Intracellular recordings were performed in the lateral thalamic nuclei of cats under barbiturate anesthesia. The nature of cyclic hyperpolarizations triggered in relay cells by cortical stimulation was analyzed. These long-lasting hyperpolarizations were made of three different components. The early component, which was reversed by current and Cl injections, was identified as a Cl-dependent inhibitory postsynaptic potential (IPSP). A depolarizing hump was usually present in the depth of the long-lasting hyperpolarization. This intermediate component was identified as a voltage-dependent dendritic Ca conductance on the basis of recordings and ethylene glycol tetraacetic acid (EGTA) injections performed in relay cell dendrites. The late phase of hyperpolarization was dissociated from the early IPSP by its differential sensitivity to current and Cl injections and to conditioning tetanic stimulation. This late component was abolished by EGTA and, thus, was interpreted as a Ca-dependent K conductance increase. Activation of intrinsic somatic or dendritic conductances by current pulses never generated rhythmic hyperpolarizations in thalamic relay neurons. Oscillations appear to be imposed on these cells by synaptic inputs. It is then proposed that other thalamic neurons would have pacemaker properties and/or that oscillations would be produced in thalamic cellular pools by feedback interconnections.