Rockefeller University

About: Rockefeller University is a education organization based out in New York, New York, United States. It is known for research contribution in the topics: Population & Gene. The organization has 15867 authors who have published 32938 publications receiving 2940261 citations. The organization is also known as: Rockefeller University & Rockefeller Institute.

Chronic stress alters synaptic terminal structure in hippocampus

Abstract: Repeated psychosocial or restraint stress causes atrophy of apical dendrites in CA3 pyramidal neurons of the hippocampus, accompanied by specific cognitive deficits in spatial learning and memory. Excitatory amino acids mediate this atrophy together with adrenal steroids and the neurotransmitter serotonin. Because the mossy fibers from dentate granule neurons provide a major excitatory input to the CA3 proximal apical dendrites, we measured ultrastructural parameters associated with the mossy fiber–CA3 synapses in control and 21-day restraint-stressed rats in an effort to find additional morphological consequences of stress that could help elucidate the underlying anatomical as well as cellular and molecular mechanisms. Although mossy fiber terminals of control rats were packed with small, clear synaptic vesicles, terminals from stressed animals showed a marked rearrangement of vesicles, with more densely packed clusters localized in the vicinity of active zones. Moreover, compared with controls, restraint stress increased the area of the mossy fiber terminal occupied by mitochondrial profiles and consequently, a larger, localized energy-generating capacity. A single stress session did not produce these changes either immediately after or the next day following the restraint session. These findings provide a morphological marker of the effects of chronic stress on the hippocampus that points to possible underlying neuroanatomical as well as cellular and molecular mechanisms for the ability of repeated stress to cause structural changes within the hippocampus.

BIOGENESIS OF ENDOPLASMIC RETICULUM MEMBRANES I. Structural and Chemical Differentiation in Developing Rat Hepatocyte

Abstract: The development of the endoplasmic reticulum of rat hepatocytes was studied during a period of rapid cell differentiation, i.e., from 3 days before to 8 days after birth. Before birth, the ER increases in volume, remaining predominantly rough surfaced; after birth, the increase continues but affects mainly the smooth-surfaced part of the system. These changes are reflected in variations of the RNA/protein and PLP/protein ratios of microsomal fractions: the first decreases, while the second increases, with age. The analysis of microsomal membranes and of microsomal lipids indicates that the PLP/protein ratio, the distribution of phospholipids, and the rate of P32 incorporation into these phospholipids show little variation over the period examined and are comparable to values found in adult liver. Fatty acid composition of total phosphatides undergoes, however, drastic changes after birth. During the period of rapid ER development in vivo incorporation of leucine-C14 and glycerol-C14 into the proteins and lipids of microsomal membranes is higher in the rough-than in the smooth-surfaced microsomes, for the first hours after the injection of the label; later on (∼10 hr) the situation is reversed. These results strongly suggest that new membrane is synthesized in the rough ER and subsequently transferred to the smooth ER.

Leptin-specific patterns of gene expression in white adipose tissue

Abstract: Leptin is a hormone that regulates body weight by decreasing food intake and increasing energy expenditure. ob/ob mice carry leptin mutations and are obese and hyperphagic. Leptin administration to lean and ob/ob mice activates a novel metabolic program that depletes adipose tissue. Although this response is physiologically distinct from that evident after food restriction, the molecular nature of these differences is as yet unknown. Expression monitoring of 6500 genes using oligonucleotide microarrays in wild-type, ob/ob, and transgenic mice expressing low levels of leptin revealed that differences in ambient leptin levels have dramatic effects on the phenotype of white adipose tissue. These data identified a large number of genes that are differentially expressed in ob/ob mice. To delineate the components of the transcriptional program specifically affected by leptin, the level of the same 6500 genes was monitored in wild-type and ob/ob mice at various times after leptin treatment or food restriction. A novel application of k-means clustering identified 8 clusters of adipose tissue genes whose expression was different between leptin treatment and food restriction in ob/ob mice and 10 such clusters in wild-type experiments. One of the clusters was repressed specifically by leptin in both wild-type and ob/ob mice and included several genes known to be regulated by SREBP-1/ADD1. Further studies confirmed that leptin decreases the levels of SREBP-1/ADD1 RNA and transcriptionally active SREBP-1/ADD1 protein in white adipose tissue. Future studies of the molecular basis for the apparent coordinate regulation of the other clusters of leptin-regulated genes may reveal additional mechanisms by which leptin exerts its weight-reducing effects.