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
GABAB-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 brain stem 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 GABAB-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
brain stem input and weaker GABAB-mediated inhibition than POm thalamus.
Our analysis leads to the prediction that the latency code will disappear if GABAB-mediated
transmission is blocked in POm thalamus or if the onset of sensory input is too abrupt.
We suggest that GABAB-mediated inhibition is a substrate of temporal coding in normal brain function.