Previous studies have demonstrated that tooth pulp deafferentation is associated with statistically significant alterations in the low-threshold facial mechanoreceptive field properties of brain stem neurons in trigeminal (V) subnucleus oralis. A loss of spinal afferent-induced presynaptic inhibition as a consequence of a decrease in primary afferent depolarization (PAD) following spinal nerve deafferentation has been invoked as a mechanism underlying deafferentation-induced somatosensory neuroplasticity. Therefore, this study was initiated to determine if these pulp deafferentation-induced neuroplastic changes could be accounted for by an alteration in PAD of low-threshold facial afferent endings in subnucleus oralis of anesthetized rats. In control (unoperated) rats (n = 7) and rats (n = 7) that had undergone mandibular pulp deafferentation 6-10 days previously, antidromic compound action potentials evoked by test stimulation in V subnucleus oralis were recorded in branches of the infraorbital (IO) and supraorbital (SO) nerves, and conditioning stimuli were applied to some of the same nerves. PAD of the afferent endings in oralis of these nerve branches was documented in all animals, and there was no significant difference between the two groups in the incidence or any of the other features of PAD. The features of the PAD were consistent with those described in several previous studies of normal animals. These findings indicate that the reported deafferentation-induced loss of spinal presynaptic regulatory mechanisms cannot be entrapolated to all forms of deafferentation injury and that the mechanoreceptive field changes that can occur in central V somatosensory neurons as a result of tooth pulp deafferentation may not reflect an alteration in PAD.