This study was designed to investigate direct effects of [D-$Pen^2$, D-$Pen^5$]-enkephalin, a $delta$-opioid receptor agonist on the neuronal activity of medial vestibular nuclear (MVN) neurons by whole-cell configuration patch clamp experiments. The spike frequency of MVN neuron was increased to $9.50{pm}0.55$ (P<0.05) and $10.56{pm}0.66$ (P<0.05) by 5 and $10{mu}M$ [D-$Pen^2$, D-$Pen^5$]-enkephalin from the control level of $8.05{pm}0.55$ spikes/sec, respectively (n=18). The resting membrane potential of the neurons was increased to $-37.86{pm}0.92$ and $-36.97{pm}0.97$ (P<0.05) from $-38.74{pm}1.13;mV$ by 5 and $10{mu}M$ [D-$Pen^2$, D-$Pen^5$]-enkephalin, respectively. The amplitude of afterhyperpolarization was decreased to $23.78{pm}0.65$ and $21.67{pm}0.89$ (P<0.05) from $23.73{pm}0.53;mV$ by 5 and $10{mu}M$ [D-$Pen^2$, D-$Pen^5$]-enkephalin, respectively. The spike width was changed to $2.22{pm}0.08$ and $2.24{pm}0.07$ from $2.20{pm}0.08;mV$ by 5 and $10{mu}M$ [D-$Pen^2$, D-$Pen^5$]-enkephalin, respectively. After pretreatment of naltrindole, a highly selective 8-opioid receptor antagonist, [D-$Pen^2$, D-$Pen^5$]-enkephalin did not change firing rate, resting membrane potential, afterhyperpolarization amplitude, and spike width of MVN neurons. The above experimental results suggest that [D-$Pen^2$, D-$Pen^5$]-enkephalin increases the neuronal activity of MVN neurons via inhibition of calcium-dependent potassium currents underlying the afterhyperpolarization.