Prevalence, symptoms, and treatment of depression suggest that major depressive disorders (MDD) present sex differences. Social stress-induced neurovascular pathology is associated with depressive symptoms in male mice; however, this association is unclear in females. Here, we report that chronic social and subchronic variable stress promotes blood-brain barrier (BBB) alterations in mood-related brain regions of female mice. Targeted disruption of the BBB in the female prefrontal cortex (PFC) induces anxiety- and depression-like behaviours. By comparing the endothelium cell-specific transcriptomic profiling of the mouse male and female PFC, we identify several pathways and genes involved in maladaptive stress responses and resilience to stress. Furthermore, we confirm that the BBB in the PFC of stressed female mice is leaky. Then, we identify circulating vascular biomarkers of chronic stress, such as soluble E-selectin. Similar changes in circulating soluble E-selectin, BBB gene expression and morphology can be found in blood serum and postmortem brain samples from women diagnosed with MDD. Altogether, we propose that BBB dysfunction plays an important role in modulating stress responses in female mice and possibly MDD.

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To isolate the anatomical locus of the neural activity most important for generating or modulating the scalp-recorded N400 and P600 components elicited during continuous recognition memory tasks, intracranial event-related potentials (ERPs) were recorded from medial and lateral aspects of the temporal, frontal, parietal, and occipital lobes in 25 patients undergoing stereoelectroencephalography for seizure localization. Large-amplitude and polarity-inverted ERPs were recorded from various temporal, frontal, and parietal structures, whereas the memory-related ERP modulation assessed by the ERP repetition effect was present only in those brain areas that play the most important role in memory processing. These data suggest that the scalp-recorded N400 and P600 components may represent the most readily observable aspect of synchronous activity occurring across widely distributed brain structures and neural systems underlying different cognitive mechanisms, which all contribute to some aspect of information processing during recognition memory.

Prior exposure to a stimulus can facilitate the performance to subsequent presentations of that stimulus. ERP studies have shown that this facilitation is associated with the modulation of two components (N400 and P600). Investigation of the time course of both behavioral and ERP repetition effects have led to the assumption that it is subserved by the combination of at least two mechanisms operating at different time-points: a short-delay semantic activation and a long-lasting episodic mechanism. The present experiment recorded intracranial ERPs from various structures during a continuous recognition memory task to investigate the respective contribution of the different brain regions to short- and long-delay ERP repetition effects. The results are in good agreement with both the classical neuropsychological literature and the more recent data obtained with functional imagery techniques. They provide electrophysiological evidence of multiple anatomo-functional memory systems in the human brain: a short-term semantic activation system and a long-term episodic memory system, with interface structures that coordinate the functioning of these two systems.

Rivastigmine treatment did not appear to enhance cognition in SZ patients with important cognitive impairments. This finding needs to be interpreted with care and requires substantiation with larger sample size studies with patients treated with cognitive enhancer for longer periods.

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