A temporal sensory code occurs in posterior medial (POm) thalamus of the rat vibrissa system, where the latency for the spike-rate to peak is observed to increase with increasing frequency of stimulation between 2 and 11 Hz. In contrast, the latency of the spike rate in the ventroposterior medial (VPm) thalamus is constant in this frequency range. We consider the hypothesis that two factors are essential for latency coding in the POm. The first is GABA_B-mediated feedback inhibition from the reticular thalamic (Rt) nucleus, which provides delayed and prolonged input to thalamic structures. The second is sensory input that leads to an accelerating spike-rate in brainstem nuclei. Essential aspects of the experimental observations are replicated by the analytical solution of a rate-based model with a minimal architecture that includes only the POm and Rt nuclei, i.e., an increase in stimulus frequency will increase the level of inhibitory output from Rt thalamus and lead to a longer latency in the activation of POm thalamus. This architecture, however, admits period-doubling at high levels of GABA_B-mediated conductance. A full architecture that incorporates the VPm nucleus suppresses period-doubling. A clear match between the experimentally measured spike-rates and the numerically calculated rates for the full model occurs when VPm thalamus receives stronger brainstem input and weaker GABA_B-mediated inhibition than POm thalamus. Our analysis leads to the prediction that the latency code will disappear if GABA_B-mediated transmission is blocked in POm thalamus or if the onset of sensory input is too abrupt. We suggest that GABA_B-mediated inhibition is a substrate of temporal coding in normal brain function.