Plasticity in mammalian somatosensory cerebellar maps

Abstract

The organization of sensory maps in mammalian brains can change following peripheral injury or experience. Such plasticity has been demonstrated for somatotopic somatosensory maps in various cortical and subcortical areas. In contrast to somatotopic maps, whose representation is distorted but nevertheless shows a detectable relationship to the topography of the body surface, cerebellar somatosensory maps have a fractured organization. Fractured cerebellar tactile maps display a mosaic of discrete, irregular patches representing nonadjacent areas of the body surface. This thesis describes the effect of peripheral injury on somatosensory maps in the cerebellum and the influence of their cortical and subcortical afferent structures on the pattern of reorganization. In normal rats, cerebellar granule cell layer field potentials evoked by a brief tactile stimulus consist of two components at different latencies. We carefully investigated the temporal relationship between the evoked tactile responses of the somatosensory cortex (SI) and the cerebellar granule cell layer, and demonstrated that SI is the primary contributor to the long-latency cerebellar response to peripheral tactile stimulation. Following lesion of the infraorbital branch of the trigeminal nerve, we investigated the developmental plasticity of the fractured tactile map in crus IIa. The tactile maps in the granule cell layer of crus IIa reorganized, maintaining a fractured somatotopy, after lesions made at all ages (from 1 to 90 days postnatal). The denervated upper lip region was consistently and predominantly replaced by representation of the upper incisors, a surprising result since this pattern does not correspond with plasticity studies in somatotopic somatosensory areas. The age of the animal at deafferentation affected the short-latency component of the cerebellar field potential but not the long-latency component. This suggests a difference in the developmental sensitivity of the cerebellum-related pathways to nerve lesion. Possible cerebellar mechanisms for the reorganization were examined. We also explored reorganization in SI, an afferent structure, which we found to have a strong influence on cerebellar granule cell activity. The upper incisor representation in SI, which we showed to be adjacent to the upper lip representation in the cortex of normal animals, increased significantly in SI of deafferented rats. Our results suggest that the site of plasticity following deafferentation is not in the cerebellum itself but in its afferent pathways. To explore this possibility, a network model of the major somatosensory pathways to the cerebellum was developed. Computer simulations, assuming plasticity only in the cerebellar afferent pathways, produced patterns of cerebellar reorganization similar to those observed experimentally.