Triel Bonds, pi-Hole-pi-Electrons Interactions in Complexes of Boron and Aluminium Trihalides and Trihydrides with Acetylene and Ethylene

MP2/aug-cc-pVTZ calculations were performed on complexes of aluminium and boron trihydrides and trihalides with acetylene and ethylene. These complexes are linked through triel bonds where the triel center (B or Al) is characterized by the Lewis acid properties through its -hole region while -electrons of C2H2 or C2H4 molecule play the role of the Lewis base. Some of these interactions possess characteristics of covalent bonds, i.e., the Al--electrons links as well as the interaction in the BH3-C2H2 complex. The triel--electrons interactions are classified sometimes as the 3c-2e bonds. In the case of boron trihydrides, these interactions are often the preliminary stages of the hydroboration reaction. The Quantum Theory of Atoms in Molecules as well as the Natural Bond Orbitals approach are applied here to characterize the -hole--electrons interactions.

Cytokine pathway disruption in a mouse model of schizophrenia induced by Munc18-1a overexpression in the brain

Background: An accumulating body of evidence points to the significance of neuroinflammation and immunogenetics in schizophrenia, and an imbalance of cytokines in the central nervous system (CNS) has been suggested to be associated with the disorder. Munc18-overexpressing mice (Munc18-OE) have provided a model for the study of the alterations that may underlie the symptoms of subjects with schizophrenia. The aim of the present study was to elucidate the involvement of neuroinflammation and cytokine imbalance in this model. Methods: Cytokines were evaluated in the cortex and the striatum of Munc18-OE and wild-type (WT) mice by enzyme-linked immunosorbent assay (ELISA). Protein levels of specific microglia and macrophage, astrocytic and neuroinflammation markers were quantified by western blot in the cortex and the striatum of Munc18-OE and WT mice. Results: Each cytokine evaluated (Interferon-gamma (IFN-gamma), Tumor Necrosis Factor-alpha (TNF-alpha), Interleukin-2 (IL-2) and CCL2 chemokine) was present at higher levels in the striatum of Munc18-OE mice than WT. Cortical TNF-alpha and IL-2 levels were significantly lower in Munc18-OE mice than WT mice. The microglia and macrophage marker CD11b was lower in the cortexes of Munc18-OE mice than WT, but no differences were observed in the striatum. Glial Fibrillary Acidic Protein (GFAP) and Nuclear Factor-kappaB (NF-kappa B)p65 levels were not different between the groups. Interleukin-1beta (IL-1 beta) and IL-6 levels were beneath detection limits. Conclusions: The disrupted levels of cytokines detected in the brain of Munc18-OE mice was found to be similar to clinical reports and endorses study of this type for analysis of this aspect of the disorder. The lower CD11b expression in the cortex but not in the striatum of the Munc18-OE mice may reflect differences in physiological activity. The cytokine expression pattern observed in Munc18-OE mice is similar to a previously published model of schizophrenia caused by maternal immune activation. Together, these data suggest a possible role for an immune imbalance in this disorder.