RESUMO
Inhibitory γ-aminobutyric acid (GABA)-ergic interneurons mediate inhibition in neuronal circuitry and support normal brain function. Consequently, dysregulation of inhibition is implicated in various brain disorders. Parvalbumin (PV) and somatostatin (SST) interneurons, the two major types of GABAergic inhibitory interneurons in the hippocampus, exhibit distinct morpho-physiological properties and coordinate information processing and memory formation. However, the molecular mechanisms underlying the specialized properties of PV and SST interneurons remain unclear. This study aimed to compare the transcriptomic differences between these two classes of interneurons in the hippocampus using the ribosome tagging approach. The results revealed distinct expressions of genes such as voltage-gated ion channels and GABAA receptor subunits between PV and SST interneurons. Gabrd and Gabra6 were identified as contributors to the contrasting tonic GABAergic inhibition observed in PV and SST interneurons. Moreover, some of the differentially expressed genes were associated with schizophrenia and epilepsy. In conclusion, our results provide molecular insights into the distinct roles of PV and SST interneurons in health and disease.
RESUMO
Herein, we report a "threading followed by shrinking" approach for the synthesis of rotaxanes by using an "oxygen-deficient" macrocycle that contained two arylmethyl sulfone units and the dumbbell-shaped salt bis(3,5-dimethylbenzyl)ammonium tetrakis(3,5-trifluoromethylphenyl)borate as the host and guest components, respectively. The extrusion of SO2 from both of the arylmethyl sulfone units of the macrocyclic component in the corresponding [2]pseudorotaxane resulted in a [2]rotaxane that was sufficiently stable to maintain its molecular integrity in CD3 SOCD3 at 393 K for at least 5 h.
RESUMO
Making the right choice: Tetrakis(3,5-trifluoromethylphenyl)borate (TFPB) counter anions can facilitate the threading of dibenzylammonium (DBA(+)) ions through macrocycles in cases where the corresponding PF(6)(-) salts fail to exhibit complexation.