Genes and disease

Pharmacological rescue of synaptic plasticity, courtship behavior, and mushroom body defects in a Drosophila model of fragile X syndrome.McBride, S. M. J. et al. Neuron 45, 753–764 (2005)

In humans, the loss of FMR1 gene function, which causes fragile X syndrome, is the leading cause of inherited mental retardation. Loss of function of the homologous gene in fruit flies produces a model of the syndrome, with abnormalities in circadian and courtship behaviour and neuroanatomical changes. In addition, McBride et al. find that the flies show impaired learning. The authors show that treatment with antagonists of metabotropic glutamate receptors or with lithium can rescue the behavioural, neuroanatomical and cognitive abnormalities in the fly model. The pharmacological rescue of the symptoms indicates that it might be possible to treat patients with fragile X syndrome using a similar approach.

Brain evolution

The brain of LB1, Homo floresiensis. Falk, D. et al. Science 3 March 2005 (10.1126/science.1109727)

Homo floresiensis was a diminutive species of human — nicknamed 'hobbits' by their discoverers — that lived about 18,000–38,000 years ago on the island of Flores in Indonesia. Falk and colleagues have assessed the brain of H. floresiensis by studying a three-dimensional reconstruction based on the skull of the type specimen, LB1. Comparisons with endocasts from the skulls of apes, Homo erectus, Homo sapiens, Australopithecus africanus and Paranthropus aeithiopicus indicate that although LB1's brain/body size ratio is similar to that of A. africanus, the shape is more similar to that of H. erectus, but with an expanded temporal lobe. The authors suggest that, despite its small brain, H. floresiensis was capable of relatively advanced cognition.

Axon guidance

β1,3- N -Acetylglucosaminyltransferase 1 glycosylation is required for axon pathfinding by olfactory sensory neurons.Henion, T. R. et al. J. Neurosci. 25, 1894–1903 (2005)

Axonal pathfinding in the embryonic olfactory system enables olfactory sensory neurons to send their axons to specific glomeruli in the olfactory bulb, so that each glomerulus receives inputs from neurons that express the same odorant receptor. The odorant receptors themselves, along with other guidance factors, have been implicated in axonal pathfinding, but the mechanism by which this precision is achieved remains unclear. Henion et al. now show that glycans are also crucial for precise axonal pathfinding in the olfactory system — mice that lack the glycosyltransferase β1,3-N-acetylglucosaminyltransferase 1 have abnormal olfactory bulb innervation and impaired formation of glomeruli in the olfactory bulb.