Spatial symmetry groups as sensorimotor guidelines

While some aspects of neuroanatomical organization are related to packing and access rather than to function, other aspects of anatomical/physiological organization are directly related to function. The mathematics of symmetry groups can be used to determine logical structure in projections and to relate it to function. This paper reviews two studies of the symmetry groups of vestibular projections that are related to the spatial functions of the vestibular complex, including gaze, posture, and movement. These logical structures have been determined by finding symmetry groups of two vestibular projections directly from physiological and anatomical data. Logical structures in vestibular projections are distinct from mapping properties such as the ability to maintain two- and three-dimensional coordinate systems; rather, they provide anatomical/physiological foundations for these mapping properties. The symmetry group of the direct projection from the semicircular canal primary afferents to neck motor neurons is that of the cube (O, the octahedral group), which can serve as a discrete skeleton for coordinate systems in three-dimensional space. The symmetry group of the canal projection from the secondary vestibular afferents to the inferior olive and thence to the cerebellar uvula-nodulus is that of the square (D8), which can support coordinates for the horizontal plane. While the mathematical relationship between these symmetry groups and functions of the vestibular complex are clear, these studies open a larger question: what is the causal logic by which neural centers and their intrinsic organization affect each other and behavior? The relationship of vestibular projection symmetry groups to spatial function make them ideal projections for investigating this causal logic. The symmetry group results are discussed in relationship to possible ways they communicate spatial structure to other neural centers and format spatial functions such as body movements. These two projection symmetry groups suggest that all vestibular projections may have symmetry groups significantly related to function, perhaps all to spatial function.

Asymmetric gene expression in the brain during acute compensation to unilateral vestibular labyrinthectomy in the Mongolian gerbil

Commercial microarrays were used to identify transcriptome expression within vestibular related brain regions (vestibular brainstem and cerebellum, and caudotemporal cortical regions) during the acute period of recovery following unilateral surgical vestibular labyrinth ablation in the gerbil. As a representative model of vestibular compensation, vestibular lesions in the gerbil produced activation in a common set of genes related to vestibular compensation. The total RNA was prepared and amplified using Affymetrix Gene Chip™ probes from the Rat U34 Neurobiology and R230, and Mouse M430 gene sets, resulting in GCRMA summarized data from S+AA software. Matched rat and mouse genes from gerbil hybridization produced good interspecies synteny. Multiple gene target trends supported global increases in neuron excitability throughout the vestibular brainstem and cerebellum. We focused further on gene expression with anatomically asymmetric activation relative to the lesion, indicative of involvement in rebalancing central vestibular tone during the vestibular compensation process. Cluster analysis revealed distinct spatial (regional and ipsi-contra) and temporal patterns. The asymmetric genes were part of well-defined neuron-related networks and included multiple members of the glutamate and GABA neurotransmitter systems. Transcripts for D3 dopamine, glycine, and some GABA receptor signals increased quickly in the ipsilesional vestibular complex and then increased gradually in the contralateral region, restoring the expression symmetry. Alternatively, the NMDA binding subunit decreased gradually over the acute compensation period in the contralateral vestibular complex. There was evidence for numerous associations between signaling systems with PKC as one possible mediator between early changes in GABA and progressive changes in NMDA signaling. These data begin to define the compensatory response at the level of molecular cascades.