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M L Aléssio

Publications and source records attributed to M L Aléssio.

4 recordsLinked to original sources

Effect of essential fatty acid deficiency on membrane fatty acid content and growth hormone stimulation of rat pituitaries during postnatal development.

Fatty acid composition of anterior pituitary cell membranes of rats deprived of essential fatty acids (EFA) and of rats receiving a standard diet was determined during postnatal development and in adults. Pregnant rats were fed an EFA-deficient diet and the offspring were fed the same diet after weaning. In parallel, effects of the diet on growth and on growth hormone (GH) responsiveness to GHRH stimulation were determined in control animals. Membrane content of arachidonic acid (20:4n-6) and of its elongation product adrenic acid (22:4n-6) increased regularly from day 2 to day 12 after birth. EFA-deficiency resulted on day 2 in increased oleic acid and in substitution of arachidonic and adrenic acids by corresponding elongation-desaturation products of oleic acid: eicosatrienoic (20:3n-9) and docosatrienoic (22:3n-9) acids. At the age of 24 days, n-9 series fatty acid reached the same level as in adult animals. Two-day-old EFA-deficient rats paradoxically exhibited a higher level of 20:4n-6 as compared to control rats. EFA-deficiency also decreased growth rate and GH pituitary responses to GHRH during the prepubertal period. These results suggest that changes in the lipid structure and in pituitary secretion properties elicited by EFA-deficiency depend upon the stage of development.

Animals↗

Selective effect of a diet-induced decrease in the arachidonic acid membrane-phospholipid content on in vitro phospholipase C and adenylate cyclase-mediated pituitary response to angiotensin II.

Young rats were fed on an essential fatty acid (EFA)-deprived diet for 6 weeks after weaning. Their pituitary was removed and adenohypophyseal cells dispersed and maintained in culture. Membrane lipids were analyzed and basal and stimulated levels of hormone secretion were measured after 4-day incubation in a culture medium containing or not 160 microM arachidonic acid 20:4n-6 (AA) in order to obtain EFA-deficient or EFA-restored pituitary cells, respectively. In EFA-deficient cells membrane phosphoglycerides (PGL) were depleted in AA and adrenic acid 22:4n-6; the deficit was overcome by incubation in the presence of AA. Depletion diversely affected PGL classes. AA was highly depleted in choline phosphoglycerides (ChoPG), only moderately depleted in serine and ethanolamine phosphoglycerides (SerPG and EtnPG) and not depleted at all in inositol phosphoglycerides, suggesting preferential preservation of AA in that class of PGL. Restoration of AA by addition of the fatty acid to the culture medium was complete for ChoPG and EtnPG and only partial for SerPG. Depressed levels of AA and adrenic acid in PGL were compensated for by a concomitant increase in 20:3n-9 and 22:3n-9. Growth hormone and prolactin (PRL) secretion was assessed by radioimmunoassay and possible effects of a membrane AA deficit on hormone regulation were tested in cells challenged by either growth hormone-releasing hormone, thyrotropin-releasing hormone, angiotensin II (AII), vasoactive intestinal peptide (VIP) or dopamine. Neither basal nor stimulated growth hormone secretion was different from controls in EFA-deficient cells. PRL modulation by VIP or dopamine was not affected either in EFA-deficient cells. In contrast, the capacity of AII, but not of thyrotropin-releasing hormone, to release PRL was markedly decreased in EFA-deprived cells. It was restored by addition of AA to the incubation medium. Parallel depression of AII-induced inositol phosphates and cAMP accumulation was also observed after EFA deficiency. When tested on membranes, the paradoxical inhibition of adenylate cyclase by AII documented by previous observations was reinforced in EFA-deficient membranes. In contrast, binding of AII was not affected by EFA deficiency. It is concluded that under our experimental conditions EFA deficiency affects selectively coupling of the AII receptor to its effectors without alteration of binding. The effect could involve changes in receptor interactions with coupling proteins.

Adenylyl Cyclases↗

Distribution of motoneurones innervating extraocular muscles in the brain of the marmoset (Callithrix jacchus).

Extraocular muscle motoneurones were localised in the oculomotor nucleus (ON), trochlear nucleus (TN) and abducens nucleus (AN) in the marmoset brain using the horseradish peroxidase (HRP) retrograde labelling technique. HRP pellets injected into individual extraocular muscles revealed one or more groups of labelled neurones occupying discrete loci within these nuclei. Relatively little overlap of motoneurone pools was observed, except in the case of the inferior oblique and superior rectus muscles. Injections of HRP into the medial rectus muscle revealed three separate populations of labelled cells in the ipsilateral ON. Motoneurones innervating the inferior rectus muscle were mainly localised in the lateral somatic cell column of the ipsilateral ON. A second smaller grouping was observed in the medial longitudinal fasciculus. The inferior oblique muscle motoneurones were localised in the ipsilateral medial somatic cell column intermingled with motoneurones supplying the superior rectus muscle of the opposite eye. The superior oblique muscle motoneurones occupied the entire TN and the lateral rectus muscle motoneurones the AN. It was concluded that the organisation of nuclei and subnuclei responsible for controlling the extraocular muscles in the marmoset is broadly similar to that of other primates.

Abducens Nerve↗

Distribution of parasympathetic motoneurones in the oculomotor complex innervating the ciliary ganglion in the marmoset (Callithrix jacchus).

Parasympathetic motoneurones in the oculomotor complex which innervate the ciliary ganglion were identified using the horseradish peroxidase (HRP) retrograde axonal tracer technique. The ciliary ganglion was located behind the eye by a lateral orbital approach and injected with HRP pellets mounted on the tips of microelectrodes. Most of the labelled cells were distributed throughout the whole Edinger-Westphal nucleus (EW). Outside the EW, only a small number of labelled cells were found, and most of these were located in the median zone ventral to the EW. There was no evidence of a division of the EW into rostral and posterior subnuclei, nor for separate cell populations in the EW and the anterior median nucleus (AM), respectively. At rostral levels labelled cells were confined to the EW with no overlap into the AM. In contrast to most previous studies no labelled cells were found in the AM. The possible physiological functions of the EW and the ventral components of the EW are discussed.

Animals↗