mohammed benyamina
Publications et Ouvrages : mohammed benyamina
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The distribution of a-melanocyte-stimulating hormone (a-MSH) in the central nervous system of the frogRana ridibunda was determined by immunofluorescence using a highly specific antiserum, a-MSH-like containing perikarya were localized in the infundibular region, mainly in the ventral hypothalamic nucleus. A rich plexus of immunoreaetive fibers directed towards the ventral telencephalic region was detected.
Reverse-phase high-performance liquid chromatography and radioimmunoassay were used to characterizea-MSH-like peptides in the frog brain. Chromatographic separation revealed that immunoreaetive a-MSH coeluted with synthetic des-Na-acetyl a-MSH, authentic a-MSH and their sulfoxide derivatives. The heterogeneity of a-MSH-like material in the frog brain was in marked contrast with the figure observed in the intermediate lobe of the pituitary gland where only des-Na-acetyl a-MSH ispresent. These findings support the existence of discrete a-MSH immunoreactive neurons in the frog brain containing both desacetyl and authentic a-MSH.
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The effect of cholinergic agonists on glucocorticoid
and mineralocorticoid production by frog interrenal
(adrenal) tissue was studied in vitro by means of
continuous perifusion. Acetylcholine, at doses ranging
from 1 to 100 \g=m\mol/l,stimulated both corticosterone
and aldosterone output in a dose-dependent manner,
with a half-maximal effective dose of 2\m=.\5 \g=m\mol/l.
Corticosteroid production was also stimulated by
muscarine (10 \g=m\mol/l).In contrast, neither nicotine
nor nicotine bitartrate (1\p=n-\100 \g=m\mol/l)enhanced corticosteroid
biosynthesis. The kinetics of the response of
adrenal cells to acetylcholine and muscarine were
similar to those observed during angiotensin II stimulation.
In particular, a significant reduction (20\p=n-\40%)
in the spontaneous level of corticosteroid production
was recorded after the initial infusion of muscarinic
agents, but no further decrease in the basal level
occurred after a second cholinergic administration.
The effect of acetylcholine was blocked by the
muscarinic receptor antagonist atropine (10 \g=m\mol/l).
These results indicate that acetylcholine can stimulate
frog adrenocortical cells through muscarinic receptors.
Repeated 20-min pulses of acetylcholine (50 \g=m\mol/l)or
muscarine (10 \g=m\mol/l),given at one pulse per 130 min,
resulted in a marked reduction in the secretory response
to the second pulse. No reduction in the stimulatory
effect of acetylcholine or muscarine was observed when
a 6\m=.\5-h interval separated two 20-min infusions of the
secretagogue. In contrast with these findings, iterative
pulses of the muscarinic agonist pilocarpine (in the
range 1\p=n-\100 \g=m\mol/l)did not cause any desensitization.
These data show that the neurotransmitter acetylcholine
can modulate frog adrenocortical function
and suggest that, in addition to more conventional
regulators, i.e. ACTH and angiotensin II, the
cholinergic endings of the splanchnic nerve might
participate in the regulation ofcorticosteroid secretion,
at least under so
[ Modifié: dimanche 24 janvier 2021, 21:11 ]