Perineuronal nets (PNNs) are extracellular matrix (ECM) structures that envelop neurons and regulate synaptic functions. Long thought to be stable structures, PNNs have been recently shown to respond dynamically during learning, potentially regulating the formation of new synapses. We postulated that PNNs vary during sleep, a period of active synaptic modification. Notably, PNN components are cleaved by matrix proteases such as the protease cathepsin-S. This protease is diurnally expressed in the mouse cortex, coinciding with dendritic spine density rhythms. Thus, cathepsin-S may contribute to PNN remodeling during sleep, mediating synaptic reorganization. These studies were designed to test the hypothesis that PNN numbers vary in a diurnal manner in the rodent and human brain, as well as in a circadian manner in the rodent brain, and that these rhythms are disrupted by sleep deprivation. In mice, we observed diurnal and circadian rhythms of PNNs labeled with the lectin Wisteria floribunda agglutinin (WFA1 PNNs) in several brain regions involved in emotional memory processing. Sleep deprivation prevented the daytime decrease of WFA1 PNNs and enhances fear memory extinction. Diurnal rhythms of cathepsin-S expression in microglia were observed in the same brain regions, opposite to PNN rhythms. Finally, incubation of mouse sections with cathepsin-S eliminated PNN labeling. In humans, WFA1 PNNs showed a diurnal rhythm in the amygdala and thalamic reticular nucleus (TRN). Our results demonstrate that PNNs vary in a circadian manner and this is disrupted by sleep deprivation. We suggest that rhythmic modification of PNNs may contribute to memory consolidation during sleep.

Perineuronal Nets (PNNs) are extracellular matrix (ECM) structures that envelop neurons and regulate synaptic functions. Long thought to be stable structures, PNNs have been recently shown to respond dynamically during learning, potentially regulating the formation of new synapses. We postulated that PNNs may vary during sleep, a period of active synaptic modification. Notably, PNN components are cleaved by matrix proteases such as the protease cathepsin-S, synthesized by microglia. Cathepsin-S is expressed in a diurnal manner in the mouse cortex, coinciding with dendritic spine density rhythms. Thus, cathepsin-S may induce PNN remodeling during sleep, mediating synaptic reorganization. These studies were designed to test the hypothesis that PNN numbers vary in a diurnal manner in the rodent and human brain, and in a circadian manner in the rodent brain, in association with cathepsin-S expression rhythms coinciding with reported rhythms in synaptic plasticity. In mice, we observed diurnal and circadian rhythms of PNNs labeled with the lectin wisteria floribunda agglutinin (WFA+PNNs) in several brain regions involved in emotional memory processing. Sleep deprivation prevented the daytime decrease of WFA+ PNNs. Diurnal rhythms of cathepsin-S expression in microglia were observed in the same brain regions, opposite to PNN rhythms. Finally, incubation of mouse sections with cathepsin-S eliminated PNN labeling. In humans, WFA+PNNs showed a diurnal rhythm in the amygdala and thalamic reticular nucleus (TRN). Our results demonstrate that PNNs vary in a circadian manner that coincides with expression rhythms of cathepsin-S in the mouse hippocampus. We suggest that rhythmic modification of PNNs may contribute to memory consolidation during sleep.

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Objective: Smith and Burger developed the Structured Inventory of Malingered Symptomatology (SIMS) in 1997 as a self-report measure for malingering of psychiatric symptoms. The SIMS consists of 75 dichotomous (True-False) items that form into five subscales Psychosis (P), Neurologic Impairment (NI), Affective Disorder (AF), Amnestic Disorders (AM), Low Intelligence (LI), with each subscale containing 15 items. In this study, we aimed to examine the reliability, validity, and factor structure of the SIMS in a Turkish forensic psychiatry sample. Methods: A sample of 103 forensic patients (9 female, 94 male), aged 18-75, undergoing an inpatient forensic evaluations for competency assessment for criminal responsibility were recruited from a large forensic hospital in Turkey. The study protocol was approved by the local ethics committee. Socio-demographic information of the participants was collected and the SIMS, Miller Forensic Assessment of Symptoms Test (M-FAST), the Scales of Psychological Well-being, 36-Item Short Form Survey (SF-36), Beck Depression Inventory (BDI) and Beck Anxiety Inventory (BAI) were administered. All statistical analyses were performed by using SPSS version 23.0 for Windows. Results: The Cronbach's alpha coefficients for the Turkish SIMS were ranging from 0.42 to 0.87. The lowest alpha coefficient was observed for the Amnestic Disorders (0.46). For the whole scale, Cronbach's alpha coefficient was found to be 0.93. The test-retest (at after 1 week) correlation coefficients for Psychosis (P), Neurologic Impairment (NI), Affective Disorder (AF), Amnestic Disorders (AM), Low Intelligence (LI), and whole scale were found to be 0.97, 0.97, 0.95, 0.91, and 0.96, respectively. A positive and statistically significant correlation was found between the Turkish SIMS and BDI (r = 0.593, p < .