Self-Regulation and Economic Stress in Children of Hispanic Immigrants and Their Peers: Better Regulation at a Cost?

RESEARCH FINDINGS: Although there is a well-established relationship between economic stress and children's self-regulation, few studies have examined this relationship in children of Hispanic immigrants (COHIs), a rapidly growing population. In a sample of preschool children (N = 165), we examined whether economic stress predicted teacher evaluations of children's self-regulation, whether economic stress predicted children's physiological reactivity (via cortisol levels), and whether economic stress had a similar effect on self-regulation and children's cortisol for COHI versus nonimmigrant children. Greater economic stress was associated with poorer child self-regulation and heightened physiological reactivity across a challenging classroom task for the sample as a whole. However, when we examined children by group, greater economic stress was associated with poorer teacher-reported self-regulation for nonimmigrant children only. In contrast, greater economic stress was related to greater cortisol reactivity across a challenge task for COHIs but not for nonimmigrants. PRACTICE OR POLICY: Results demonstrate the importance of considering physiological indices of self-regulation (heightened stress physiology), in addition to traditional external indices (teacher report), when assessing self-regulation or risk more generally among preschool samples that are diverse in terms of ethnicity, economic risk, and parents' nativity.

Increased basement membrane thickness, pericyte ghosts, and loss of retinal thickness and cells in dopamine beta hydroxylase knockout mice.

Diabetes can cause damage to sympathetic nerves, and we have previously shown that experimental sympathectomy can produce capillary abnormalities in the retina similar to those seen in early diabetes. We postulate that the diabetes-induced loss of the sympathetic system, and at least in part the sympathetic neurotransmitter norepinephrine (NE), contributes to the development of retinal vascular and neural abnormalities in diabetes. Thus, we predict that non-diabetic animals that lack NE will develop microvascular and neural changes that are similar to those that are characteristic of diabetic retinopathy. To test this, retinas from non-diabetic dopamine beta hydroxylase (Dbh, Dbh(-/-)) knockout mice and their littermate controls were assessed for diabetic-like capillary and neural changes at 5 months of age. Genetic deletion of Dbh resulted in a significant decrease in retinal thickness and number of cells in the retinal ganglion cell layer (central retinal region). In addition, the number of pericyte ghosts and the basement membrane of retinal capillaries were significantly increased in the Dbh(-/-) mice. These results provide evidence that loss of sympathetic neurotransmission may contribute to the microvascular and neural changes of diabetic retinopathy. Restoration of sympathetic neurotransmission may be a new target for therapeutic intervention to inhibit the early phases of diabetic retinopathy.

Distinct intracellular signaling mediates C-MET regulation of dendritic growth and synaptogenesis.

Hepatocyte growth factor (HGF) activation of the MET receptor tyrosine kinase influences multiple neurodevelopmental processes. Evidence from human imaging and mouse models shows that, in the forebrain, disruptions in MET signaling alter circuit formation and function. One likely means of modulation is by controlling neuron maturation. Here, we examined the signaling mechanisms through which MET exerts developmental effects in the neocortex. In situ hybridization revealed that hgf is located near MET-expressing neurons, including deep neocortical layers and periventricular zones. Western blot analyses of neocortical crude membranes demonstrated that HGF-induced MET autophosphorylation peaks during synaptogenesis, with a striking reduction in activation between P14 and P17 just before pruning. In vitro analysis of postnatal neocortical neurons assessed the roles of intracellular signaling following MET activation. There is rapid, HGF-induced phosphorylation of MET, ERK1/2, and Akt that is accompanied by two major morphological changes: increases in total dendritic growth and synapse density. Selective inhibition of each signaling pathway altered only one of the two distinct events. MAPK/ERK pathway inhibition significantly reduced the HGF-induced increase in dendritic length, but had no effect on synapse density. In contrast, inhibition of the PI3K/Akt pathway reduced HGF-induced increases in synapse density, with no effect on dendritic length. The data reveal a key role for MET activation during the period of neocortical neuron growth and synaptogenesis, with distinct biological outcomes mediated via discrete MET-linked intracellular signaling pathways in the same neurons. © 2016 Wiley Periodicals, Inc. Develop Neurobiol 76: 1160-1181, 2016.