Synaptic dysfunction represents the core pathological basis underlying cognitive impairment in the pathological progression of Alzheimer''s disease (AD). Owing to the early onset of amyloid-β (Aβ) deposition and its rapid pathological progression, the 5xFAD mouse has become a widely utilized transgenic animal model for investigating AD-related synaptic pathological mechanisms. ThePatch-clamp techniques enable the electrophysiological characterization of this model at multiple levels, including synaptic transmission, synaptic plasticity, and intrinsic neuronal excitability. Current studies have shown that 5xFAD mice exhibit alterations in synaptic transmission, long-term potentiation(LTP), and intrinsic excitability at different ages stages, displaying distinct phenotypes characterized by marked age dependence, brain region specificity, and cell type differences. The underlying mechanisms potentially involve amyloid-β deposition-induced pre- and postsynaptic dysfunction, impairment of inhibitory interneurons, disruption of excitatory/inhibitory(E/I) balance, and abnormal ion channel regulation. Future studies are warranted to systematically compare the electrophysiological features of 5xFAD mice across various ages, sexes, and brain regions under standardized experimental conditions,, and to establish a more standardized phenotypic evaluation system, thereby providing valuable reference for the application of 5xFAD mice as an AD model and for elucidating the mechanisms underlying synaptic dysfunction.