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Drug relapse can be mainly ascribed to the retrieval of drug withdrawal memory induced by conditioned context. Previous studies have shown that the central nucleus of the amygdala lateral division (CeL) could be activated by conditioned context. However, what source of input that activates the CeL during conditioned context-induced retrieval of morphine-withdrawal memory remains unknown. In this study, using retrograde labeling, immunohistochemistry, local microinjection and chemogenetic technologies, we found that (1) Conditioned context induced an activation of the CeL and the inhibition of the CeL inhibited the context-induced retrieval of morphine-withdrawal memory; (2) the inhibition of the paraventricular nucleus of thalamus (PVT) or PVT-CeL projection neurons caused an attenuation of the activation of the CeL by conditioned context and conditioned place aversion (CPA); (3) the inhibition of the locus coeruleus (LC) or LC-CeL projection neurons decreased the activation of the CeL by conditioned context and CPA. These results suggest that the CeL is necessary for conditioned context-induced retrieval of morphine-withdrawal memory and inputs from PVT and LC contribute to the activation of the CeL during context-induced retrieval of morphine withdrawal memory. • CeL plays an important role in conditioned context-induced retrieval of morphine-withdrawal memory • PVT is an upstream brain region activating CeL during conditioned context-induced retrieval of morphine-withdrawal memory • LC is another upstream brain region of the activation of CeL which plays the same role as PVT [ABSTRACT FROM AUTHOR]

Chronic morphine withdrawal memory formation is a complex process influenced by various molecular mechanisms. In this study, we aimed to investigate the contributions of the basolateral amygdala (BLA) and complement component 1, q subcomponent-like 3 (C1QL3), a secreted and presynaptically targeted protein, to the formation of chronic morphine (repeat dosing of morphine) withdrawal memory using conditioned place aversion (CPA) and chemogenetic methods. We conducted experiments involving the inhibition of the BLA during naloxone-induced withdrawal to assess its impact on CPA scores, providing insights into the significance of the BLA in the chronic morphine memory formation process. We also examined changes in C1ql3 /C1QL3 expression within the BLA following conditioning. Immunofluorescence analysis revealed the colocalization of C1QL3 and the G protein-coupled receptor, brain-specific angiogenesis inhibitor 3 (BAI3) in the BLA, supporting their involvement in synaptic development. Moreover, we downregulated C1QL3 expression in the BLA to investigate its role in chronic morphine withdrawal memory formation. Our findings revealed that BLA inhibition during naloxone-induced withdrawal led to a significant reduction in CPA scores, confirming the critical role of the BLA in this memory process. Additionally, the upregulation of C1ql3 expression within the BLA postconditioning suggested its participation in withdrawal memory formation. The colocalization of C1QL3 and BAI3 in the BLA further supported their involvement in synaptic development. Furthermore, downregulation of C1QL3 in the BLA effectively hindered chronic morphine withdrawal memory formation, emphasizing its pivotal role in this process. Notably, we identified postsynaptic density protein 95 (PSD95) as a potential downstream effector of C1QL3 during chronic morphine withdrawal memory formation. Blocking PSD95 led to a significant reduction in the CPA score, and it appeared that C1QL3 modulated the ubiquitination-mediated degradation of PSD95, resulting in decreased PSD95 protein levels. This study underscores the importance of the BLA, C1QL3 and PSD95 in chronic morphine withdrawal memory formation. It provides valuable insights into the underlying molecular mechanisms, emphasizing their significance in this intricate process. • BLA inhibition reduces chronic morphine withdrawal memory conditioned place aversion scores. • Downregulation of C1QL3 in the BLA hinders chronic morphine withdrawal memory formation. • PSD95 was identified as a downstream effector of C1QL3, influencing chronic morphine withdrawal memory. [ABSTRACT FROM AUTHOR]

Compared with lithium-ion batteries, sodium-ion batteries possess the advantages of low cost and high energy density. The research and development of the positive, negative and electrolyte materials of sodium-ion batteries is of great significance to develop sodium-ion energy storage devices. The sodium superionic conductor (NASICON) with a stoichiometric ratio of Na 3 Sc 2 P 3 O 12 (NSP) has a variety of crystal types, namely α-, β- and γ-phase. Different crystal structures exhibit different ion transport characteristics, resulting in the varied ionic conductivity and other electrochemical performance. The effect of different crystalline-type Na 3 Sc 2 P 3 O 12 (α-Na 3 Sc 2 P 3 O 12 , β-Na 3.5 Sc 2 P 2.5 Si 0.5 O 12 and γ-Na 4 Sc 2 P 2 SiO 12) fillers on gel polymer electrolytes (GPE) was investigated in detail. Due to the difference in the adsorption capacity of the gel electrolyte added three types of crystalline-type fillers and the difference in the conductivity of fillers, the composite gel electrolytes exhibited various performances. The optimal gel electrolyte with 7 ​% γ-Na 4 Sc 2 P 2 SiO 12 filler delivers the optimal conductivity as high as 2.783 ​× ​10−3 ​S ​cm−1. The optimal performance of Na 3 V 2 (PO 4) 3 /C| GPE |Na cell shows that the first discharge specific capacity was 92.3 mAh g−1 with a capacity retention rate of 98.18% after 100 cycles. Different crystalline-type sodium conductive filler (α-Na 3 Sc 2 P 3 O 12 , β-Na 3.5 Sc 2 P 2.5 Si 0.5 O 12 and γ-Na 4 Sc 2 P 2 SiO 12) modified GPEs membranes with enhanced ionic conductivity were fabricated and the application performances in sodium ions batteries (SIBs) were demonstrated. [Display omitted] • Sodium conductive Na 3 Sc 2 P 3 O 12 filler with three types of crystal phases modified GPEs were fabricated. • Ionic conductivity of GPEs was enhanced with the presence of Na 3 Sc 2 P 3 O 12 filler. • Na 3 Sc 2 P 3 O 12 filler decreased the crystallinity and enlarged the porosity of GPEs. • GPEs membranes delivered competitive electrochemical performances applied in SIBs. [ABSTRACT FROM AUTHOR]