PubMed · 2438716
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D S Forman. 1987. Fast axonal transport: recent developments.. https://doi.org/10.1016/s0079-6123(08)61817-8
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In the homozygous (but not the heterozygous) reeler mutant, disruption of neuron migration leads to a major perturbation of the cortical environment that in turn could modify (1) the specification of neuronal fate and (2) the proliferation dynamics of cortical precursors. To investigate these issues, tritiated thymidine injections during cortical neurogenesis were coupled with postnatal injections of a retrograde tracer in the spinal cord to accurately measure the neurogenesis of corticospinal neurons in the heterozygous and homozygous mutant. The homozygous reeler shows (1) strict conservation of area-specific timetables of corticospinal neuron generation; (2) neurons with the appropriate birthdates show an enhanced probability of projecting to the spinal cord; (3) during early stages of corticogenesis, there is a reduced rate of neuron production followed at later stages by an increased rate of neuron production; and (4) these changes in the rate of neuron production were shown to be at least partially attributable to changes in the proportions of differentiative divisions. Taken together, our results show that in the developing cortex, the neurogenesis and specification of a given neuronal phenotype are partially controlled by the postmigratory compartment. On the other hand, neither areal identity nor the chronology of production of layer-specific neuronal phenotype seems to depend on the integrity of the cellular environment.
The expression of three cadherins (cadherin-6B, cadherin-7, and R-cadherin) was analyzed by immunohistochemistry at early to intermediate stages of chicken cerebellar development (4.5-12 days of incubation [E4.5-E12]). Expression was first detected at approximately E5. On the cerebellar surface, expression of cadherin-6B and cadherin-7 is initially observed in transverse domains that subsequently elongate into parasagittal stripes. The sequence of emergence, the borders, and the orientation of these expression domains suggest a parcellation of the cerebellum into distinct medial, lateral, and caudal embryonic subdivisions. These subdivisions relate to histologic features, to the expression of gene regulatory proteins, and, possibly, to patterns of clonal restriction. Individual cadherin-expressing cell clusters can be observed to split into cortical and nuclear subdivisions, which are connected by nerve fibers expressing the same cadherin, thus establishing the parasagittal corticonuclear connectivity pattern found at later developmental stages. Our results suggest that cadherins may play a role in the transition from the early embryonic to the later functional organization of the cerebellum by providing a scaffold of potential adhesive cues.
Neurotrophic factors, particularly the neurotrophin gene family of neurotrophic factors, are implicated in activity-dependent anatomical plasticity in the visual cortex and at the neuromuscular junction. Accumulating evidence implicates neurotrophic factors as possible mediators of activity-dependent competition between afferents, leading to the segregation of afferents' arbors on the target space. We present a biologically plausible mathematical model of competition for neurotrophic factors. We show that the model leads to anatomical segregation, provided that the levels of neurotrophic factors released in an activity-independent manner, or the levels available by exogenous infusion, are below a critical value, which we derive. Above this critical value, afferent segregation breaks down. We also show that the model segregates afferents even in the presence of very highly correlated patterns of afferent activity. The model is therefore ideally suited for application to the development of ocular dominance columns in the kitten visual cortex.