Neuromodulators like dopamine are critical regulators of associative learning. Indeed, dopaminergic neurons in the dorsal tegmental area interact with the lateral central amygdala (CEl) circuitry involved in fear behavior. Thus, fear learning modulates the microcircuit of the CEl composed of somatostatin-positive (SST+) and protein kinase C-positive (PKCδ+) neurons. During this process, dopamine 1 receptor (D1R) activation enables LTP induction in SST+ CEl neurons (Groessl et al. 2018, Nat Neurosci 21:952-962).In fact, a detailed analysis of dopaminergic cellular effects on synaptic transmission in SST+ and PKCδ+ neurons in the CEl is lacking. Therefore, we conducted patch-clamp recordings in an in vitro slice preparation of the lateral central amygdala (CEl). EPSCs were evoked by a stimulating electrode positioned in the basal amygdala. Neurons were identified by fluorescence in the progeny of the respective driver mouse line bred with a reporter mouse line.Interestingly, the amplitude of evoked EPSCs (eEPSCs) declined reversibly in the presence of dopamine in both cell types. This effect was abolished in the continuous presence of the dopamine 2 receptor (D2R) antagonist sulpiride. In SST+ as well as PKCδ+ neurons, dopamine application did not affect paired-pulse facilitation. Analysis of miniature EPSC amplitude and frequency revealed a significant reduction in frequency only, indicating a presynaptic site of action.These results show reduced efficacy of glutamatergic synaptic transmission in the presence of dopamine in SST+ as well as PKCδ+ neurons in the CEl.Supported by Deutsche Forschungsgemeinschaft (DFG) – Project number 449735246, and by the Austrian Science Fund (FWF) grant I5074.