Search

A series of low-cost Lewis acidic deep eutectic solvents (DESs) was synthesized and applied for the first time for catalyzing the polymerization of α-pinene to produce terpene resins. The DES catalyst of [AlCl3]3[CPL] prepared via the self-assembly of AlCl3 and caprolactam (CPL) exhibited the highest catalytic activity, and polymerization conditions were optimized by a single-factor method: 15 g α-pinene, 3 g catalyst, 1 g initiator, −5 °C reaction temperature, and 4 h reaction time. Under these conditions, the softening point of the terpene resin reached (annular spheroid method) 118.3 °C, the acid value was 0.22 mg KOH g−1, and the depth of color (Fe–Co method) was 5. The structure of [AlCl3]3[CPL] was characterized using FT-IR, 1H-NMR, and UV-vis spectroscopy. GPC measure showed that the number-average molecular weight of the terpene resin was 510, the weight-average molecular weight was 776, and the polydispersity index was 1.523. TG results indicated that the terpene resin had favorable thermal stability. After the reaction, the product and the catalyst could be automatically divided into two phases, which was beneficial for recycling the catalyst. The results revealed that [AlCl3]3[CPL] exhibited good recyclability. [ABSTRACT FROM AUTHOR]

Aims: The basolateral amygdala (BLA) plays an integral role in anxiety disorders (such as post traumatic stress disorder) stem from dysregulated fear memory. The excitability of glutamatergic neurons in the BLA correlates with fear memory, and the afterhyperpolarization current (IAHP) mediated by small‐conductance calcium‐activated potassium channel subtype 2 (SK2) dominates the excitability of glutamatergicneurons. This study aimed to explore the effect of MPP2 interacts with SK2 in the excitability of glutamatergic neurons in the BLA and the extinction of conditioned fear in mice. Methods: Fear memory was analyzed via freezing percentage. Western blotting and fluorescence quantitative PCR were used to determine the expression of protein and mRNA respectively. Electrophysiology was employed to measure the excitability of glutamatergic neurons and IAHP. Results: Fear conditioning decreased the levels of synaptic SK2 channels in the BLA, which were restored following fear extinction. Notably, reduced expression of synaptic SK2 channels in the BLA during fear conditioning was caused by the increased activity of protein kinase A (PKA), while increased levels of synaptic SK2 channels in the BLA during fear extinction were mediated by interactions with membrane‐palmitoylated protein 2 (MPP2). Conclusions: Our results revealed that MPP2 interacts with the SK2 channels and rescues the excitability of glutamatergic neurons by increasing the expression of synaptic SK2 channels in the BLA to promote the normalization of anxiety disorders and provide a new direction for the treatment. [ABSTRACT FROM AUTHOR]