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Biomedical subjects

G Anglade

Publications and source records attributed to G Anglade.

13 recordsLinked to original sources
PubMed1999

Olfactory bulbectomy increases vasopressin, but not corticotropin-releasing hormone, content in the external layer of the median eminence of male rats.

Removal of the olfactory bulbs results in numerous physiological and behavioral changes in rats. The most frequent and characteristic change is an abnormally high level of corticosterone in the blood, possibly due to changes in the activity of the hypothalamic neurons which synthesize corticotrophin-releasing hormone (CRH). Some of these neurons also synthesize vasopressin (AVP). They are located in the parvocellular part of the paraventricular nucleus of the hypothalamus, which projects into the external layer of the median eminence. We investigated whether there was such a change in activity by studying the synthesis and storage activity of CRH neurons in bulbectomized rats. CRH and AVP axon terminals in frozen sections of the external layer of the median eminence were labeled by immunofluorescence techniques and the degree of labeling was analyzed semi quantitatively. There was no difference in the area or intensity of CRH-labeling in control and bulbectomized rats. However, a significantly larger area was stained for AVP in the bulbectomized than in control rats. We also used in situ hybridization, with single- and double-labeling, to study the effects of bulbectomy on expression of the genes encoding CRH and AVP. No significant difference was found in the levels of mRNA for CRH and the number of CRH+/AVP+ cell bodies was similar in the parvocellular part of the paraventricular nucleus in bulbectomized and normal rats. Our results suggest that the hypothalamo-pituitary-adrenal (HPA) axis changes observed after olfactory bulbectomy may be due to plastic changes in hypothalamic CRH neurons, resulting in greater storage of increased AVP in CRH neurosecretory nerve terminals in the external layer of the median eminence.

Adrenal Glands↗
PubMed1999

An investigation of serotonergic involvement in the regulation of ACTH and corticosterone in the olfactory bulbectomized rat.

The bilateral olfactory bulbectomy resulted in significantly higher plasma concentration of corticosterone, but not of ACTH in basal conditions and much higher plasma ACTH and corticosterone concentrations after 15 min of immobilization stress than were observed in sham-operated animals. Daily treatment with fluoxetine-a specific serotonin reuptake inhibitor-(15 mg/kg/day) had no effect on basal ACTH and corticosterone concentrations in OB rats. Fluoxetine treatment caused lower levels of ACTH, but not of corticosterone secretion, in response to immobilization stress. Bulbectomy significantly reducing 5-HT concentration in the amygdala. Stress increased serotonergic activity in the hypothalamus but not in the amygdala of OB rats. Chronic fluoxetine treatment of both unstressed and stressed OB rats resulted in a lower turnover rate in the two structures. Our results suggest that the hypercorticosteronemia observed after bulbectomy in unstressed OB rats is independent of the serotonergic system in both hypothalamus and amygdala. In contrast, they also demonstrate hypothalamic 5-HT changes in the HPA hyperactivity of OB rats in response to stress. Chronic fluoxetine treatment may normalize pituitary ACTH secretion in response to stress, possibly desensitization of the 5-HT receptors in the hypothalamus due to 5-HT being move available at the synapses.

Adrenocorticotropic Hormone↗
PubMed1999

Effects of bilateral olfactory bulbectomy on the anterior pituitary corticotropic cell activity in male rats.

Bilateral olfactory bulbectomy (OB) has drastic biochemical and behavioral effects and is often associated with an increase in plasma corticosterone concentrations. This experiment examined the effects of OB on adrenocorticotropin (ACTH) and corticosterone release under basal and stress conditions and on proopiomelanocortin (POMC) gene expression. Bulbectomy potentiated hypophysal ACTH and adrenal corticosterone release induced by ether stress but had no effect on ACTH release under basal conditions, despite a significant increase of circulating corticosterone. POMC gene expression was stronger (+60%) in OB rats than in sham-operated rats. These results suggest that olfactory bulbectomy substantially altered the negative feed-back exerted by glucocorticoids on anterior pituitary corticotropic cells in the male rat.

Adrenocorticotropic Hormone↗
PubMed1997

Effects of bilateral olfactory bulbectomy on circadian rhythms of ACTH, corticosterone, motor activity and body temperature in male rats.

Bilateral olfactory bulbectomy (BOX) has major biochemical and behavioral effects, and is one of the most widely investigated of animal models of depression. We studied the consequences of BOX in male rats, on the organization of endogenous circadian rhythms for ACTH, corticosterone (Cort), motor activity (MA) and body temperature (BT). Mean levels were increased for Cort and MA, whereas no significant changes were observed for ACTH and BT. Significantly higher plasma Cort morning values were evidenced in BOX than sham-operated animals. In addition, compared with the single prominent power spectrum for the 24 hours period of control rats, the BOX animals displayed substantially lower 24 hours spectral power for the MA and BT circadian rhythms. These alterations suggest that olfactory bulbectomy, by disruption of the afferences and efferences, induced drastic changes in the function of the endogenous clock or of its regulating systems. From this point of view, bulbectomized rats may therefore be a valuable model to studying the etiology of psychiatric disorders with rhythm disturbance.

Adrenocorticotropic Hormone↗
PubMed1995

[Regulation of corticotropic function in stressful situations].

ACTH secretion is mainly controlled by two hypothalamic neurohormones: corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP). Both peptides are synthesized in the hypothalamic paraventricular nucleus (PVN) (in parvo-cellular neurons for CRH and in magnocellular neurons for most AVP). Under basal conditions, some CRH neurons coexpress AVP (CRH+/AVP+ neurons). This colocalisation represents a form of functional plasticity since the number of CRH+/AVP+ neurons increases after acute or repeated stress exposure. Experiments in sheep and rat (studies on the secretion of both peptides in hypophysial portal blood, effects of anti-CRH and anti-AVP immunisation upon ACTH secretion) indicate that stress-induced ACTH stimulation involves both CRH and AVP. Unlike CRH which participates also in the maintenance of basal ACTH and glucocorticoids secretion, the role of AVP appears to be limited to corticotropic response to stress.

Adrenocorticotropic Hormone↗
PubMed1994

Blockade of alpha 2-adrenoceptors stimulates basal and stress-induced adrenocorticotropin secretion in the developing rat through a central mechanism independent from corticotropin-releasing factor and arginine vasopressin.

In the neonatal rat, the response of the hypothalamo-pituitary-adrenal axis to stressful stimuli is markedly reduced during the first 2 weeks of life [stress-hyporesponsive period (SHRP)]. In this report, we studied the effect of idazoxan (an alpha 2-adrenergic antagonist) on plasma ACTH and corticosterone levels in 8-day-old rats. Indeed, it is known that in the adult rat, blockade of alpha 2-adrenoceptors increases ACTH secretion stimulated by CRF and arginine vasopressin (AVP) injection. Injection of 2.5 micrograms/g idazoxan induced a rapid (within 30 min) increase in basal plasma ACTH and corticosterone levels that lasted for 60 min. Injection of increasing doses of idazoxan led to a dose-dependent stimulation of ACTH and corticosterone levels. Administration of 2.5 micrograms/g idazoxan significantly increased the ACTH response to insulin-induced hypoglycemia, whereas it potentiated and accelerated the ACTH response to ether exposure stress. We next examined ACTH secretion from superfused anterior pituitary glands. Neither the alpha 2-adrenergic agonist clonidine nor idazoxan changed the basal ACTH secretory rate. Idazoxan had no effect on CRF- and AVP-stimulated ACTH secretion. This indicates that in vivo, idazoxan acts at a suprapituitary level. To investigate a possible effect of idazoxan on presynaptic alpha 2-adrenoceptors, we studied the effect of idazoxan on the concentrations of norepinephrine (NE) and L-DOPA in punches of locus coeruleus after dopa-decarboxylase blockade. Idazoxan injection induced a decrease in the NE content, without changing L-DOPA levels, indicating that idazoxan can act at the level of presynaptic alpha 2-adrenoceptors, inducing an increased release and/or degradation of NE without any effect on catecholamines synthesis. Finally, we investigated a possible involvement of CRF and AVP in mediating the effect of alpha 2-adrenoceptor blockade on ACTH secretion. Passive immunization against CRF or AVP did not change the ACTH response to idazoxan administration, whereas idazoxan pretreatment had simply an additive effect on CRF- and lysine vasopressin-stimulated ACTH secretion. In conclusion, our data demonstrate that during the SHRP, blockade of alpha 2-adrenoceptors induces an increase in both basal and stress-induced ACTH secretion. They suggest that a decreased catecholaminergic tone, consecutive to an increased occupation of alpha 2-adrenoceptors, acting through a central mechanism independent from CRF and AVP may be responsible for the SHRP in the developing rat.

Adrenergic alpha-Antagonists↗
PubMed1994

Insulin-induced hypoglycaemia increases colocalization of corticotrophin-releasing factor and arginine vasopressin mRNAs in the rat hypothalamic paraventricular nucleus.

The regulation of ACTH secretion during stress is a multifactorial process that mainly involves two hypothalamic neurohormones: corticotrophin-releasing factor (CRF) and arginine vasopressin (AVP). In this report we measured, using semiquantitative in situ hybridization, the concentrations of CRF and AVP mRNA in hypophyseotrophic paraventricular parvocellular cell bodies of male rats after an acute (3-h) exposure to insulin-induced hypoglycaemia. Insulin injection (2.5 IU/kg) induced a significant decrease in blood glucose levels and a strong increase in plasma ACTH concentrations. The concentration of CRF mRNA in the paraventricular nucleus (PVN) was significantly increased after insulin-induced hypoglycaemia (150% of control levels), while the number of CRF mRNA-containing cell bodies was not changed. Double-labelling experiments demonstrated that the number of CRF mRNA-containing cell bodies that also contained AVP mRNA was doubled after insulin injection. These data demonstrate that the established increased colocalization of AVP immunoreactivity in nerve terminals immunoreactive for CRF after exposure to stress follows a pretranslational activation of AVP synthesis. Cell-by-cell analysis indicated that the mean CRF hybridization signal was increased in double-labelled cells (about 150% of control levels), suggesting that the increase in CRF gene expression occurs equally in the AVP-synthesizing and in the AVP-deficient CRF mRNA-containing cell bodies. The mean AVP hybridization signal in the double-labelled cells was decreased, suggesting that the amount of AVP mRNA was unchanged in the cell bodies that expressed both CRF and AVP in the basal state and that AVP mRNA levels in the cell bodies recruited after insulin-induced hypoglycaemia were below control values.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed1994

Effect of POMC-derived peptides on corticosterone secretion during the stress hypo-responsive period in rat.

During the stress hyporesponsive period (postnatal days 2-10), the stimulation of corticosterone secretion by ACTH is very low. In our study, we have observed that administration of ACTH during 3 consecutive days is followed by a striking increase in corticosterone response to an acute ACTH test. A comparable potentiation of corticosterone secretion was observed after a similar treatment with Lys gamma 3-MSH. The 3 day-treatment with each peptide induced an increase in adrenal weight. Similar data were obtained with alpha-MSH. However, corticosterone response to ACTH was not significantly altered following the same pattern of alpha-MSH administration.

Adrenal Cortex↗
PubMed1993

Antibodies raised against a peptide corresponding to a Gs alpha domain reveal a vimentin-associated protein.

In an attempt to localize the guanine nucleotide binding protein Gs alpha by immunocytochemistry, we synthetized peptides corresponding to several stretches of residues deduced from the published cDNA sequence of Gs alpha and raised antibodies against them. Among the peptides, one corresponding to residues 367-381 elicited antibodies that immunocytochemically detected, at the optical level, what appeared to be vimentin in several cells and tissues. Studies at the ultrastructural level confirmed this observation and also showed weak staining of some areas of plasma membranes of glial and nerve cells. Analysis by Western blots of rat brain subcellular fractions indicated that: (a) the protein stained by the anti-peptide antibodies was associated with the cytoskeleton; and (b) it was not vimentin but a protein of higher molecular weight, 65 KD. We accordingly suggest that the Gs alpha-derived peptide elicited two types of antibodies, one recognizing Gs alpha in fixed tissues, the other recognizing an epitope located in a vimentin-associated protein. This study emphasizes the caution that is needed when conclusions are drawn on the basis of immunocytochemical studies using antipeptide antibodies.

Amino Acid Sequence↗