Social support before and after childbirth is a possible protective factor for perinatal depression. Currently, there is a lack of longitudinal studies beyond the first year postpartum exploring the relationship of social support with depression and anxiety. Social support is also a possible protective factor for adverse child development, which is a known consequence of perinatal depression. The present study followed up a cohort of depressed women (n = 54) from a randomised controlled trial of psychological treatment for antenatal depression. We examined the trajectory of the relationships between perceived social support (Social Provisions Scale), depression (Beck Depression Inventory), and anxiety (Beck Anxiety Inventory) twice in pregnancy and twice postpartum up to two years. The influence of social support on child development and parenting-related stress was also explored. Two aspects of social support, Reassurance of Worth and Reliable Alliance, were strongly related to perinatal depression and anxiety, particularly when predicting symptoms in late pregnancy. However, the effect of postnatal depression on child development at 9 and 24 months post-birth was not mediated by social support. These results suggest the importance of adjusting current interventions for depressed perinatal women to focus on social support in late pregnancy and the first six months postpartum.

Deep brain stimulation (DBS) is an established treatment for advanced Parkinson's disease (PD).The procedure entails intracranial implantation of an electrode in a specific brain structure followed by chronic stimulation. Although the beneficial effects of DBS on motor symptoms in PD are well known, it is often accompanied by cognitive impairments the origin of which is not fully understood. To explore the possible contribution of the surgical procedure itself, we studied the effect of electrode implantation in the subthalamic nucleus (STN) on regional neuroinflammation and memory function in rats implanted bilaterally with stainless steel electrodes. Age-matched sham and intact rats were used as controls. Brains were removed one week or eight weeks post implantation and processed for in vitro autoradiography with [3H]PK11195, an established marker of microglial activation. Memory function was assessed by the novel object recognition test (ORT) before surgery and two and eight weeks after surgery. Electrode implantation produced region-dependent changes in ligand binding density in the implanted brains at one week as well as eight weeks post implantation. Cortical regions showed more intense and widespread neuroinflammation than striatal or thalamic structures. Furthermore, implanted animals showed deficits in ORT performance two and eight weeks post implantation. Thus, electrode implantation resulted in a widespread and persistent neuroinflammation and sustained memory impairment. These results suggest that the insertion and continued presence of electrodes in the brain, even without stimulation, may lead to inflammationmediated cognitive deficits in susceptible individuals, as observed in patients treated with DBS.

Anhedonia is defined as a diminished ability to obtain pleasure from otherwise positive stimuli. Anxiety and mood disorders have been previously associated with dysregulation of the reward system, with anhedonia as a core element of major depressive disorder (MDD). The aim of the present study was to investigate whether stress-induced anhedonia could be prevented by treatments with escitalopram or novel herbal treatment (NHT) in an animal model of depression. Unpredictable chronic mild stress (UCMS) was administered for 4 weeks on ICR outbred mice. Following stress exposure, animals were randomly assigned to pharmacological treatment groups (i.e., saline, escitalopram or NHT). Treatments were delivered for 3 weeks. Hedonic tone was examined via ethanol and sucrose preferences. Biological indices pertinent to MDD and anhedonia were assessed: namely, hippocampal brain-derived neurotrophic factor (BDNF) and striatal dopamine receptor D2 (Drd2) mRNA expression levels. The results indicate that the UCMS-induced reductions in ethanol or sucrose preferences were normalized by escitalopram or NHT. This implies a resemblance between sucrose and ethanol in their hedonic-eliciting property. On a neurobiological aspect, UCMS-induced reduction in hippocampal BDNF levels was normalized by escitalopram or NHT, while UCMS-induced reduction in striatal Drd2 mRNA levels was normalized solely by NHT. The results accentuate the association of stress and anhedonia, and pinpoint a distinct effect for NHT on striatal Drd2 expression.

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