We used whole-cell patch recording to study 102 local interneurons in the rat dorsal lateral geniculate nucleus in vitro. Input impedance with this technique (607.0+/-222.4 MOhm) was far larger than that measured with sharp electrode techniques, suggesting that interneurons may be more electrotonically compact than previously believed. Consistent and robust burst firing was observed in all interneurons when a slight depolarizing boost was given from a potential at, or slightly hyperpolarized from, resting membrane potential. These bursts had some similarities to the low-threshold spike described previously in other thalamic neuron types. The bursting responses were blocked by Ni+, suggesting that the low-threshold calcium current I(T), responsible for the low-threshold spike, was also involved in interneuron burst firing. Compared to the low-threshold spike of thalamocortical cells, however, the interneuron bursts were of relatively long duration and low intraburst frequency. The requirement for a depolarizing boost to elicit the burst is consistent with previous reports of a depolarizing shift of the I(T) activation curve of interneurons relative to thalamocortical cells, a finding we confirmed using voltage-clamp. Voltage-clamp study also revealed an additional long-lasting current that could be tentatively identified as the calcium activated non-selective cation current, I(CAN), based on reversal potential and on pharmacological characteristics. Computer simulation of the interneuron burst demonstrated that its particular morphology is likely due to the interaction of I(T) and I(CAN). In the slice, bursts could also be elicited by stimulation of the optic tract, suggesting that they may occur in response to natural stimulation. Synaptically triggered bursts were only partially blocked by Ni+, but could then be completely blocked by further addition of (+/-)-2-amino-5-phosphonopentanoic acid. The existence of robust bursts in this cell type suggests an additional role for interneurons in sculpting sensory responses by feedforward inhibition of thalamocortical cells. The low-threshold spike is a mechanism whereby activity in a neuron is dependent on a prior lack of activity in that same neuron. Understanding of the low-threshold spike in the other major neuron types of the thalamus has brought many new insights into how thalamic oscillations might be involved in sleep and epilepsy. Our description of this phenomenon in the interneurons of the thalamus suggests that these network oscillations might be even more complicated than previously believed.