Breathing in mammals depends on inspiratory-related neural activity generated in the preBoetzinger complex (preBoetC), where neurokinin receptor-expressing neurons (NKR⁺) have been hypothesized to play a critical rhythmogenic role. Currently, the extent to which the preBoetC is populated by rhythmogenic NKR⁺ neurons, and whether neurons without neurokinin receptor expression (NKR^-) share similar electrical properties with NKR⁺ neurons, are not well understood. These interrelated problems must be resolved to understand the widespread excitatory effects of neuropeptides and the mechanism of respiratory rhythmogenesis. We recorded and imaged inspiratory neurons in neonatal mouse slices that isolate the preBoetC and generate respiratory motor output in vitro. Using tetramethylrhodamine conjugated to the endogenous NKR agonist substance P (TMR-SP) to tag neurons that express NKRs, we show that early inspiratory neurons with small whole-cell capacitance (C_M) are 36% TMR-SP⁺ and 64% TMR-SP^-. Also, late inspiratory neurons with large C_M are 67% TMR-SP⁺ and 33% are TMR-SP^-. Thus NKR⁺ and NKR^- neurons exhibit the same phenotypic properties, which suggests that they may share functional roles too. Substance P (SP) alone evoked a voltage-insensitive inward current (I_SP) that reversed at -19 mV and was associated with an increase in membrane conductance in both NKR⁺ and NKR^- neurons. Gap junctions may be required to confer SP sensitivity to neurons that appear to lack NKR expression. We propose that cell death in NKR⁺ preBoetC neurons, by targeted lesion or neurodegeneration, may impair breathing behavior by killing less than half of the rhythmogenic preBoetC neurons and a large number of respiratory premotoneurons.