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Volume 35 / No. 3 / 2001
Francesca Fernandez, Marlene Durand, Valerie Coomans, Pierre Mormede, Francis Chaouloff
NeuroGenetics & Stress, INSERM U471-INRA, 33077 Bordeaux Cιdex, France
E-mail: francis.chaouloff@bordeaux.inserm.fr
Objective. There is evidence for a regulatory impact of corticoids
on hippocampal serotonergic systems, including serotonin (5-HT) synthesis and
5-HT1A receptor expression and/or activity. On the other hand,
contradictory data have emerged as to the regulation of the 5-HT transporter by
corticoids. Using male Spontaneously Hypertensive Rats (SHRs) and Wistar-Kyoto
(WKY) rats, we have analysed whether subchronic corticosterone alters in a strain-dependent
manner the reuptake activity of the hippocampal 5-HT transporter.
Methods. Two separate experiments were performed. In the first
experiments, we assessed the impact of corticosterone ingestion (400 ΅g/ml in
drinking water for 7 days) on hippocampal reuptake of increasing concentrations
of [3H]5-HT (6.25-100 nM). In the second series of experiments, we
measured whether such a corticosterone regimen affected the potency of the
antidepressant citalopram to block the reuptake of 10 nM of [3H]5-HT.
Results. Corticosterone administration, which markedly reduced body
weight gains and adrenal weights in both strains, increased Km and Vmax values
in SHRs but decreased these values in WKY rats, compared to vehicle (2.4 %
ethanol) administration. In addition, it was observed that neither the basal
reuptake of 10 nM [3H]5-HT nor the potency of citalopram to block
selectively such a reuptake (IC50 = 2.88-3.63 nM) differred
between vehicle- and corticosterone-treated animals.
Conclusion. Under our experimental conditions, both the reuptake of a physiological
concentration of 5-HT and the potency of an antidepressant to inhibit such a reuptake
proved insensitive to repeated corticosterone administration.
Key words: Corticosterone [3H]Serotonin reuptake
Hippocampus Citalopram Wistar Kyoto Rats Spontaneously Hypertensive
Rats
ENDOCRINE REGULATIONS, Vol. 35, 119126, 2001
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Angelina I. Russinova, Christina A. Valkova, Roumiana T. Denkova
Institute of Experimental Morphology and Anthropology, Department of Cell
Differentiation, Bulgarian Acadamy of Sciences and
Institute of Molecular Biology, Department of Cell Biology, Bulgarian Academy of
Sciences, 1113 Sofia, Bulgaria
Objective. In the present study we employed a monoclonal antibody
(Mab 3D8) obtained against a rat ovarian antigen and indentified a 76
kDa protein in porcine ovarian follicles.
Methods. The localization of this antigen was studied by light and
electron-microscopic immunocytochemistry and further characterized by
polyacrylamide gel elctrophoresis and immunoblotting on nitrocellulose
membranes.
Results. We found that the antigen recognized by Mab 3D8 is localized in
granulosa cells (GCs) and oocytes. The expression of the 76 kDa protein
apparently depends on the developmental stage. A particularly strong
reaction was observed in cumulus cells and oocytes in early and late antral
follicles. In granulosa cells the reaction product was localized in rough
endoplasmic reticulum (RER), cis and trans faces of the Golgi stack, the outer
nuclear envelope and in numerous transport vesicles budding from the endoplasmic
reticulum. In the oocyte the reaction product was localized in structures
related to specific endocytosis small pits at the cell surface, two subsets
of endosomes, endocytic carrier vesicles and the prelysosomal compartment (PLC).
Conclusions. The results obtained suggest that porcine oocytes possess
the cellular structures which allow them to bind and internalize this protein,
which is most probably produced by granulosa cells. During oocyte development
the intracellular site of accumulation of the 76 kDa protein varies, which
implies that it is under developmental control.
Key words: Monoclonal antibody Immunocytochemistry Endocytosis-
Porcine ovarian follicle
ENDOCRINE REGULATIONS, Vol. 35, 127137, 2001
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Marek Pawlikowski, Anna Gruszka, Slavomir Mucha, Gabriela Melen-Mucha
Department of Experimental Endocrinology and Hormone Diagnostics and
Department of Clinical Endocrinology, Institute of Endocrinology, Medical
University of Lodz, 91425 Lodz, Poland
E-mail: m.pawlikowski@mail.e.pl
Objective. The effects of angiotensins II (AngII) and IV (Ang IV,3-8
fragment of angiotensin II) on the adrenocortical cell proliferation have been
investigated in the rat.
Methods. The male adult Wistar rats were injected subcutaneously with saline,
captopril or captopril together with either Ang II or Ang IV. A part of animals
received additionally losartan an antagonist of AT1 subtype of angiotensin
receptors. Bromodeoxyuridine (BrDU) incorporation into cell nuclei was used as
the index of cell proliferation.
Results. It was found that both Ang II and Ang IV increased the BrDU
labeling in the adrenal cortex of captopril-pretreated rats. This effect
involved mainly the zona glomerulosa cells.The proliferogenic effect of Ang II
was blocked by AT1 receptor antagonist losartan. In contrast, losartan did not
block the effect of Ang IV.
Conclusion. Both Ang II and Ang IV stimulate the adrenocortical cell
proliferation in the rat, but they act via different receptors AT1 in the
case of Ang II and non-AT1 (probably AT4) in the case of Ang IV.
Key words: Adrenal cortex Cell proliferation Angiotensin II
Angiotensin IV
ENDOCRINE REGULATIONS, Vol. 35, 139142, 2001
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Josef Thalhamer, Wolfgang Leitner, Peter Hammerl, Julius Brtko
Immunology Group, Institute of Chemistry and Biochemistry, University of
Salzburg, Austria,
Surgery Branch, National Cancer Institute, NIH, Bethesda MD 20892, USA
Institute of Experimental Endocrinology, Slovak Academy of Sciences, Bratislava,
Slovak Republic
Email: Josef.Thalhamer@sbg.ac.at
Genetic immunization or DNA vaccination represents a rapidly developing
technology with new perspectives for the prevention and therapy of infectious
diseases and it offers new approaches for the treatment of autoimmunity, tumors
and even allergy. DNA vaccines are comprised of plasmid DNA which encodes
antigen molecules directly in the transfected cells of a target organism.
In contrast to protein-induced immune responses, DNA vaccines stimulate both
humoral and cell-mediated immune reactions.
In the present review we present a palette of unique features of genetic
immunization like the effect of CpG motifs, the influence of mode and site of
gene delivery and the modulation of immune responses by co-delivery of
cytokines, colony stimulating factors, adhesion molecules and other stimulatory
molecules. In addition, modulation of the immune response via translation,
processing and presentation will be discussed, which in sum demonstrate the
elegant possibilities of genetic immunization to induce tailor-made immune
responses.
ENDOCRINE REGULATIONS, Vol. 35, 143166, 2001
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Magdalena Matejkova-Behanova
Institute of Endocrinology, 116 94 Prague, Czech Republic
E-mail: mbehanova@endo.cz
Latent autoimmune diabetes in adults (LADA) is characterised by clinical
presentation as type 2 diabetes after 25 years of age, initial control achieved
with diet or oral hypoglycaemic agents during at least 6 months, presence of
autoantibodies (first of all GADA) and some immunogenetic features of diabetes
mellitus type 1. In patients with an autoimmune endocrine disease, which could
be also autoimmune diabetes, there is a high risk of development of another
autoimmune endocrine disorder. The coexistence of two or more autoimmune
endocrine diseases is pathognomonic for autoimmune polyglandular syndrome.
Autoimmune thyroiditis and type 1 diabetes mellitus are the most common
combination of autoimmune endocrine diseases reported. Most studies reported the
prevalence of autoimmune thyroiditis in typical type 1 adult diabetic
subjects about 20 40%. Little is known about the prevalence of autoimmune
thyroiditis in subjects with LADA. Only a few studies confirmed a high
prevalence of thyroid autoantibodies in type 2 diabetic subjects with GADA
compared to type 2 diabetic subjects without GADA and compared to non-diabetic
population too.
Key words: Diabetes mellitus type 1 LADA Autoimmune thyroiditis
Autoimmune polyglandular syndrome
ENDOCRINE REGULATIONS, Vol. 35, 167172, 2001
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