Neurogenetics

A new chromosome 17q21.31 microdeletion syndrome associated with a common inversion polymorphism. Koolen, D. A. et al. Nature Genet. 38, 999–1001 (2006)

Microdeletion encompassing MAPT at chromosome 17q21.3 is associated with developmental delay and learning disability. Shaw-Smith, C. et al. Nature Genet. 38, 1032–1037 (2006)

Discovery of previously unidentified genomic disorders from the duplication architecture of the human genome. Sharp, A. J. et al. Nature Genet. 38, 1038–1042 (2006)

Advances in the detection of submicroscopic chromosome deletions are helping to uncover genomic disorders that cause mental retardation. Three studies have identified a microdeletion syndrome affecting chromosome 17q21.3, estimated to account for up to 1% of mental retardation cases. The deletion was associated with an inversion polymorphism found in 20% of Europeans and gave rise to a clinically recognizable phenotype. The deletion encompassed several genes, including microtubule-associated protein tau, which has been linked to neural development and neurodegeneration.

Synaptic plasticity

Cooperative astrocyte and dendritic spine dynamics at hippocampal excitatory synapses. Haber, M., Zhou, L. & Murai, K. K. J. Neurosci. 26, 8881–8891 (2006)

Although the role of morphological rearrangements in dendritic spines in synaptic plasticity is well appreciated, less is known about glial motility at synapses, despite evidence that glia can modulate synaptic function. To enable the visualization of synaptic interactions in live cells, Haber et al. infected hippocampal slices with viral vectors to mediate the expression of two different fluorescent proteins in astrocytes and neurons. Time-lapse imaging revealed that astrocytes exhibit dynamic morphological plasticity, rapidly extending and retracting processes in a manner that was often coordinated with changes in dendritic spines. Astrocyte plasticity might therefore make an important contribution to the function of synapses, by regulating communication between neurons and glia.

Behavioural neuroscience

A role for the macaque anterior cingulate gyrus in social valuation. Rudebeck, P. H. et al. Science 313, 1310–1312 (2006)

In humans, damage to the frontal lobe can lead to impairments in social interaction, and in extreme cases, sociopathy, but the exact region that is responsible for these deficits has been unclear. New work in macaques shows that damage to the anterior cingulate cortex disrupts normal patterns of social interest in other macaques. By contrast, the orbitofrontal cortex did not seem to be necessary for this type of social functioning, but was instead associated with fear responses. It is therefore likely that the anterior cingulate cortex contributes, along with other brain regions, to normal social behaviour.