The amygdala contributes towards emotional processes such as fear, anxiety and social cognition. Further, evidence suggests that increased excitability of basolateral amygdala (BLA) principal neurons underlie certain neuropsychiatric disorders. Gain-of-function mutations in neuronal L-type calcium channels (LTCCs) are linked to neurodevelopmental diseases including autism spectrum disorders (ASDs). While LTCCs are expressed throughout the BLA, direct evidence for increased LTCC activity affecting BLA excitability and potentially contributing to disease pathophysiology is lacking. Here, we utilized a pharmacological approach to examine the contributions of LTCCs to BLA principal cell excitability and synaptic activity at immature (P7) and juvenile (P21) developmental stages. Acute upregulation of LTCC activity in brain slices by application of the agonist (S)-Bay K8644 resulted in increased intrinsic excitability properties including firing frequency response, plateau potential and spike frequency adaptation selectively in P7 neurons. Contrastingly, for P21 neurons the main effect of (S)-Bay K8644 was to enhance burst-firing. (S)-Bay K8644 increased spontaneous inhibitory synaptic currents at both P7 and P21 but did not affect evoked synaptic currents at either stage. (S)-Bay K8644 did not alter P7 spontaneous excitatory synaptic currents although increased current amplitude in P21 neurons. Overall, the results provide support for the notion that alteration of LTCC activity at specific periods of early brain development may lead to functional alterations to neuronal network activity, and subsequently contribute to underlying mechanisms of amygdala-related neurological disorders.