Hypothalamic neuronal histamine is a factor regulating feeding behaviors. Autoradiographic mappings have shown that high densities of histamine receptors were found in the trigeminal motor nucleus as well as the mesencephalic trigeminal nucleus (Mes V). However, the detailed function of histaminergic inputs to trigeminal motoneurons is unclear. In the present study, we used whole-cell patch-clamp recordings from masseter motoneurons (MMNs) in transverse brainstem preparations from postnatal day 7-13 Wistar rats to examine effects of application of histamine on the membrane potential of MMNs. We also examined the effects of histamine on postsynaptic inward currents (PSCs) in the MMNs evoked by electrical stimulation of the Mes V that relays spindle afferents from the jaw-closing muscle or periodontal afferents to jaw-closing motoneurons. MMNs were retrogradely labeled by tetramethylrhodamine injected into the masseter muscle one to 3 days prior to the preparation of the slices. Bath-application of 100 μM histamine in the presence of 0.5 μM tetrodotoxin induced membrane depolarizations (mean 7.1 mV, n= 6) in MMNs at the resting potential. Bath-application of 100 μM 2-pyridylethlamine dihydrochloride, a H1 receptor agonist, and 100 μM immethridine dihydrobromide, a H3 receptor agonist, also induced the membrane depolarization of 5.9 mV (n = 5) and 6.6 mV (n = 6), respectively. In contrast, bath-application of the H1 receptor agonist reduced the peak amplitude of the PSCs in MMNs evoked by electrical stimulation of the Mes V, to 53% of the control (n = 12), whereas the H3 receptor agonist had no effects on the Mes V-induced PSCs (n= 5). These results suggest that MMNs express both histamine H1 and H3 receptors, and that histaminergic inputs are involved in regulating the jaw-closing reflex through H1 receptors.