Received cradling bias during the first year of life: A retrospective study on children with typical and atypical development

A population-level left cradling bias exists whereby 60-90% of mothers hold their infants on the left side. This left biased positioning appears to be mutually beneficial to both the mother and the baby’s brain organization for processing of socio-emotional stimuli. Previous research connected cradling asymmetries and Autism Spectrum Disorders (ASD), entailing impairment in socio- communicative relationships and characterized by an early hypo-lateralization of brain functions. In this explorative study, we aimed to provide a contribution to the retrospective investigations by looking for early behavioral markers of neurodevelopmental disorders such as ASD. We hypothesized that an atypical trajectory in maternal cradling might be one of the possible signs of an interference in mother-infant socio-emotional communication, and thus of potential neurodevelopmental dysfunctions. To this aim, we examined photos depicting mother-child early cradling interactions by consulting family albums of 27 children later diagnosed with autism and 63 typically developing children. As regards the first half of the first year of life, no differences were shown between maternal cradling-side preferences in typical and ASD groups, both exhibiting the left-cradling bias in the 0-3 months period, but not in the 3-6 months period. However, our results show dissimilar patterns of cradling preferences during the second half of the first year of life. In particular, the absence of left-cradling shown in typical mothers was not observed in ASD mothers, who exhibited a significant left-cradling bias in the 6-12 months age group. This difference might reflect the fact that mother-infant relationship involving children later diagnosed with ASD might remain “basic” because mothers experience a lack of social activity in such children. Alternatively, it may reflect the overstimulation in which mothers try to engage infants in response to their lack of responsiveness and social initiative. However, further investigations are needed both to distinguish between these two possibilities and to define the role of early typical and reversed cradling experiences on neurodevelopment

Poor screening and nonadiabatic superconductivity in correlated systems

In this paper we investigate the role of the electronic correlation on the hole doping dependence of electron-phonon and superconducting properties of cuprates. We introduce a simple analytical expression for the one-particle Green's function in the presence of electronic correlation and we evaluate the reduction of the screening properties as the electronic correlation increases by approaching half-filling. The poor screening properties play an important role within the context of the nonadiabatic theory of superconductivity. We show that a consistent inclusion of the reduced screening properties in the nonadiabatic theory can account in a natural way for the $T_c$-$\delta$ phase diagram of cuprates. Experimental evidences are also discussed.Comment: 12 Pages, 6 Figures, Accepted on Physical Review

ex-dimorphic behavioral and neuroendocrine effects of the organophosphate chlorpyrifos in a mouse model of autism spectrum disorders.

Autism is a neurodevelopmental disorder characterized by impaired social and communicative skills and repetitive behaviors with a male-female ratio of 4:1. The etiology of autism results from complex interaction between multiple genes and diverse environmental contaminants. Chlorpyrifos (CPF) is a widely diffused organophosphate insecticide. Recent epidemiological studies indicate that environmentally prenatal exposure to CPF in children can alter the morphology of some brain areas involved in cognitive and behavioural processes. Several rodent studies have confirmed that CPF developmental exposure influences serotonergic neurotransmission and neuroendocrine markers in hypothalamic and amygdaloidal regions in a sex-dimorphic fashion. In the present study we analyzed the effects of low-dose developmental exposure to CPF in a mouse model of autism-spectrum disorders, the BTBR T+tf/J mouse strain, which displays several behavioral traits relevant to autism. To this aim, pregnant BTBR mice were administered from gestational day 14-17 with either vehicle or CPF at a dose of 6 mg/kg/bw by oral gavages. Offspring of both sexes underwent early assessment of sensorimotor milestones and ultrasound emission. At adulthood, the social responses of females were assessed in a free social interaction test with a same-sex companion, whereas the courtship behavior of adult males with a sexually receptive female was analyzed. Our findings evidenced significant effects of CPF on neonatal motor patterns and ultrasound emission, in the male offspring. At adulthood, CPF males showed an abnormal pattern of social investigation of the receptive female, associated to marked increase in the rate of ultrasonic vocalizations emitted during the courtship. Analysis of mRNA expression in hypothalamus and amygdala evidenced in CPF males a significant decrease of vasopressin receptor 1A in the hypothalamus and ERα in the amygdala, and a diminished expression of ERβ and oxytocin precursor in the hypothalamus. These findings open the way for future experimental studies on the interaction among vulnerable gene backgrounds and environmental neurotoxicants in the etiology of sex-biased neurodevelopmental disorders. Supported by: Project Italy/US 11US/11 and Italian Ministry of Health Grant (GR3), Young Researcher 2008, “Non-invasive tools for early detection of Autism Spectrum Disorders”

Sex-dimorphic effects of gestational exposure to the organophosphate insecticide chlorpyrifos on social investigation in mice.

Several pieces of evidence from animal and human studies indicate that the organophosphate insecticide chlorpyrifos (CPF) acts as a developmental neurotoxicant at environmentally relevant doses, and it is possibly endowed with endocrine-disrupting activity. Data collected in rodent models show that developmental exposure to CPF at sub-toxic doses induces long-lasting and sex-dimorphic changes in social and investigative responses in exposed offspring. The aim of this study was to evaluate the effects of gestational CPF treatment on social and olfactory discrimination in adult mice of both sexes. Pregnant CD1 out-bred mice were exposed to CPF per os on gestational days (GD) 14–17 at the sub-toxic dose of 6 mg/kg/bw. At adulthood, male and female offspring underwent the same experimental paradigms, namely i) a social discrimination test where mice were presented with a simultaneous binary choice between a novel conspecific and a familiar one, and ii) an olfactory habituation/dishabituation test to evaluate their capability to discriminate between odors with different eco-ethological salience (non-social vs. social odors). Results showed that in the social discrimination test prenatal CPF primarily affected the female sex by raising the investigation time in females to the same levels as found in vehicle- and CPF-exposed males. The ability to discriminate between a familiar and a novel social mate was not affected by CPF in either sex. In the olfactory habituation/dishabituation test, mice of both sexes successfully discriminated non-social from social odors regardless of the prenatal treatment received. These results confirm previous evidence indicating that developmental exposure to CPF causes long-lasting and sex-dimorphic changes in responsiveness to social cues, in the absence of significant impairment of social and olfactory discrimination capacity. These findings are discussed within the framework of recent data pointing to the limbic/hypothalamic circuitry and steroid hormonal regulations as possible targets for CPF neurotoxicity

Behavioural and neuroendocrine effects of developmental exposure to a common organophosphate insecticide in two mouse strains: relevance for vulnerability to human neurodevelopment disorders.

Chlorpyrifos (CPF) is the most largely used organophosphate insecticide worldwide. Epidemiological studies have indicated that assumption of CPF by diet and indoor exposure at environmentally relevant doses affects behaviour and brain maturation in exposed children. We found that developmental exposure of the out bred CD1 mouse strain to low dose of CPF altered neonatal behaviour patterns, adult social responses and neuroendocrine markers in a sex-dimorphic fashion. In the present study the prenatal treatment schedule used for CD1 mice was applied to the inbred BTBR T+tf/J mouse strain, a validated model of autism-spectrum disorders. The etiology of autism is still obscure but it has become increasingly clear that both defective genes and environmental factors (including chemicals) concur to the pathogenesis of this clinical heterogeneous condition. BTBR mice exhibit an abnormal immune responses that may also contribute to a proper vulnerability to environmental insults. Moreover while the BTBR mouse has been shown to exhibit behavioural patterns thought to be relevant to the core domains of ASD, it is unknown whether these behaviour, relevant to ASD, can be further exacerbated by the effects of environmental insults, such as chlorpyrifos exposure. Pregnant BTBR mice were orally administered on gestational days 14-17 with either vehicle or CPF at a dose of 6 mg/kg/bw. Offspring of both sexes underwent neonatal assessment of sensorimotor milestones and ultrasound emission, and social investigation and/or courtship behaviour were investigated at adulthood. Our findings evidenced significant effects of CPF on neonatal behaviours and ultrasound emission with a different pattern of effects between CD1 and BTBR mice. BTBR-CPF males showed an abnormal courtship behaviour pattern of the receptive female, an effect not found in the CD1 males. Analysis of mRNA expression of oxytocin, vasopressin and steroid receptors in hypothalamus and amygdala evidenced important baseline differences between the two strains, which might be relevant for their different behavioural phenotypes and susceptibility to neurotoxicants' effects