The goal of the present study was to investigate developmental differences in the effectiveness of parent support to alleviate hypothalamic-pituitary-adrenal (HPA) axis stress responses of children (ages 9-10, N = 40) and adolescents (ages 15-16, N = 41). We experimentally manipulated the provision of parent support during the speech preparation period before a modified Trier Social Stress Test (TSST) and examined its effect on levels of salivary cortisol secreted in response to this laboratory stressor. Analyses revealed a significant interaction of condition and age group such that social support from the parent (versus a stranger) significantly eliminated the cortisol stress response in children, but had no effect on the response among adolescents.

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Background Children reared in deprived environments, such as institutions for the care of orphaned or abandoned children, are at increased risk for attention and behavior regulation difficulties. This study examined the neurobehavioral correlates of executive attention in post-institutionalized (PI) children. Methods The performance and event-related potentials (ERPs) of 10- and 11-year-old internationally adopted PI children on two executive attention tasks, Go/No-go and Flanker, were compared to two groups: children internationally adopted early from foster care (PF) and non-adopted children (NA). Results Behavioral measures suggested problems with sustained attention, with PIs performing more poorly on Go trials and not on No-go trials of the Go/No-go and made more errors on both congruent and incongruent trials on the Flanker. ERPs suggested differences in inhibitory control and error monitoring, as PIs had smaller N2 amplitude on Go/No-go and smaller error-related negativity on Flanker. Conclusions This pattern of results raises questions regarding the nature of attention difficulties for PI children. The behavioral errors are not specific to executive attention and instead likely reflect difficulties in overall sustained attention. The ERP results are consistent with neural activity related to deficits in inhibitory control (N2) and error monitoring (error-related negativity). Questions emerge regarding the similarity of attention regulatory difficulties in PIs to those experienced by non-PI children with ADHD.

Associations between early deprivation/neglect in the form of institutional care with the cortisol awakening response (CAR) were examined as a function of pubertal status among 12- and 13-year-old post-institutionalized youth. CARs indexed hypothalamic-pituitary-adrenocortical reactivity. Post-institutionalized youth were compared to youth adopted internationally from foster care (adoption control) and to nonadopted youth reared in families comparable in parental education and income to the adoptive families. Post-institutionalized youth exhibited a blunted CAR if they were at earlier but not if they were at later stages of puberty. Similarly, for both groups of internationally adopted youth combined, earlier but not later stages of puberty were associated with more blunted CARs at higher but not lower levels of parent-reported pre-adoption physical and social neglect.

The goal of the present study was to investigate the role of early social deprivation in shaping the effectiveness of parent support to alleviate hypothalamic-pituitary-adrenal (HPA) axis stress responses of children (ages 8.9–11, M = 9.83 years, SD = .55). The sample was equally divided between children who had been adopted internationally from orphanage care by age 5 (N = 40) and an age- and gender-matched group of non-adopted children (N = 40). On average, internationally adopted children were invited to the laboratory 7.6 years post-adoption (SD = 1.45). We experimentally manipulated the provision of parent support during the 5-minute speech preparation period before a modified Trier Social Stress Test (TSST) and examined its effect on levels of salivary cortisol secreted in response to this laboratory stressor. All participants were randomly assigned to receive support from their parent or a stranger. Analyses revealed a significant interaction of support condition and group such that parent support significantly dampened the cortisol stress response in non-adopted children compared to support from a stranger, whereas the cortisol response curves of post-institutionalized children did not differ between the parent and stranger support conditions. Cortisol reactivity for PI children in both conditions was lower than that of non-adopted children in the stranger support condition. Social deprivation during the first few years of life may shape neurobehavioral development in ways that reduce selective responses to caregivers versus strangers.

Inactivation of the perlecan gene leads to perinatal lethal chondrodysplasia. The similarity to the phenotypes of the Col2A1 knock-out and the disproportionate micromelia mutation suggests perlecan involvement in cartilage collagen matrix assembly. We now present a mechanism for the defect in collagen type II fibril assembly by perlecan-null chondrocytes. Cartilage perlecan is a heparin sulfate or a mixed heparan sulfate/chondroitin sulfate proteoglycan. The latter form binds collagen and accelerates fibril formation in vitro, with more defined fibril morphology and increased fibril diameters produced in the presence of perlecan. Interestingly, the enhancement of collagen fibril formation is independent on the core protein and is mimicked by chondroitin sulfate E but neither by chondroitin sulfate D nor dextran sulfate. Furthermore, perlecan chondroitin sulfate contains the 4,6-disulfated disaccharides typical for chondroitin sulfate E. Indeed, purified glycosaminoglycans from perlecan-enriched fractions of cartilage extracts contain elevated levels of 4,6-disulfated chondroitin sulfate disaccharides and enhance collagen fibril formation. The effect on collagen assembly is proportional to the content of the 4,6-disulfated disaccharide in the different cartilage extracts, with growth plate cartilage glycosaminoglycan being the most efficient enhancer. These findings demonstrate a role for perlecan chondroitin sulfate side chains in cartilage extracellular matrix assembly and provide an explanation for the perlecan-null chondrodysplasia.

The goal of this study was to examine whether growth delay can serve as an index of allostatic load during early development, as it is well known that the activity of stress-mediating systems inhibits growth. The participants were children adopted internationally from institutional care (n = 36), children adopted internationally from foster care (n = 6), and nonadopted children (n = 35). For the adopted children, height-for-age and weight-for-height were assessed at adoption; for all children, disinhibited social approach (DSA; termed elsewhere as “indiscriminate friendliness”) and diurnal cortisol were assessed at 6–8 years (M = 6.9 years). For internationally adopted children in general, and postinstitutionalized children specifically, linear growth delay assessed at the time of adoption was associated with more dysregulated behavior in response to an unfamiliar adult (i.e., greater DSA) and a more dysregulated diurnal cortisol rhythm (i.e., higher late-afternoon and evening values). Further, among the most growth-delayed children, higher cortisol levels later in the day were correlated with DSA. The potential for using growth delay as an allostatic load indicator and the possible problems and limitations in its use in child populations are discussed.

SLC7A10 (Asc-1) is a sodium-independent amino acid transporter known to facilitate transport of a number of amino acids including glycine, L-serine, L-alanine, and L-cysteine, as well as their D-enantiomers. It has been described as a neuronal transporter with a primary role related to modulation of excitatory glutamatergic neurotransmission. We find that SLC7A10 is substantially enriched in a subset of astrocytes of the caudal brain and spinal cord in a distribution corresponding with high densities of glycinergic inhibitory synapses. Accordingly, we find that spinal cord glycine levels are significantly reduced in Slc7a10-null mice and spontaneous glycinergic postsynaptic currents in motor neurons show substantially diminished amplitudes, demonstrating an essential role for SLC7A10 in glycinergic inhibitory function in the central nervous system. These observations establish the etiology of sustained myoclonus (sudden involuntary muscle movements) and early postnatal lethality characteristic of Slc7a10-null mice, and implicate SLC7A10 as a candidate gene and auto-antibody target in human hyperekplexia and stiff person syndrome, respectively.