GABA (gamma-aminobutyric acid) regulates neuronal excitability and network activity by activating GABAA channels that generate phasic and tonic currents. The pancreatic hormone insulin, in addition to its critical role in peripheral glucose regulation, has effects on neuronal excitability and memory functions. Hippocampus and amygdala , both important components of the limbic system participate in the memory formation. We have previously shown that insulin can enhance the GABAA mediated tonic conductance in rat hippocampal CA1 neurons (Jin Z, et al., 2011). The aim of this study is to investigate 1) if insulin receptor is expressed in the rat and human amygdala 2) the effect of insulin on GABAA channels-mediated inhibition in rat hippocampal and amygdala neurons. Quantitative RT-PCR was run on total RNAs isolated from rat and human post-mortem amygdala. Standard whole-cell and single channel recordings were performed on hippocampal and amygdala slices were prepared from postnatal 16-22 days old Wistar rats and incubated with ACSF (artificial cerebrospinal fluid) or low physiological concentration of insulin. The mRNA transcript for insulin receptor was detected in both rat (n=3) and human (n=12) amygdala samples. In the rat amygdala, the insulin receptor was expressed in both the central nucleus and the basolateral nucleus. The incubation of 1nM insulin increased GABAA-mediated tonic currents in rat hippocampal CA1 neurons (n=24) and reduced the action potential firing frequency (n=13). The enhanced tonic current is partially carried by alpha5, gamma2 containing GABAA channels. The insulin-induced GABAA channels have very high-affinity (pM) with novel pharmacological profile. Our results suggest GABAA-mediated tonic conductance regulate basal neuronal excitability when it is prominently expressed.