Repeat investigation during social preference behavior is suppressed in male mice with prefrontal cortex (Ca1.2)-deficiency through the dysregulation of neural dynamics.

Impairments in social behavior are observed in a range of neuropsychiatric disorders and several lines of evidence have demonstrated that dysfunction of the prefrontal cortex (PFC) plays a central role in social deficits. We have previously shown that loss of neuropsychiatric risk gene that codes for the Ca1.2 isoform of L-type calcium channels (LTCCs) in the PFC result in impaired sociability as tested using the three-chamber social approach test.

Exploring opportunities for tuning phenyltris(pyrazol-1-yl)borate donation by varying the extent of phenyl substituent fluorination.

The importance of electron deficient Tp ligands motivates the introduction of electron-withdrawing substituents into the scorpionate framework. Since perfluorophenyltris(pyrazol-1-yl)borate affects significant anodic shifts in half-cell potentials in their metal complexes relative those of phenyltris(pyrazol-1-yl)borate analogues, the tuning opportunities achieved using 3,4,5-trifluorophenyl- and 3,5-bis(trifluoromethyl)phenyl(pyrazol-1-yl)borates were explored. Bis(amino)boranes ((3,4,5-F)CH)B(NMe) and ((3,5-CF)CH)B(NMe) are precursors to fluorinated tris(pyrazol-1-yl)phenylborates.