamine (DA) uptake complex was investigated in vivo (in control, reserpine- and L-DOPA-treated mice) and in vitro (on membrane preparations of the striatum of the rat). In both cases increasing doses of DA exerted a non-competitive inhibition of binding of [3H]BTCP, with a Ki value close to its K0.5, determined in competition experiments. Amphetamine and cocaine were also non-competitive inhibitors of the binding of [3H]BTCP, while GBR 12783 was competitive. In the presence of DA, the amount of cocaine required to inhibit the binding of [3H]BTCP was increased both in vitro and in vivo. These results suggest that inhibitors of the uptake of DA, such as BTCP or GBR 12783, modulate allosterically the uptake of DA, by binding to a site different from the DA recognition site. Cocaine, however, seems to share the same recognition site as DA.

Animals↗
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↗
PubMed1990

[Implication of alpha-2 adrenergic post-synaptic receptors in the central catecholaminergic stimulation of the corticotropic axis in rats].

We have recently assigned a major stimulatory role to the brain catecholamines (CA) via alpha 1 and beta receptors on CRH-ACTH secretion, e.g. in the physiological response to stress. In the present study, we explored the possible participation in this regulation of post-synaptic alpha 2 receptors in free moving rats, one week after CA denervation of the hypothalamus by bilateral neurotoxic lesions of the noradrenergic ascending brain stem bundles (NAB). Intracerebroventricular (i.c.v.) injection of clonidine (alpha 2 agonist; 1 nmol) induced a 3 fold rise of ACTH release (measured by RIA) above vehicle (PBS) injected controls (p less than 0.001). This stimulatory effect was completely reversed by an i.c.v. pretreatment with the alpha 2 antagonist idazoxan (10 nmol; without action by itself), whereas it was only slightly affected by an i.c.v. pretreatment with a combination of an alpha 1 and beta blocker (prazosin + propranolol; 5/5 nmol; p greater than 0.1). The results strongly suggest the participation of alpha 2 post-synaptic receptors in the central catecholaminergic activation of ACTH secretion.

Adrenergic alpha-Antagonists↗
PubMed1989

The organization of prolactin-like-immunoreactive neurons in the rat central nervous system. Light- and electron-microscopic immunocytochemical studies.

The localization and distribution of prolactin-like-immunoreactive perikarya and nerve fibers in the rat central nervous system have been studied by a preembedding immunoperoxidase method using well-characterized specific immunsera to rat prolactin. Although the localization of labeled neuronal structures in a number of brain areas correlates with the data of previous immunocytochemical studies, we found prolactin-immunoreactive neurons in various regions not previously reported. In untreated animals, the highest concentrations of prolactin-fibers were observed: (i) in the external layers of the median eminence where they exhibited close contact with blood vessels, and (ii) in the bed nucleus of the stria terminalis and in the central nucleus of the amygdala where they closely surrounded unlabeled perikarya. Dense networks of finely varicose prolactin fibers were also observed in the organum vasculosum of the lamina terminalis, in the subfornical organ, and in the dorsolateral regions of the medulla oblongata and the spinal cord. Lastly, a number of large, varicose, intensely immunoreactive fibers were found in the olfactory bulb, the cingulum, and the periventricular regions of the hypothalamus and central gray, whereas isolated fibers could be detected in the caudate nucleus and in the cerebral cortex. In animals treated with colchicine, prolactin-immunoreactive perikarya were essentially located within the periventricular and perifornical regions of the hypothalamus, and within the bed nucleus of the stria terminalis. Although corticotropin (ACTH 17-39)-immunoreactive fibers could be detected in several regions found to contain prolactin fibers, the distribution and organization of both fiber types clearly differed in numerous brain regions, and the regions containing the corresponding perikarya did not overlap.(ABSTRACT TRUNCATED AT 250 WORDS)

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↗
PubMed1988

Axons containing a prolactin-like peptide project into the perivascular layer of the median eminence: an immunocytochemical light and electron microscope study in adult and infant rats.

A light and electron microscopic immunocytochemical study was undertaken to explore the fine structural organization of prolactin-immunoreactive axons in the rat median eminence. In adult intact males and females and in hypophysectomized females, light microscopic immunocytochemical labeling of the mediobasal hypothalamus revealed a marked concentration of prolactin-like immunoreactive fibers in the perivascular layer throughout the median eminence and the hypophysial stalk. At the electron microscopic level, immunostaining was associated with typical neurosecretory axons located either in the palisade layer where they displayed numerous contacts with tanycyte processes, or in the perivascular layer where they frequently contacted the perivascular space. Within the labeled axonal profiles, immunostaining was essentially located on secretory granules, 90-120 nm in diameter, whereas the microvesicles accumulated in some perivascular profiles constantly remained unlabeled. These data strongly suggest that most prolactin-immunoreactive axons of the median eminence release their content into the hypophysial portal vessels. In 1-day-old infant rats, intensely prolactin-like immunoreactive fibers were similarly localized in the most external layer of the median eminence, in which, contrary to adult animals, very slight if any tyrosine-hydroxylase-immunoreactive fibers were detected. Since earlier studies have provided evidence for a nondopaminergic prolactin-release-inhibiting factor in the hypothalamus of infant rats, and for an inhibitory effect of prolactin on pituitary mammotrophs, we propose that hypothalamic prolactin may contribute, as an additional prolactin-release-inhibiting factor, to the multifactorial control of pituitary mammotrophs.

Aging↗
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

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↗