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In order to improve the flame retardancy of polycarbonate/acrylonitrile-butadiene-styrene (PC/ABS) alloy, the flame retardant formula system was explored by the method of compound synergy. Taking the limiting oxygen index (LOI) and vertical combustion grade (UL-94) of PC/ABS composites as the main indexes, a binary flame retardant formula system with aluminum diethylphosphinate (ADP) as the main flame retardant and 9, 10-dihydro-9-oxa-10-phosphaphenanthrene-10-oxide (DOPO) as the synergistic flame retardant was constructed. PC/ABS/binary flame retardant composites were prepared by mixing PC/ABS and binary flame retardant systems. The flame retardancy, mechanical properties, combustion characteristics and thermal stability of PC/ABS composites were studied by UL-94 vertical combustion test, oxygen index (LOI) test, mechanical property test, cone calorimetry test and thermogravimetric analysis test. The results show that when the mass ratio of ADP to DOPO is 3:1 and the total addition amount of binary flame retardant formula system is 15.0%, PC/ABS composites have excellent flame retardancy, mechanical properties, combustion characteristics and thermal stability. [ABSTRACT FROM AUTHOR]

Aims: Central melanocortin 4 receptor (MC4R) has been reported to induce anhedonia via eliciting dysfunction of excitatory synapses. It is evident that metabolic signals are closely related to chronic stress‐induced depression. Here, we investigated that a neural circuit is involved in melanocortin signaling contributing to susceptibility to stress. Methods: Chronic social defeat stress (CSDS) was used to develop depressive‐like behavior. Electrophysiologic and chemogenetic approaches were performed to evaluate the role of paraventricular thalamus (PVT) glutamatergic to nucleus accumbens shell (NAcsh) circuit in stress susceptibility. Pharmacological and genetic manipulations were applied to investigate the molecular mechanisms of melanocortin signaling in the circuit. Results: CSDS increases the excitatory neurotransmission in NAcsh through MC4R signaling. The enhanced excitatory synaptic input in NAcsh is projected from PVT glutamatergic neurons. Moreover, chemogenetic manipulation of PVTGlu‐NAcsh projection mediates the susceptibility to stress, which is dependent on MC4R signaling. Overall, these results reveal that the strengthened excitatory neurotransmission in NAcsh originates from PVT glutamatergic neurons, facilitating the susceptibility to stress through melanocortin signaling. Conclusions: Our results make a strong case for harnessing a thalamic circuit to reorganize excitatory synaptic transmission in relieving stress susceptibility and provide insights gained on metabolic underpinnings of protection against stress‐induced depressive‐like behavior. [ABSTRACT FROM AUTHOR]

Summary: Aims: Palmitoylation of α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid receptors (AMPARs) subunits or their "scaffold" proteins produce opposite effects on AMPAR surface delivery. Considering AMPARs have long been identified as suitable drug targets for central nervous system (CNS) disorders, targeting palmitoylation signaling to regulate AMPAR function emerges as a novel therapeutic strategy. However, until now, much less is known about the effect of palmitoylation‐deficient state on AMPAR function. Herein, we set out to determine the effect of global de‐palmitoylation on AMPAR surface expression and its function, using a special chemical tool, N‐(tert‐Butyl) hydroxylamine (NtBuHA). Methods: BS3 protein cross‐linking, Western blot, immunoprecipitation, patch clamp, and biotin switch assay. Results: Bath application of NtBuHA (1.0 mM) reduced global palmitoylated proteins in the hippocampus of mice. Although NtBuHA (1.0 mM) did not affect the expression of ionotropic glutamate receptor subunits, it preferentially decreased the surface expression of AMPARs, not N‐methyl‐d‐aspartate receptors (NMDARs). Notably, NtBuHA (1.0 mM) reduces AMPAR‐mediated excitatory postsynaptic currents (mEPSCs) in the hippocampus. This effect may be largely due to the de‐palmitoylation of postsynaptic density protein 95 (PSD95) and protein kinase A‐anchoring proteins, both of which stabilized AMPAR synaptic delivery. Furthermore, we found that changing PSD95 palmitoylation by NtBuHA altered the association of PSD95 with stargazin, which interacted directly with AMPARs, but not NMDARs. Conclusion: Our data suggest that the palmitoylation‐deficient state initiated by NtBuHA preferentially reduces AMPAR function, which may potentially be used for the treatment of CNS disorders, especially infantile neuronal ceroid lipofuscinosis (Batten disease). [ABSTRACT FROM AUTHOR]