The basolateral amygdala (BLA) is critical for the generation of emotional behavior and the formation of emotional memory. Understanding the neuronal mechanisms that contribute to emotional information processing in the BLA will ultimately require knowledge of the anatomy and physiology of its constituent neurons. Two major cell classes exist in the BLA, pyramidal projection neurons and nonpyramidal interneurons. Although the properties of projection neurons have been studied in detail, little is known about the properties of BLA interneurons. We have used whole‐cell patch clamp recording techniques to examine the physiological properties of 48 visually identified putative interneurons from the rat anterior basolateral amygdalar nucleus. Here, we report that BLA interneurons can be differentiated into four electrophysiologically distinct subtypes based on their intrinsic membrane properties and their response to afferent synaptic input. Interneuron subtypes were named according to their characteristic firing pattern generated in response to transient depolarizing current injection and were grouped as follows: 1) burst‐firing interneurons (n = 13), 2) regular‐firing interneurons (n = 11), 3) fast‐firing interneurons (n = 10), and 4) stutter‐firing interneurons (n = 14). Post hoc histochemical visualization confirmed that all 48 recorded neurons had morphological properties consistent with their being local circuit interneurons. Moreover, by using triple immunofluorescence (for biocytin, calcium‐binding proteins, and neuropeptides) in conjunction with patch clamp recording, we further demonstrated that over 60% of burst‐firing and stutter‐firing interneurons also expressed the calcium‐binding protein parvalbumin (PV⁺). These data demonstrate that interneurons of the BLA show both physiological and neurochemical diversity. Moreover, we demonstrate that the burst‐ and stutter‐firing patterns positively correlate with PV⁺ immunoreactivity, suggesting that these neurons may represent functionally distinct subpopulations. J. Comp. Neurol. 498:142–161, 2006. © 2006 Wiley‐Liss, Inc.