Development

Tangential migration in neocortical development.Jiménez, D. et al. Dev. Biol. 25 February 2002 (10.1006/dbio.2002.0586)

Ventricle-directed migration in the developing cerebral cortex.Nadarajah, B. et al. Nature Neurosci. 5, 218–224 (2002)

It is known that some cortical neurons migrate tangentially from the basal telencephalon during development, but their precise site of origin has not been clear. Jiménez et al. have now shown that distinct populations of cortical neurons are derived from two regions — the medial and lateral ganglionic eminence. Nadarajah et al. have addressed a different but related question; namely, how do tangentially migrating cells know where to go once they have reached the cortex? Their data indicate that the cells initially migrate towards the cortical ventricular zone, where they acquire the information that determines their final position in the cortex.

Aging

Under-recruitment and nonselective recruitment: dissociable neural mechanisms associated with aging.Logan, J. M. et al. Neuron 33, 827–840 (2002)

Using functional magnetic resonance imaging, Logan et al. found that older adults showed less recruitment of frontal regions during the self-initiated memory encoding of words than did younger adults. This under-recruitment could be reversed if the memory encoding was supported, for example, by requiring semantic elaboration. A second difference between younger and older adults — nonselective activation of multiple frontal regions for both words and faces — was not reversed by this strategy. The results might have implications for understanding and ameliorating age-related cognitive decline.

Ion channels

Models of the extracellular domain of the nicotinic receptors and of agonist- and Ca2+-binding sites.Le Novère, N. et al. Proc. Natl Acad. Sci. USA 99, 3210–3215 (2002)

Experimentally based model of a complex between a snake toxin and the α7 nicotinic receptor.Fruchart-Gaillard, C. et al. Proc. Natl Acad. Sci. USA 99, 3216–3221 (2002)

These two papers constitute significant progress in the elucidation of the extracellular domain of nicotinic acetylcholine receptors (nAChRs). The authors took advantage of the crystal structure of a molluscan acetylcholine-binding protein (AChBP), which shows substantial homology to nAChRs, and constructed three-dimensional models of the receptor. They identified key differences between AChBP and nAChRs in the binding pocket, and provided a structural basis for previous mutagenesis experiments. In the second paper, the authors model the α7 nAChR subunit in association with a toxin antagonist, identifying the interaction sites and paving the way to the design of new receptor blockers.