Identifying and avoiding potentially harmful food is crucial for the survival of many organisms. Conditioned taste aversion (CTA) is an associative learning paradigm when a novel appetitive tastant (e.g., saccharin) paired with a malaise-inducing agent, such as intraperitoneal injection of lithium chloride (LiCl), induces an aversion towards the same tastant when presented again. Recently, we have demonstrated that taste valence is encoded, at least in part, by changes in the intrinsic and synaptic properties of layer V/VI projecting neurons in aIC. Recent rodent studies have demonstrated that conditioned immune suppression or activation leads to taste aversion. This can be achieved by pairing a neutral stimulus (CS) with an unconditioned stimulus (US), the drugs that elicit the physiological and immune response like lipopolysaccharide (LPS). It has been shown that the aIC and pIC are reciprocally connected. However, the functional connectivity within the insula, especially following the retrieval of conditioned taste aversion, remains largely unknown. Using retrograde viral tracing and whole-cell patch-clamp electrophysiology, we demonstrated that at the baseline level, the excitability of aIC to pIC neurons is different from that of pIC–aIC neurons. The retrieval of conditioned taste changes the intrinsic excitability of layer V/VI, aIC-pIC, but not the pIC-aIC projection neurons. In addition, we have demonstrated that these intrinsic changes are correlated with an increased synaptic inhibition of aIC-pIC neurons. Our study highlights the importance of the plasticity changes in neuronal intrinsic and synaptic properties of aIC-pIC projecting neurons in the confidence of taste valence encoding.