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H Vaudry

Publications and source records attributed to H Vaudry.

At least 307 records · Page 17Linked to original sources
PubMed1993

Analysis of inositol phosphate metabolism in melanotrope cells of Xenopus laevis in relation to background adaptation.

The present study examined inositol phosphate metabolism in melanotrope cells of Xenopus laevis to determine if inositol phosphates are involved in regulating the biosynthetic or secretory activity of these cells. No correlation could be found between inositol phosphate metabolism and the secretory activity of the melanotrope cells. Therefore, we conclude that inositol phosphate production is not directly involved in the regulation of release of alpha-MSH from these cells. However, there were dramatic differences in the capacity of the melanotrope cells to produce inositol phosphates dependent on the state of background adaptation of the animals from which the melanotropes were derived; cells from white-adapted animals had a low capacity to produce inositol phosphates, whereas melanotropes from black-adapted animals had a high capacity in this regard. During adaptation of animals from a white to a black background, the capacity of the melanotrope cells to produce inositol phosphates was only very slowly acquired, reminiscent of the slow acquisition displayed by these cells to produce POMC during background adaptations. Likewise, during black to white background adaptation, the melanotrope cells very slowly lost the capacity to phosphorylate inositol, which correlates with the slow loss of the biosynthetic capacity of melanotrope cells during such adaptations. Altogether we conclude that inositol phospholipid metabolism is likely involved in the regulation of the biosynthetic processes of melanotrope cells of Xenopus laevis.

Acclimatization↗
PubMed1993

Quantitative autoradiography of somatostatin receptors in the rat limbic system.

The distribution of somatostatin receptors (SRIF-R) was analyzed in the limbic system of the adult rat by in vitro autoradiography with [125I-Tyr0,DTrp 8]S14 as a radioligand. Precise quantification of the density of binding sites, at 0.2 mm intervals throughout the different areas revealed a marked heterogeneity of labeling in most structures. In particular, SRIF-R were concentrated in the basal (104.4 +/- 3.3 fmol/mg proteins) and basolateral amygdaloid nuclei (94.8 +/- 4.3 fmol/mg proteins), and in the nucleus of the lateral olfactory tract (121.6 +/- 2.4 fmol/mg proteins), whereas moderate densities were detected in the amygdalo-hippocampal nucleus (76.4 +/- 2.8 fmol/mg proteins). The medial (41.3 +/- 1.9 fmol/mg proteins) and the central (24.0 +/- 1.4 fmol/mg proteins) amygdaloid nuclei contained lower SRIF-R concentrations. It appears from these observations, in the light of the anatomical pathways of the amygdala, that intra-amygdalian SRIF-containing neurons project to the amygdalo-hippocampal nucleus, and that SRIF-R in the basolateral complex are the target of afferents from limbic cortical areas. SRIF-R were detected at different levels of the hippocampal formation but their distribution was more restricted than that of SRIF-containing fibers. The maximal density of sites was detected in the ventral and dorsal parts of the subiculum (115.0 +/- 3.4 and 87.0 +/- 2.8 fmol/mg proteins, respectively) and in the parasubiculum (100.1 +/- 5.4 fmol/mg proteins). In Ammon's horn, the stratum oriens and stratum radiatum of the CA1 field were the only sites enriched in SRIF-R (74.1 +/- 2.0 and 74.6 +/- 1.9 fmol/mg proteins, respectively). The apparent lack of receptors in the pyramidal cell layer indicated that, in Ammon's horn, SRIF is involved in intra-hippocampal communication. Low levels of receptors were found in the hippocampal CA2 and CA3 fields. SRIF-R in the dentate gyrus were mainly concentrated in the molecular layer (57.3 +/- 1.2 fmol/mg proteins). A very high density of sites was also observed in the entorhinal cortex (up to 123.1 +/- 1.5 fmol/mg proteins). A clear mismatch between SRIF and SRIF-R was detected in the septum and the habenula. In the profound layers of the cingulum and retrosplenial cortex, a heterogeneous distribution of SRIF-R was observed. High concentrations of sites were detected in the rostral zone of the cingulate cortex (93.4 +/- 2.0 fmol/mg proteins) while the posterior cingulate only exhibited moderate concentrations of sites (66.5 +/- 0.7 fmol/mg proteins).(ABSTRACT TRUNCATED AT 400 WORDS)

Amygdala↗
PubMed1993

Effects of central and peripheral administration of arginine vasotocin and related neuropeptides on blood pressure and heart rate in the conscious trout.

The cardiovascular activity of neurohypophyseal peptides has been investigated in conscious trout bearing an intracerebroventricular guide cannula and a permanent intraarterial catheter. Changes in diastolic pressure, systolic pressure and heart rate were monitored during the 25-min period following intracerebroventricular or intraarterial administration of arginine vasotocin and related neuropeptides, including arginine vasopressin, oxytocin, hydrin-2, mesotocin, isotocin and conopressin-S. Intracerebroventricular injection of increasing doses of arginine vasotocin (0.62-5 pmol) induced a dose-dependent increase of diastolic and systolic pressures. The onset of the response occurred within 3-5 min after intracerebroventricular administration of arginine vasotocin and the maximal increase was reached at 10-15 min. Central administration of vasopressin and oxytocin induced a significant rise in diastolic and systolic pressures at a dose of 5 pmol while hydrin-2 only caused a significant elevation of blood pressure at a dose of 50 pmol. Central administration of mesotocin, isotocin and conopressin-S (5-500 pmol each) had no significant effect on blood pressure. No changes in heart rate occurred after intracerebroventricular injection of any of the seven neuropeptides tested. Intraarterial injection of arginine vasotocin (50 pmol) induced a significant rise in blood pressure and bradycardia. Peripheral injection of the other neuropeptides did not cause any modification of the cardiovascular activity, whatever the doses administered (5-500 pmol). The V1A receptor antagonist [d(CH2)5, Tyr(OMe)2]arginine vasopressin had no intrinsic effect on blood pressure and heart rate when injected centrally (50 pmol) or in the peripheral circulation (200 pmol). At the same doses, [d(CH2)5, Tyr(OMe)2]arginine vasopressin reduced by 50 and 66%, respectively, the increase in blood pressure evoked by intracerebroventricular (5 pmol) or intraarterial (50 pmol) injections of arginine vasotocin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Short- and long-term effects of nucleus basalis magnocellularis lesions on cortical levels of somatostatin and its receptors in the rat.

Cognitive and histological alterations in human Alzheimer's disease (AD) are correlated with selective neuronal loss in nucleus basalis of Meynert. In search of an animal model of AD-linked neurochemical deficits, we examined the effects of short- (2 weeks) and long- (3 and 6 months) term lesions of the nucleus basalis magnocellularis (NBM) on somatostatinergic parameters in rat forebrain. NBM lesions were performed by unilateral injection of ibotenic acid into the NBM. Cortical choline-acetyl transferase (ChAT) activity and acetylcholinesterase staining in the NBM remained significantly decreased ipsi- as compared to contralaterally up to 6 months after the placement of the lesion. Somatostatin (SRIF) content was increased by 120% in the ipsilateral frontal cortex 6 months post-lesion but not at shorter time intervals. Levels of neuropeptide Y (which is extensively co-localized with SRIF in the forebrain) were not significantly altered after unilateral NBM lesions at any time point. A 30% decrease in SRIF binding capacity as well as a marked reduction of SRIF inhibition of adenylate cyclase, indicative of a loss of functional SRIF receptors, was observed in ipsilateral versus contralateral frontal cortex on brain tissue homogenates after short-term unilateral NBM lesion. By film radioautography, the loss in SRIF binding sites was localized to both superficial and deep layers of the frontal cortex. This loss persisted up to 3 months but was no longer apparent after 6 months due to a decrease in SRIF binding capacity on the contralateral side.

Adenylyl Cyclase Inhibitors↗