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Abstract: In this work, a systematic theoretical investigation on a series of dimeric complexes formed between MH2 and HX has been carried out by employing correlated ab initio methods. It was shown that besides dihydrogen bonds, there also exists novel noncovalent X⋯H interactions between the two molecules, which have similar characteristics to traditional halogen bonds. Upon complexation, the Hend to elongate in all cases, concomitant with red-shifts of the Hing frequencies. X⋯H interaction energies, calculated at the MP2/aug-cc-pvtz level, range from −2.11 to −11.78kJ/mol; the interactions are much weaker than corresponding dihydrogen bonds. The major stabilization source of dihydrogen and halogen bonds arises from the electrostatic force, while charge-transfer force plays a minor role in the formation of the complexes. AIM analyses further confirm the presence of X⋯H interactions in the systems, and the electron density at bond critical points correlates fairly well with the interaction energy. [Copyright &y& Elsevier]

Background: The underlying molecular mechanisms of the excitatory/inhibitory (E/I) imbalance induced by sevoflurane exposure to neonates remain poorly understood. This study aimed to investigate the long-term effects of prolonged sevoflurane exposure to neonatal rats during the peak period of synaptogenesis on the changes of trans-synaptic neurexin-neuroligin interactions, synaptic ultrastructure in the hippocampus and cognition.Methods: A total of 30 rat pups at postnatal day (P) 7 was randomly divided into two groups: the control group (exposed to 30 % oxygen balanced with nitrogen) and the sevoflurane group (exposed to 2.5 % sevoflurane plus 30 % oxygen balanced with nitrogen) for 6 h. Neurocognitive behaviors were assessed with the Open field test at P23-25 and the Morris water maze test at P26-30. The expression of β-neurexin (β-NRX), N-methyl-d-aspartate receptor 2 subunit (NR2A and NR2B), neuroligin-1 (NLG-1), neuroligin-2 (NLG-2), postsynaptic density protein-95 (PSD-95), α1-subunit of the γ-aminobutyric acid A receptor (GABAAα1) and gephyrin in the hippocampus at P30 were measured by Western blot. The ultrastructure of synapses was examined under electron microscope.Results: Prolonged sevoflurane exposure at P7 resulted in cognitive deficiency in adolescence, as well as the downregulation of β-NRX, NR2A, NR2B, NLG-1, and PSD-95, and the upregulation of GABAAα1, NLG-2, and gephyrin in the hippocampal CA3 region. Sevoflurane anesthesia also increased the number of symmetric synapses in the hippocampus.Conclusions: Prolonged sevoflurane exposure during the brain development leads to cognitive deficiency and disproportion of excitatory/inhibitory synapses which may be caused by dysregulated expression of synaptic adhesion molecules of β-NRX and neuroligins. [ABSTRACT FROM AUTHOR]