Compelling evidence now suggests that early life immune challenges during key developmental stages can have long lasting effects on brain excitability, neurochemistry, and behaviour. Perinatal and neonatal rat exposure to the inflammatory molecule, lipopolysaccharide (LPS), has demonstrable effects on memory formation and retrieval, anxiety, depression and fear responses. The amygdala complex has been identified as a likely locus for many of these functions and behaviours. I have thus hypothesized that neonatal exposure to LPS in rats will cause long-term alterations in the synaptic and membrane properties of amygdalar neurons. Neonatal (post natal day (P) 14) male and female Sprague Dawley rats were injected with LPS (100 µg/kg, ip) or saline and slices of the amygdalar complex were collected at various time points in adolescence and adulthood (P21-P60). Whole-cell voltage and current clamp recordings were obtained in basolateral amygdala neurons. Comparison of resting membrane potential, input resistance, and action potential characteristics in neonatal LPS- and saline-pretreated animals revealed that cells in LPS-treated rats are less excitable, with elevated firing thresholds. These alterations were not affected by age or sex of animals. I also stimulated afferent pathways to these cells and isolated glutamatergic synaptic currents. Compared to saline pretreated litter mates, LPS pretreated animals had increased glutamatergic paired pulse ratios, suggesting a depression in glutamatergic transmission. However, miniature excitatory post synaptic currents were similar in both groups. In contrast, GABAergic miniature inhibitory post synaptic currents occurred at higher frequencies. Thus neonatal LPS has long lasting effects upon some regenerative membrane properties and on synaptic transmission in the basolateral amygdala.