Due to the inappropriate use and overuse of antibiotics, the emergence and spread of antibiotic-resistant bacteria are increasing and have become a major threat to human health. A key factor in the treatment of bacterial infections and slowing down the emergence of antibiotic resistance is to perform antimicrobial susceptibility testing (AST) of infecting bacteria rapidly to prescribe appropriate drugs and reduce the use of broad-spectrum antibiotics. Current phenotypic AST methods based on the detection of bacterial growth are generally reliable but are too slow. There is an urgent need for new methods that can perform AST rapidly. Bacterial metabolism is a fast process, as bacterial cells double about every 20 to 30 min for fast-growing species. Moreover, bacterial metabolism has shown to be related to drug resistance, so a comparison of differences in microbial metabolic processes in the presence or absence of antimicrobials provides an alternative approach to traditional culture for faster AST. In this review, we summarize recent developments in rapid AST methods through metabolic profiling of bacteria under antibiotic treatment.

Antimicrobial resistance (AMR) is a global medical threat that seriously endangers human health. Rapid bacterial identification and antimicrobial susceptibility testing (AST) are key interventions to combat the spread and emergence of AMR. Although current clinical bacterial identification and AST provide comprehensive information, they are labor-intensive, complex, inaccurate, and slow (requiring several days, depending on the growth of pathogenic bacteria). Recently, Raman-based identification and AST technologies have played an increasingly important role in fighting AMR. This review summarizes major Raman-based techniques for bacterial identification and AST, including spontaneous Raman scattering, surface-enhanced Raman scattering (SERS), and coherent Raman scattering (CRS) imaging. Then, we discuss recent developments in rapid identification and AST methods based on Raman technology. Finally, we highlight the major challenges and potential future efforts to improve clinical outcomes through rapid bacterial identification and AST.

L-type Ca²⁺ (Ca_V1) channels transduce channel activities into nuclear signals critical to neuritogenesis. Also, standalone peptides encoded by Ca_V1 DCT (distal carboxyl-terminus) act as nuclear transcription factors reportedly promoting neuritogenesis. Here, by focusing on exemplary Ca_V1.3 and cortical neurons under basal conditions, we discover that cytosolic DCT peptides downregulate neurite outgrowth by the interactions with Ca_V1’s apo-calmodulin binding motif. Distinct from nuclear DCT, various cytosolic peptides exert a gradient of inhibitory effects on Ca²⁺ influx via Ca_V1 channels and neurite extension and arborization, and also the intermediate events including CREB activation and c-Fos expression. The inhibition efficacies of DCT are quantitatively correlated with its binding affinities. Meanwhile, cytosolic inhibition tends to facilitate neuritogenesis indirectly by favoring Ca²⁺-sensitive nuclear retention of DCT. In summary, DCT peptides as a class of Ca_V1 inhibitors specifically regulate the channel activity-neuritogenesis coupling in a variant-, affinity-, and localization-dependent manner.