Complete understanding of the role of the mammalian main olfactory bulb in sensory processing has remained elusive despite many detailed studies on its anatomy and physiology. Several lines of recent evidence viewed in the context of earlier knowledge have provided new insights into the bulbar mechanisms of olfactory coding. The output cells of the olfactory bulb receive a localized olfactory nerve input and interneuronal input via dendrodendritic synapses on distinct sets of dendrites. The spatial arrangement of granule cell contacts on output cell basal dendrites suggests that lateral inhibitory interactions may occur between neighboring output cells. The input from olfactory receptor cell axons to the bulb also has spatial order, but does not represent a precise map of the receptor surface. Recent studies with antibodies and lectins suggest that different groups of axons from chemically similar receptor cells collect into certain glomeruli, even if the axons originate from cells that are not contiguous in the mucosa. Electrophysiological studies have begun to explore the participation of spatially organized circuits in olfactory processing. The degree to which neighboring output cells respond similarly to odor stimulation, for example, depends on the distance between the cells, with those further apart showing complementary responses. Also, a single output cell can show 2 or more different temporal response patterns when different odors are presented. Intracellular recordings indicate that these responses are shaped by IPSPs. Electrical stimulation during such recordings shows that some mitral cells are excited by nerve inputs close to their glomerular tufts, while they are inhibited by nerve inputs to other parts of the bulb. Finally, recordings from granule and periglomerular cells indicate their potential in mediating components of output cell odor responses. These considerations suggest that the olfactory bulb performs a spatially based analysis on the information coming from the receptor cells. While the spatial organization of the olfactory bulb is probably not faithfully represented in the projections to the olfactory cortex, bulbocortical projections are not random. The fact that spatial factors exist at each of these levels in the olfactory system must be considered in developing models of central olfactory processing.
The trigeminal region of the chick was studied with indirect immunofluorescence in order to determine whether extracellular matrix components might be distributed in such a way as to guide trigeminal axons to their peripheral targets in the mandibular arch. Tissue sections from stages 13-15 and 21/22 were immunolabeled indirectly with affinity-purified antibodies raised against fibronectin and laminin, two extracellular matrix glycoproteins that support axon growth in vitro. Fibronectin was distributed ubiquitously throughout the head mesenchyme prior to and during initial axon growth from the brainstem (stages 13-15). Shortly after trigeminal axons reached their target tissues (stage 21/22), fibronectin immunolabeling was distributed throughout the head mesenchyme, but was present only at low levels in the trigeminal ganglion and motor nerve. Laminin immunolabeling was distributed in the lateral head mesenchyme at stage 13 as small specks and patches. At stage 14, when the motor axons first exit from the brainstem, short, linear arrays of laminin immunostaining were present from the basement membrane of the neural tube to the core of the mandibular arch, and many were parallel to the direction of axon growth. By stage 21/22 the trigeminal ganglion and motor root showed intense antilaminin immunofluorescence as did the central core of the mandibular arch. These studies suggest that the distribution of fibronectin within the head mesenchyme cannot give directional information to the growing trigeminal axons because of its homogeneous distribution. However, the initial distribution of laminin during the earliest stages of axon outgrowth may provide an extracellular matrix pathway that permits trigeminal axons to reach their targets.
Ganglioside stimulated neurite outgrowth may be due to ganglioside binding to membrane proteins or to intercalation into the membrane. To test that ganglioside binding proteins could be found on neuronal surfaces, anti-idiotypic ganglioside monoclonal antibodies (AIG mAbs) were generated to mimic the biological properties of the GM1 ganglioside. The AIG mAbs were identified by their ability to bind to a known GM1 binding protein, the beta-subunit of cholera toxin. For the two AIG mAbs studied, AIG5 and AIG20, binding to beta-CT was blocked most strongly by GM1. This data also suggests that AIG5 and AIG20 mimic different but overlapping epitopes of the ganglioside GM1. Western blotting and immunoprecipitation of mammalian tissues reveals four potential ganglioside binding proteins of molecular weight 93, 66, 57, and 45 kDa. Immunocytochemistry demonstrates neuronal surface label with the AIG mAbs, which suggests that gangliosides, enriched on the neuronal surface membrane, are co-localized with putative ganglioside binding proteins. In bioassays, the AIG mAbs promote neuronal sprouting. This shows that these antibodies can be used to study the biological effects of ganglioside binding to neuronal surface proteins, and the role of gangliosides in the activation of neurite outgrowth.
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