a b s t r a c tAdolescence is increasingly recognized as a critical period for the development of the social system, through the maturation of social competences and of their underlying neural circuitries. The present study sought to test the utility of resveratrol, a dietary phenol recently reported to have mood lifting properties, in modulating social interaction that is deficient following early life adversity. The main aims were to 1) pharmacologically restore normative social investigation levels dampened by peripubertal stress in rats and 2) identify neural pathways engaged by this pharmacological approach. Following peripubertal (P28e42) stress consisting of unpredictable exposures to fearful experiences, at adulthood the subjects' propensity for social exploration was examined in the three-chamber apparatus, comparing time invested in social or non-social investigation. Administered intraperitoneally 30 min before testing, resveratrol (20 mg/kg) normalized the peripubertal stress-induced social investigation deficit seen in the vehicle group, selectively altering juvenile but not object exploration. Examination of prefrontal cortex subregion protein samples following acute resveratrol treatment in a separate cohort revealed that while monoamine oxidase A (MAOA) enzymatic activity remained unaltered, nuclear AKT activation was selectively increased in the infralimbic cortex, but not in the prelimbic or anterior cingulate cortex. In contrast, androgen receptor nuclear localization was increased in the prelimbic cortex, but not in the infralimbic or anterior cingulate cortex. This demonstration that social contact deficits are reversed by resveratrol administration emphasizes a prosocial role for this dietary phenol, and evokes the possibility of developing new treatments for social dysfunctions.
The aim of this study was to investigate the effect of three metal priming agents on the bond strength of adhesive resin cement to Silver-Zinc-Tin-Indium (Ag-Zn-Sn-In) alloy and pure Ag, Zn, Sn, and In. The specimens were air-abraded with alumina and then primed with one of three metal priming agents: V-Primer, Estenia Opaque Primer, or Alloy Primer. The metal disks were bonded with adhesive resin cement (Super-Bond Bulk-mix technique). Shear bond strengths (n=10/group) were determined before and after 50,000 thermocycles for Ag-Zn-Sn-In alloy as well as after 5,000 thermocycles for pure Ag, Zn, Sn and In. For Ag-Zn-Sn-In alloy, the post-thermocycling bond strength of the Alloy Primer group was significantly higher than that of the other primers. It can be concluded that Alloy Primer containing both the vinyl-thione monomer (VBATDT) and hydrophobic phosphate monomer (MDP) is effective for bonding Ag-Zn-Sn-In alloy and pure Ag, Zn and Sn.
Homer1a, an activity-dependent induced member of the scaffold protein family Homer, plays an essential role in synaptic reorganization and is widely used as a neuronal activity marker. However, the cell type transcribing Homer1a remains unidentified. Here, we investigated the main cell types of the amygdala, hippocampus, primary somatosensory cortex, and dorsal striatum that express Homer1a. Homer1a expression relevant to the baseline neural activity as well as exposure to unfamiliar and conditioned contexts was preferentially detected in the excitatory neurons within the basolateral amygdala, hippocampus, and neocortex, and in inhibitory neurons within the central amygdala and dorsal striatum. These findings indicate that Homer1a is expressed in the principal neurons of each region regardless of whether they are excitatory or inhibitory neurons.
Conditioned fear is extinguished if a conditioned animal receives the conditioned stimulus without an unconditioned stimulus. The extinguished fear response can be reinstated after the animal experiences a mild unconditioned stimulus. Although extensive studies on the neuronal circuitry and neurochemical mechanisms leading to fear acquisition and extinction have been carried out, few studies have focused on reinstatement. In this study, we investigated the effects of N-methyl-D-aspartic acid receptor (NMDAR) antagonists, protein synthesis inhibitors, cannabinoid receptor type 1 (CB1R) antagonists, and benzodiazepine on reinstatement of conditioned fear in mice. An intraperitoneal injection of the NMDAR antagonist MK-801 or the protein synthesis inhibitor anisomycin before the reminder shock attenuated fear reinstatement tested the next day. However, anisomycin had no effect on fear reinstatement tested 2 h after the reminder shock. CB1R antagonists, SR141716, and a benzodiazepine, diazepam, had no effect on fear reinstatement. These results suggested that NMDAR and protein synthesis-dependent plasticity contributed toward the reinstatement of conditioned fear and that protein synthesis was involved in consolidation of reinstated fear.
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