Ocular distribution of keratan sulfates during pre- and postnatal development in rabbits.

Twenty-six monoclonal antibodies (MAbs) developed against rabbit corneal proteokeratan sulfate (PKS), were used to evaluate immunohistochemically the ocular distribution of PKS during prenatal and early postnatal development in rabbits. These MAbs were directed against epitopes located in the keratan sulfate (KS) chains of the proteoglycan (SundarRaj et al., 1985). Staining of cryostat sections of the eyes was carried out using an indirect peroxidase-conjugated technique. Only one of the MAbs reacted with the presumptive corneal region at day 13 or 16 of fetal development. By day 20, more MAbs reacted with the corneal stroma. There were distinct differences, however, in the distribution of the epitopes recognized by the various MAbs. A few of them stained only the posterior region of the cornea, whereas others showed a decreasing staining gradient from the posterior to the anterior region. By day 24, all of the MAbs reacted with the corneal stroma, but some reacted also with the limbal region and with the conjunctival stromal matrix. One MAb also reacted with the conjunctival epithelial layer, but only at this stage of development. Conjunctival staining was more intense at day 28 of fetal development and at day 2 postnatally. KS was not detectable in the conjunctiva of adult rabbits with any of the MABs. These results suggest that although KS synthesis starts at very early stages of fetal development, there are progressive changes in its antigenic structure in specific regions of the cornea and conjunctiva during corneal development.

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Molecular and genetic predictors of endothelial dysfunction and impairment of angioand neurogenesis in the perinatal period (a literature review)

Siberian medical review ◽

10.20333/25000136-2021-5-14-23 ◽

2021 ◽

Vol 5 ◽

pp. 14-23

Author(s):

S.B. Berezhanskaya ◽

◽

E.A. Lukyanova ◽

M.K. Abduragimova ◽

◽

...

Keyword(s):

Nervous System ◽

Endothelial Dysfunction ◽

Literature Review ◽

Postnatal Development ◽

Genetic Predisposition ◽

Fetal Development ◽

Perinatal Period ◽

Early Postnatal Development ◽

Genetic Predictors ◽

The Brain

Perinatal pathologies serve as the basis for a great variety of diseases in teenagers and adults including the especially frequent and important diseases of the nervous system which is vulnerable during the period of ante- and early postnatal development, especially against the background of genetic predisposition to it. This leads to development of pathology also manifesting at later stages of life. In this connection, the review presents molecular and genetic predictors of endothelial dysfunction and impairment of angio- and neurogenesis during the perinatal period. The article presents facts related to the influence of endothelial dysfunction as a trigger for pregnancy pathology and fetal-programmed diseases. A discussion regarding the contribution made by the congenital and by the acquired into basic mechanisms of fetal development including the brain and its pathologies

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Ghrelin endocrine cells in the human stomach during prenatal and early postnatal development

Archives of Biological Sciences ◽

10.2298/abs1101021m ◽

2011 ◽

Vol 63 (1) ◽

pp. 21-28 ◽

Cited By ~ 2

Author(s):

Olivera Mitrovic ◽

Mileva Micic ◽

Vera Todorovic ◽

G. Radenkovic ◽

Sanja Vignjevic ◽

...

Keyword(s):

Postnatal Development ◽

Fetal Development ◽

Endocrine Cells ◽

Prenatal Development ◽

Human Stomach ◽

Early Postnatal Development ◽

Early Stages

The aim of this study was to investigate the appearance, localization and density of ghrelin cells in the human stomach during prenatal development. For this purpose the antrum and corpus of embryos, fetuses and infants are stained immunohistochemically by the streptavidin-biotin technique. The presence of P/D1 cells at 11 weeks of fetal development, their highest density during the first detection and higher density in the corpus than in antrum, and their localization in the glandular base of stomach gland, all suggest that ghrelin plays a major role in the early stages of the developing stomach.

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Faculty Opinions recommendation of Early Postnatal Development of Corpus Callosum and Corticospinal White Matter Assessed with Quantitative Tractography.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1091144.544544 ◽

2007 ◽

Author(s):

Robert Greenwood

Keyword(s):

White Matter ◽

Corpus Callosum ◽

Postnatal Development ◽

Early Postnatal Development

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Impact of repeated co-treatment with escitalopram and aripiprazole on the schizophrenia-like behaviors and BDNF mRNA expression in the adult Sprague–Dawley rats exposed to glutathione deficit during early postnatal development of the brain

Pharmacological Reports ◽

10.1007/s43440-021-00318-z ◽

2021 ◽

Author(s):

Marta A. Lech ◽

Kinga Kamińska ◽

Monika Leśkiewicz ◽

Elżbieta Lorenc-Koci ◽

Zofia Rogóż

Keyword(s):

Mrna Expression ◽

Postnatal Development ◽

Repeated Treatment ◽

Sprague Dawley ◽

Biochemical Tests ◽

Bdnf Mrna ◽

Adult Rats ◽

Behavioral Deficits ◽

Glutathione Synthesis ◽

Early Postnatal Development

Abstract Background Preclinical and clinical studies have indicated that impaired endogenous synthesis of glutathione during early postnatal development plays a significant role in the pathophysiology of schizophrenia. Moreover, some studies have suggested that antidepressants are able to increase the activity of atypical antipsychotics which may efficiently improve the treatment of negative and cognitive symptoms of schizophrenia. Methods In the present study, we investigated the influence of repeated co-treatment with escitalopram and aripiprazole on the schizophrenia-like behavior and BDNF mRNA expression in adult rats exposed to glutathione deficit during early postnatal development. Male pups between the postnatal days p5–p16 were treated with the inhibitor of glutathione synthesis, BSO (L-buthionine-(S,R)-sulfoximine) and the dopamine uptake inhibitor, GBR 12,909 alone or in combination. Escitalopram and aripiprazole were given repeatedly for 21 days before the tests. On p90–92 rats were evaluated in the behavioral and biochemical tests. Results BSO given alone and together with GBR 12,909 induced deficits in the studied behavioral tests and decreased the expression of BDNF mRNA. Repeated aripiprazole administration at a higher dose reversed these behavioral deficits. Co-treatment with aripiprazole and an ineffective dose of escitalopram also abolished the behavioral deficits in the studied tests. Conclusion The obtained data indicated that the inhibition of glutathione synthesis in early postnatal development induced long-term deficits corresponding to schizophrenia-like behavior and decreased the BDNF mRNA expression in adult rats, and these behavioral deficits were reversed by repeated treatment with a higher dose of aripiprazole and also by co-treatment with aripiprazole and ineffective dose of escitalopram.

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Glutathione Deficiency during Early Postnatal Development Causes Schizophrenia-Like Symptoms and a Reduction in BDNF Levels in the Cortex and Hippocampus of Adult Sprague–Dawley Rats

International Journal of Molecular Sciences ◽

10.3390/ijms22126171 ◽

2021 ◽

Vol 22 (12) ◽

pp. 6171

Author(s):

Marta Anna Lech ◽

Monika Leśkiewicz ◽

Kinga Kamińska ◽

Zofia Rogóż ◽

Elżbieta Lorenc-Koci

Keyword(s):

Postnatal Development ◽

Time Course ◽

Postnatal Life ◽

Positive Symptoms ◽

Gbr 12909 ◽

Sprague Dawley ◽

Bdnf Mrna ◽

Synthesis Inhibitor ◽

Early Postnatal Development ◽

Middle Adolescence

Growing body of evidence points to dysregulation of redox status in the brain as an important factor in the pathogenesis of schizophrenia. The aim of our study was to evaluate the effects of l-buthionine-(S,R)-sulfoximine (BSO), a glutathione (GSH) synthesis inhibitor, and 1-[2-Bis(4-fluorophenyl)methoxy]ethyl]-4-(3-phenylpropyl)piperazine dihydrochloride (GBR 12909), a dopamine reuptake inhibitor, given alone or in combination, to Sprague–Dawley pups during early postnatal development (p5–p16), on the time course of the onset of schizophrenia-like behaviors, and on the expression of brain-derived neurotrophic factor (BDNF) mRNA and its protein in the prefrontal cortex (PFC) and hippocampus (HIP) during adulthood. BSO administered alone decreased the levels of BDNF mRNA and its protein both in the PFC and HIP. Treatment with the combination of BSO + GBR 12909 also decreased BDNF mRNA and its protein in the PFC, but in the HIP, only the level of BDNF protein was decreased. Schizophrenia-like behaviors in rats were assessed at three time points of adolescence (p30, p42–p44, p60–p62) and in early adulthood (p90–p92) using the social interaction test, novel object recognition test, and open field test. Social and cognitive deficits first appeared in the middle adolescence stage and continued to occur into adulthood, both in rats treated with BSO alone or with the BSO + GBR 12909 combination. Behavior corresponding to positive symptoms in humans occurred in the middle adolescence period, only in rats treated with BSO + GBR 12909. Only in the latter group, amphetamine exacerbated the existing positive symptoms in adulthood. Our data show that rats receiving the BSO + GBR 12909 combination in the early postnatal life reproduced virtually all symptoms observed in patients with schizophrenia and, therefore, can be considered a valuable neurodevelopmental model of this disease.

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