In order to determine to what extent the terminal arbors of phylogenetically and functionally distant axons are constructed according to common rules, we have compared visual callosal axons in cats (CCC axons) with thalamocortical axons to the whisker representation in mice (MTC axons). Both similarities and differences were found. Maximal order of branching, branching angles, topological distribution of branches and boutons are similar for all axons, indicating strong constraints in arbor formation. CCC and MTC axons are indistinguishable for total arbor length and number of branches, although these parameters can vary across individual axons of each group. MTC axons have longer and bouton-richer end-branches (the 'transmission compartment') while, in CCC axons, proximal, boutonless branches (the 'conduction compartment') predominate. Therefore, the two classes of axons appear to be specialized for performing different types of operations, in agreement with the available electrophysiological data and computer simulations. Differences in the length of branches were also observed between MTC axons of normal and 'barrelless' mice, suggesting that this parameter can be regulated by conditions at the terminal sites.

The corpus callosum interconnects both corresponding (homotopic) and noncorresponding (heterotopic) cortical sites of the two hemispheres. We have studied the axons that establish heterotopic connections from visual areas 17 and 18 (E axons) by using anterogradely transported biocytin and three-dimensional serial reconstructions in adult cats and in kittens. Their site of termination distinguished four types of axons. Type EI ends near the border between areas 19/21a or 7, and type EII near the PMLS/PLLS border (posteromedial and posterolateral lateral suprasylvian areas). Type EIII and EIV terminate the first near the PMLS/PLLS and PMLS/21a borders, and the second near the PMLS/PLLS and 19/21a or 7 borders. Taking into account the previously studied homotopic axons (O axons; Houzel et al. [1994] Eur. J. Neurosci. 6:898-917), it can be concluded that areas 17 and 18 are interhemispherically connected by at least five types of axons, three of which (O, EI, and EII) terminate near one areal border, the other two (types EIII and EIV), near two areal borders. All types terminate near representations of the vertical meridian of the visual field. The different types of axons can be identified already during the first postnatal week; at this age, unlike in the adult, they originate not only near the 17/18 border, but also, transiently, in area 17. This suggests that the developing cortex contains sets of neurons destined to send their axon to different targets; however, the axons grow beyond their sites of adult termination. Indeed, exuberant growth takes place at the stage of axonal elongation, and at subsequent stages of axonal differentiation, i.e., during subcortical branching, intracortical branching and synaptogenesis. The growth is progressively more constrained in its topographic distribution and the axons are subsequently reshaped by regressive events.

Endocytosis is enhanced in some cases of neuronal death. We report for the first time that intraocular injections, in chick embryos, of excitotoxic doses of kainate induce strong endocytosis in retinal amacrine cells destined to die and that even subtoxic doses can induce some degree of endocytosis. That the uptake was due to endocytosis rather than passive diffusion through the plasma membrane was shown ultrastructurally. The endocytosis was demonstrated by using three unrelated tracers--horseradish peroxidase, microperoxidase, and 4.4-kDa fluorescein isothiocyanate (FITC)-labeled dextran--suggesting that it does not depend on the binding of the tracers to a particular receptor. However, it appears to be surprisingly sensitive to the size of the ligand, because a heavier (42-kDa) FITC-dextran was not endocytosed. The induction of endocytosis by kainate can occur even when protein synthesis is blocked. These results indicate that toxic or near-toxic doses of kainate induce endocytosis, raising the question of whether this is mechanistically implicated in causing or preventing excitotoxic neuronal death.

No abstract