University College London

Two neuroscientists are surprised by the link between a brain-chemical transporter and sexual orientation.

Many nerve cells in the brain release the chemical neurotransmitter glutamate to signal to other neurons via receptors. Dedicated transporters then remove glutamate from the extracellular space to end signalling.

Cystine–glutamate exchangers are unusual glutamate transporters because they do the reverse, adding glutamate to the extracellular space while removing cystine. David Featherstone of the University of Illinois, Chicago, and his colleagues have found that in the fruitfly Drosophila melanogaster, knocking down expression of a cystine–glutamate exchanger in non-neuronal glial cells leads to a dramatic change in the sexual behaviour of male flies: they mate with both males and females owing to altered processing of sex-specific chemosensory cues (Y. Grosjean et al. Nature Neurosci. 11, 54–61; 2008).

This behaviour may be caused by an increase in the number of glutamate signalling receptors, which is induced by the fall in extracellular glutamate concentration that follows transporter knockdown. Indeed, the effect of the knockdown could be reversed by feeding the flies a drug that reduces glutamate signalling, and could be mimicked by feeding normal flies a drug that enhances glutamate signalling.

These studies raise questions about whether human sexual orientation, long assumed to be due to a mix of genes and environment, could also be altered by perturbations of neurotransmitter signalling. Could differences in such signalling contribute to different sexual preferences?

The possibility of altering sexual preference pharmacologically is worrying. We cannot rule out a future regression to the twentieth-century idea that sexual behaviour should be regulated by society.