How many of us, sitting in a schoolroom or lecture hall, have struggled to keep our attention from wandering? The parts of the brain responsible for this tricky task include the substantia innominata — literally, the 'substance with no name' — in the basal forebrain, whose cholinergic projections to the cortex help us to keep our minds on the task at hand. Turchi and Sarter have used antisense techniques to show that blocking the expression of NMDA receptors in the substantia innominata impairs attention in rats.

The animals were trained on a task that required them to pay attention — they had to press one lever if a light had come on for a short time and another one if no light had come on. If their attention lapsed and they missed the light, they got no reward; equally, they missed out on their treat if they incorrectly signalled that there had been a light. Turchi and Sarter then infused antisense oligonucleotides against NR1 subunits of the NMDA receptor into the substantia innominata and tested the rats on this task. Twenty-four hours after the third infusion, the rats seemed to be much less able to pay attention to the task — they often signalled that there had not been a light when there had, although they still correctly rejected non-light trials. They were unimpaired, however, on a cued discrimination task that did not test attentional processes.

As the prefrontal cortex sends extensive glutamate projections to the basal forebrain, these results indicate that NMDA receptors in the substantia innominata mediate attentional processes. The pattern of deficit is similar to that produced by lesioning the cholinergic projections from the basal forebrain to the cortex. The authors propose that glutamate inputs act through NMDA receptors to activate these projections, and that this activation is involved in the selection and amplification of specific sensory inputs.