BDNF increases survival of retinal dopaminergic neurons after prenatal compromise.

Purpose: Chronic placental insufficiency (CPI) severe enough to cause growth restriction (GR) results in alterations to the retina, including a reduction in tyrosine hydroxylase immunoreactive (TH-IR)-dopaminergic amacrine cells. Brain-derived neurotrophic factor (BDNF) plays a role in the development of the retinal dopaminergic network and may therefore be an appropriate therapy for restoring dopaminergic cells after prenatal compromise. This study was conducted (1) to establish whether BDNF and its receptor NTRK2 (Trk B) are altered in the retina after CPI and (2) to explore the potential of BDNF to enhance dopaminergic cell survival in organotypic retinal cultures from prenatally compromised animals.

Prenatally compromised neurons respond to brain-derived neurotrophic factor treatment in vitro.

Prenatal hypoxia affects neuronal survival and process outgrowth. Brain-derived neurotrophic factor, which influences neural growth, is decreased in these conditions. We tested whether addition of brain-derived neurotrophic factor enhances growth of neurons cultured from guinea pig fetuses (n=7) compromised by chronic placental insufficiency from 30-52 days gestation (term approximately 67 days).

The pattern of cerebral injury in a primate model of preterm birth and neonatal intensive care.

Survivors of very premature birth face an increased risk of adverse motor, cognitive, and behavior sequelae. In order to understand the pathogenesis of these adverse outcomes, an animal model of premature birth and neonatal care in a species with a close similarity to the human infant is sought. In this histological and immunohistochemical study we have defined the pattern of cerebral injury in a premature baboon model undergoing similar neonatal intensive care to that of the human premature infant.

Cardiovascular and renal disease in the adolescent guinea pig after chronic placental insufficiency.

Objective: The aim of this study was to determine the long-term effects of chronic placental insufficiency on the metabolic state and organ structure in the fetal and adolescent guinea pig.

Study Design: The maternal uterine artery was ligated at day 28-30 to reduce placental function and restrict fetal growth. Whole body and tissue weights and plasma metabolites were determined at 60 days of gestation and 8 weeks of age; tissue structure was determined at the latter age in restricted and control offspring.

Chronic placental insufficiency affects retinal development in the guinea pig.

Purpose: Very low birth weight (VLBW) and fetal growth restriction are associated with increased risks of long-term visual impairments, including alterations to contrast sensitivity, a parameter mediated in part by dopaminergic amacrine cells. This study was conducted to determine whether chronic placental insufficiency (CPI), sufficient to cause growth restriction, results in neurochemical alterations to retinal interneurons, specifically amacrine and horizontal cell populations near term.

Methods: CPI was induced just before midgestation (term approximately 67 days of gestation, dg) in guinea pigs through unilateral ligation of the uterine artery.

Is there an association between level of adult blood pressure and nephron number or renal filtration surface area?

Background: Reductions in renal filtration surface area (FSA) have been linked to development of hypertension. This study investigated whether there are direct relationships, in the adult rat, between levels of blood pressure and nephron number or total renal FSA.

Methods: F1 and F2 offspring were generated from a spontaneously hypertensive rat (SHR)/Wistar Kyoto (WKY) rat cross.