Brain repair

Functional connections are established in the deafferented rat spinal cord by peripherally transplanted human embryonic sensory neurons. Levinsson, A. et al. Eur. J. Neurosci. 12, 3589–3595 (2000).

Embryonic human sensory neurons were grafted in place of adult rat dorsal root ganglia. The grafted cells extended processes that invaded the dorsal horn, forming branches and then synaptic contacts with host neurons. In addition, the cells were capable of evoking polysynaptic reflexes in the ventral roots, revealing an significant degree of functional integration. This highlights the potential of human embryonic sensory neurons for tissue repair.

Cell biology of the neuron

Oligomeric tubulin in large transporting complex is transported via kinesin in squid giant axons. Terada, S. et al. Cell 103, 141–155 (2000).

The transport of fluorescent tubulin was measured in real time in the squid giant axon. Contrary to previous ideas, tubulin transport was found to depend on kinesin, a microtubule-based motor, and not on actin-based motors. Furthermore, by using fluorescence-correlation spectroscopy, the authors obtained an estimate of the number of fluorescent molecules transported in a complex and observed that tubulin is not transported as a stable polymer, as previously thought, but as a smaller oligomer.

Working memory

Synaptic mechanisms and network dynamics underlying spatial working memory in a cortical network model. Compte, A. et al. Cerebral cortex. 10, 910–923 (2000).

A network model accounting for the persistent activity observed in the prefrontal cortex during spatial working memory tasks. The current model shows bistability between a resting state with low frequency, spontaneous firing, and a spatially-structured state with higher-frequency firing. This is achieved by a combination of an overall recurrent inhibitory influence and NMDA receptor-mediated recurrent synaptic excitation, features not present in previous pattern formation models.

Development

Cell interactions within nascent neural crest cell populations transiently promote death of neurogenic progenitors. Maynard, T. M. et al. Development 127, 4561–4572 (2000).

During neural crest cell migration, early, but not late, migratory populations have neurogenic potential. This study shows that neurogenic precursors that fail to disperse early die as a result of cell–cell interactions. Caspase inhibitors prevent this death. Cells that migrated successfully during the early period were no longer susceptible to the influence of cell contact. This was partly mediated by Notch–Delta interactions, and may be a mechanism for assuring that late migratory populations lack neurogenic potential.