Neural cognitive control moderates the association between insular risk processing and risk-taking behaviors via perceived stress in adolescents.

Adolescence is a critical period for the initiation of risk-taking behaviors. We examined the longitudinal interplay between neural correlates of risk processing and cognitive control in predicting risk-taking behaviors via stress. The sample consisted of 167 adolescents (53% males) who were assessed twice (MAgeTime1 = 14.13, MAgeTime2 = 15.05). Neural risk processing was operationalized as blood-oxygen-level-dependent (BOLD) responses in the anterior insula during a lottery choice task and neural cognitive control as BOLD responses during an inhibitory control task. Adolescents reported on perceived stress and risk-taking behaviors. Structural equation modeling analyses indicated that low insular risk processing predicted increases in perceived stress, while perceived stress did not predict changes in insular risk processing across one year. Moreover, significant moderation by neural cognitive control indicated that low insular risk processing predicted increases in risk-taking behaviors via increases in perceived stress among adolescents with poor neural cognitive control, but not among adolescents with good neural cognitive control. The results suggest that risk processing in the anterior insular cortex plays an important role in stress experience and risk-taking behaviors particularly for vulnerable adolescents with poor neural cognitive control.

Insular atrophy and diminished disgust reactivity.

Disgust is an emotion that helps us deal with potential contamination (Rozin & Fallon, 1987). It produces a distinctive facial expression (e.g., wrinkled nose) and a physiological response that is accompanied by strong visceral sensations (e.g., nausea). Given the important role that the anterior insula plays in processing and integrating visceral information (Craig, 2009), it is likely to be centrally involved in disgust. Despite this, few studies have examined the link between insular degeneration and the experience, physiology, and expression of disgust. We studied a group that was heterogeneous in terms of insular damage: 84 patients with neurodegenerative diseases (i.e., frontotemporal dementia, corticobasal syndrome, progressive supranuclear palsy, Alzheimer's disease) and 29 controls. Subjects viewed films that elicit high levels of disgust and sadness. Emotional reactivity was assessed using self-report, peripheral physiology, and facial behavior. Regional brain volumes (insula, putamen, pallidum, caudate, and amygdala) were determined from structural MRIs using the FreeSurfer method. Results indicated that smaller insular volumes were associated with reduced disgust responding in self-report and physiological reactivity, but not in facial behavior. In terms of the specificity of these findings, insular volume did not predict sadness reactivity, and disgust reactivity was not predicted by putamen, pallidum, and caudate volumes (lower self-reported disgust was associated with smaller amygdala volume). These findings underscore the central role of the insula in the experience and physiology of disgust. (PsycINFO Database Record

Delayed early primary visual pathway development in premature infants: high density electrophysiological evidence.

In the past decades, multiple studies have been interested in developmental patterns of the visual system in healthy infants. During the first year of life, differential maturational changes have been observed between the Magnocellular (P) and the Parvocellular (P) visual pathways. However, few studies investigated P and M system development in infants born prematurely. The aim of the present study was to characterize P and M system maturational differences between healthy preterm and fullterm infants through a critical period of visual maturation: the first year of life. Using a cross-sectional design, high-density electroencephalogram (EEG) was recorded in 31 healthy preterms and 41 fullterm infants of 3, 6, or 12 months (corrected age for premature babies). Three visual stimulations varying in contrast and spatial frequency were presented to stimulate preferentially the M pathway, the P pathway, or both systems simultaneously during EEG recordings. Results from early visual evoked potentials in response to the stimulation that activates simultaneously both systems revealed longer N1 latencies and smaller P1 amplitudes in preterm infants compared to fullterms. Moreover, preterms showed longer N1 and P1 latencies in response to stimuli assessing the M pathway at 3 months. No differences between preterms and fullterms were found when using the preferential P system stimulation. In order to identify the cerebral generator of each visual response, distributed source analyses were computed in 12-month-old infants using LORETA. Source analysis demonstrated an activation of the parietal dorsal region in fullterm infants, in response to the preferential M pathway, which was not seen in the preterms. Overall, these findings suggest that the Magnocellular pathway development is affected in premature infants. Although our VEP results suggest that premature children overcome, at least partially, the visual developmental delay with time, source analyses reveal abnormal brain activation of the Magnocellular pathway at 12 months of age.

Alterations in postnatal neurogenesis and dopamine dysregulation in schizophrenia: a hypothesis.

An increasing number of studies demonstrate the important role of several susceptibility genes for schizophrenia, such as neuregulin-1 and DISC1, in early postnatal and adult neurogenesis. Its significance for the pathophysiology of the disease, including its relation to neurotransmitter systems implicated in schizophrenia (like the dopamine system), remains, however, unknown. Here, we review molecular and cellular components of the dopamine system associated with postnatal neurogenesis and plasticity, both in rodents and in primates, and discuss their possible implication in schizophrenia. We focus mainly on the islands of Calleja, complex aggregations of granule cells in the ventral striatum, generated early postnatally in the subventricular zone. In contrast to the involution of the primate olfactory bulb, the islands of Calleja attain their maximal development in humans, an evolution paralleled by a larger ventral subventricular zone and more connections with other structures, including temporal cortical areas. The islands of Calleja express high levels of neuronal nitric oxide (NO) synthase and D3 dopamine receptors and are densely interconnected by dopaminergic projections with the ventral tegmental area. D3 receptors modulate subventricular zone neurogenesis and dopamine release. Their genetic deletion induces striatal hyperdopaminergia. We review data indicating a high plasticity of postnatal islands of Calleja, potentially facilitating susceptibility to schizophrenia-related risk factors. In this context, we propose a new pathophysiological model, where altered neurogenesis of the islands of Calleja may contribute to dysfunction of the dopamine and NO systems and psychosis through convergence of genetic and environmental disease-associated factors.

Alterations in dopamine D3 receptors in the circling (ci3) rat mutant.

We have previously described a black-hooded mutant rat (BH.7A/Ztm-ci3/ci3) that displays abnormal lateralized circling behavior, but normal auditory and vestibular functions. Neurochemical determination of dopamine and dopamine metabolite levels in striatum, nucleus accumbens and substantia nigra showed that ci3 rats have a significant asymmetry in striatal dopamine in that dopamine levels were significantly lower in the hemisphere contralateral to the preferred direction of turning. Consistent with this finding, immunohistological examination of dopaminergic neurons in substantia nigra and ventral tegmental area yielded a significant laterality in the medial part of substantia nigra pars compacta with a lower density of tyrosine hydroxylase-positive neurons in the contralateral hemisphere of mutant circling rats, while no laterality was seen in unaffected rats of the background strain. In the present study, quantitative autoradiography was used to examine the binding of [(3)H]SCH 23390, [(3)H]raclopride and [(3)H]7-OH-DPAT (7-hydroxy-N,N-di-n-propyl-2-aminotetralin) to dopamine D1, D2, and D3 receptors, respectively, in various brain regions of ci3 rats and unaffected rats of the background strain (BH.7A(LEW)/Won). No significant differences between circling rats and controls were obtained for D1 and D2 receptor binding in any region, but mutant rats differed from controls in dopamine D3 binding in several regions. A significant decrease in D3 binding was seen in the shell of the nucleus accumbens, the islands of Calleja, and the subependymal zone of ci3 mutant rats. Furthermore, a significant laterality in D3 binding was determined in ci3 rats in that binding was lower in the contralateral hemisphere in the shell of the nucleus accumbens and the islands of Calleja. Our data indicate that alterations of dopamine D3 receptors may be involved in the behavioral phenotype of the ci3 rat, thus substantiating the findings from a recent genetic linkage analysis that indicated the D3 receptor gene as a candidate gene in this rat mutant.