Although the collateral branching patterns differed from one axon to another, collaterals arising from a particular axon usually exhibited similar patterns at different rostrocaudal levels.
These uniform collateral termination patterns indicate that the morphology of each neuron might be specifically related to its function.
Even for data representation the challenges are nontrivial: the conventional approach using regional connectivity matrices fails to capture the collateral branching patterns of projection neurons.
Such collateral pathway patterns are rare, and in our review of the literature, we found that only four cases have been described [1, 3, 6].
The same authors went on to identify cross-resistance and collateral sensitivity patterns in a set of multidrug-resistant human small-cell lung cancer cell lines.
Therefore, dyads and dyad-dependent collateral and broker patterns are more abundant in G4.
The most intriguing pattern was collateral sensitivity to gemcitabin in two cell lines and to ara-C in five drug-resistant cell lines, i.e. in all lines except the lines resistant to topo I poisons.
When Purkinje cells are reinnervated by the climbing fibres, either upon removal of tetrodotoxin or by the collateral sprouts that form following subtotal 3-acetylpyridine lesion, a normal spine distribution pattern is restored.
In fact, all resistant cell lines exhibited patterns of collateral sensitivity to various different classes of drugs.
The MDR lines demonstrated, as expected, cross-resistance to all topo II drugs, but also different patterns of collateral sensitivity to BCNU, cisplatin, ara-C, hydroxyurea, and to the topo I inhibitor camptothecin.
