At excitatory synapses, the postsynaptic scaffolding protein postsynaptic density 95 (PSD-95) couples NMDA receptors (NMDARs) to the Ras GTPase-activating protein SynGAP. The close association of SynGAP and NMDARs suggests that SynGAP may have an important role in NMDAR-dependent activation of Ras signaling pathways, such as the MAP kinase pathway, and in synaptic plasticity. To explore this issue, we examined long-term potentiation (LTP), p42 MAPK (ERK2) signaling, and spatial learning in mice with a heterozygous null mutation of the SynGAP gene (SynGAP(-/+)). In SynGAP(-/+) mutant mice, the induction of LTP in the hippocampal CA1 region was strongly reduced in the absence of any detectable alteration in basal synaptic transmission and NMDAR-mediated synaptic currents. Although basal levels of activated ERK2 were elevated in hippocampal extracts from SynGAP(-/+) mice, NMDAR stimulation still induced a robust increase in ERK activation in slices from SynGAP(-/+) mice. Thus, although SynGAP may regulate the ERK pathway, its role in LTP most likely involves additional downstream targets. Consistent with this, the amount of potentiation induced by stimulation protocols that induce an ERK-independent form of LTP were also significantly reduced in slices from SynGAP(-/+) mice. An elevation of basal phospho-ERK2 levels and LTP deficits were also observed in SynGAP(-/+)/H-Ras(-)/- double mutants, suggesting that SynGAP may normally regulate Ras isoforms other than H-Ras. A comparison of SynGAP and PSD-95 mutants suggests that PSD-95 couples NMDARs to multiple downstream signaling pathways with very different roles in LTP and learning.

Although prior research has established a link between exposure to peer victimization and depressive symptoms, relatively little is known about the processes underlying this association. This study examined whether maladaptive responses to a novel social stressor – specifically, lower levels of problem solving or higher levels of rumination – mediate this association. Data were gathered from 130 children (64 boys, 66 girls; M age = 9.46, SD = .33) who participated in a laboratory social stressor task with an unfamiliar peer. Results indicated that prior exposure to peer victimization in the school context was associated with ruminative responses to the novel stressor, which mediated the association between victimization and depressive symptoms. These results indicate that ruminative responses to social stress outside of the victimization context may serve as one process explaining the association between victimization and heightened depressive symptoms.

Although research links insecure adult attachment with depression, the emotional processes accounting for this association over time remain relatively unexplored. To address this gap, this study investigated whether deficits in emotional awareness serve as one explanatory process. Adult females caregivers (N = 417, M age = 37.83) completed questionnaires annually for three years. As anticipated, attachment avoidance exerted an indirect effect on depression via emotional awareness. Attachment anxiety directly predicted subsequent depression but the indirect effect through emotional awareness was nonsignificant. These results suggest that an avoidant attachment style interferes with the effective processing of emotions, thereby placing women at risk for depression. This research implicates emotional awareness as a potential target for interventions aimed at reducing depressive symptoms in mothers with avoidant attachment styles.

Executive function problems may disrupt the ability to use important adaptive coping skills, such as cognitive reappraisal, positive thinking, and acceptance, thereby resulting in greater emotional distress among YA CHD survivors.