Biomedical subjects

M Balmefrézol

Publications and source records attributed to M Balmefrézol.

4 recordsLinked to original sources

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↗

PubMed1986

Immunocytochemical evidence for stimulatory control by the ventral noradrenergic bundle of parvocellular neurons of the paraventricular nucleus secreting corticotropin releasing hormone and vasopressin in rats.

The regulation, by catecholaminergic innervation, of parvocellular neurons of the paraventricular nuclei (PVN) secreting corticotropin releasing hormone (CRH) and vasopressin (Vp) was studied by immunocytochemical visualization of both neurohormones in control rats and in rats given discrete injections of 6-hydroxydopamine in the ventral noradrenergic ascending bundle (VNAB). In both groups, the changes in immunostaining intensities observed in axon terminals of the external median eminence and in PVN perikarya 48 h after a blockade of axoplasmic transport by intraventricular injections of colchicine, served as an index for hormonal release and synthesis. In controls, this treatment induced a strong decrease in CRH and Vp immunoreactivity within the terminals, together with intense labeling of PVN perikarya containing CRH. By contrast, bilateral VNAB lesions strikingly inhibited both the colchicine-induced reduction of the CRH and Vp immunoreactivity in axons and the accumulation of CRH in the perikarya. Unilateral VNAB lesions induced similar alterations but these were restricted to the ipsilateral PVN and median eminence. Comparison of these immunocytochemical data with earlier physiological observations on the effects of VNAB lesions on ACTH secretion indicates that the catecholaminergic afferents to the PVN conveyed by the VNAB stimulate the release and the synthesis of CRH and Vp by parvocellular neurons projecting into the external median eminence.

Afferent Pathways↗

PubMed1975

Diaminobenzidine reactivity of mitochondria and peroxisomes in Tetrahymena and in wild-type and cytochrome oxidase-deficient Paramecium.

Reactivity of mitochondria and peroxisomes to diaminobenzidine was investigated in Tetrahymena pyriformis and in wild-type and cytochrome oxidase-deficient Paramecium aurelia. Wild-type and cytochrome oxidase-deficient Paramecium gave positive mitochondrial reactions in the absence of added H2O2, and the deposits were enhanced by the addition of H2O2, whereas Tetrahymena gave positive mitochondrial reactions only upon addition of H2O2. These results are discussed in the light of the current ideas concerning the mechanism of staining by diaminobenzidine. Peroxisome-like organelles which react positively to diaminobenzidine, the reaction being partially inhibited by aminotriazole, were identified in both protozoa.

3,3'-Diaminobenzidine↗

PubMed1972

The effects of erythromycin and chloramphenicol on the ultrastructure of mitochondria in sensitive and resistant strains of Paramecium.

The effects on cell structure of 12 hr to 6 days of exposure to erythromycin or chloramphenicol, two antibiotics known to inhibit specifically the mitochondrial protein synthesizing system, have been studied in the ciliate Paramecium aurelia. A wild type strain (sensitive to both antibiotics) and three mutant strains carrying cytoplasmically inherited mutations conferring resistance to one or the other antibiotic have been used In sensitive cells both antibiotics lead to a progressive and profound alteration of mitochondrial structure evidenced by an elongation of the organelle, a considerable decrease in the number of cristae, and the appearance of some abnormal lamellar cristae and of rigid plates of periodic structure. The modifications of cell structure, then, are mainly restricted to mitochondrial cristae. The three resistant mutants studied, on the contrary, retain normal or nearly normal mitochondrial structure in the presence of the antibiotic to which they are resistant. This fact is in good agreement with the postulated location in the mitochondrial DNA of the resistance mutations studied. The results are discussed in the light of present knowledge concerning the function of the mitochondrial protein-synthesizing system.

Animals↗