The primary olfactory cortex (piriform cortex) is a well-established epileptogenic site with the potential to amplify and generalize seizures. Disinhibition, caused by the synaptic inhibition of inhibitory neurons by other inhibitory neurons, increases the excitability of principal neurons and has been proposed as a contributing factor in numerous neurological diseases, including epilepsy. Therefore, unravelling inhibitory microcircuits in the piriform cortex may uncover new therapeutic avenues for treating epilepsy. Our study used whole-cell recordings from identified classes of inhibitory interneurons in the deeper, more epileptogenic layers of the piriform cortex. Consistent with earlier work, we identified four types of layer 2/3 interneurons: neurogliaform (NG), bitufted (BT), fast-spiking (FS) and regular-spiking (RS) cells. Using extracellular stimulation in the presence of glutamate receptor blockers, we found that NG and FS cells received much stronger inhibitory inputs than BT and RS cells. We next mapped electrical and synaptic connections between interneurons by using paired whole-cell recordings. We found that NG and FS cells were far more likely to inhibit other interneurons and received larger inputs from homologous interneuron types, consistent with the findings using extracellular stimulation. NG and FS cells also commonly excited each other through gap junctions. Conversely, BT and RS cells showed limited inhibition of other interneurons, although NG-BT and FS-BT gap junctions were common. Our findings suggest that NG and FS cells are the primary disinhibitory interneurons in the piriform cortex and can also mutually entrain their firing via gap junctions.