The cerebello-cerebral circuit plays an important role in the preparation and execution of voluntary movements. The neural information originating in the cerebellum is mediated to the cerebral cortex via its relay in the ventrolateral (VL) nucleus of the thalamus. Until recently VL was regarded as a simple relay station between the cerebellum and the motor cortex. This view became seriously challenged by recent work which showed that VL receives substantial sensory input from the spinal cord. Input from the periphery permits modification of intended and ongoing movement in VL and as such can change the cerebellar motor commands before they impinge onto the motor cortex. As a site of integration of cerebellar and sensory input, VL can update the motor cortex on more movement related events than was heretofore believed to be the case. It is the aim of the proposed work to fully describe the organization and mode of synaptic transmission of sensory input from the spinal cord to VL. The pathways and structures which relay the spinal information to VL will also be identified. The experiments will be performed acutely, on anesthetized cats. Intracellular recording techniques will be used to identify the relay neurons in the cerebello-cerebral circuit and to study the synaptic responses to spinal cord stimulation. Here, the two major ascending pathways to the thalamus, the dorsal columns and the spinothalamic tract will be stimulated. Most of the spinal input to VL is expected to be mediated polysynaptically. Therefore, the relay stations in the midbrain and caudal brain stem which mediate the polysynaptic input to VL will be identified. This requires lesioning procedures and recording of neural activity from these relays. The outcome of the study will provide new information on the physiology of cerebello-cerebral interactions and will give new insight into the understanding of the control of voluntary movements. The findings will also provide a means for assessing in the future the importance of sensory input to VL during recovery from cerebellar motor deficits.