The immediate premotor circuit in the brainstem for the generation of saccades has been extensively studied. It includes excitatory and inhibitory burst neurons and omnipause neurons, whose coordinated interplay is essential to execute healthy saccades. In neurodegenerative diseases, the malfunction of saccades may depend on alterations of the biology of burst and/or omnipause neurons rather than pure cell loss. Here we describe the molecular characteristics of saccadic burst and omnipause neurons in monkeys, including transmitter inputs. Both neuronal groups contain calcium-binding proteins; they are enwrapped by perineuronal nets and express voltage-gated potassium channels, T-type calcium channels, and hyperpolarization-activated cyclic nucleotide-gated channels enabling fast firing with post-inhibitory rebound. The findings will help to refine the current neuromimetic models of the saccadic circuit to find therapy strategies for saccadic disorders in patients.