Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by early non-cognitive dysfunctions. Recent studies have reported synaptic alterations in limbic circuits in AD animal models, even before amyloid plaque appearance. The basolateral amygdala (BLA) is a critical region of the limbic system involved in diverse emotional processing, and studies in human and AD animal models have reported that it is altered in early AD. However, whether synaptic and excitability properties are altered in the BLA in AD has not been studied. In this study, we used 6-month-old APP/PS1 AD mice to examine the presence of AD pathology. Immunohistochemical experiments in coronal slices showed the presence of intracellular amyloid-beta (iAβ) compared to WT mice. Subsequently, we analysed excitatory and inhibitory synaptic activities using patch clamp technique, finding that the AMPAR-mediated mEPSCs transferred charge increased significantly in APP/PS1 mice. The transferred charge in WT and APP/PS1 mice was 52.4±4 and 93.1±17pA.ms, respectively. Conversely, GABAAR-mediated mIPSCs transferred charge was reduced from 133±9pA·ms in the WT to 105±8pA·ms in the APP/PS1 mice. Intrinsic membrane properties examined by current-clamp recordings showed that the number of action potentials decreased from 8±0.5 to 6.3±0.5 (250pA pulse). The value for membrane resistance was also reduced (WT:124±6.8MΩ; APP/PS1: 104±6.9MΩ). In conclusion, the data show that iAβ is overexpressed in the BLA of 6-month-old APP/PS1 mice. This increase was accompanied by an increase in the excitatory/inhibitory balance. Action potential firing was attenuated, suggesting the presence of compensatory mechanisms.