Research from Karolinska Institutet in Sweden shows that the human olfactory bulb – a structure in the brain that processes sensory input from the nose – differs from that of other mammals in that no new neurons are formed in this area after birth. The discovery, which is published in the scientific journal Neuron, is based on the age-determination of the cells using the carbon-14 method, and might explain why the human sense of smell is normally much worse than that of other animals.
"I've never been so astonished by a scientific discovery," says lead investigator Jonas Frisén, Tobias Foundation Professor of stem cell research at Karolinska Institutet. "What you would normally expect is for humans to be like other animals, particularly apes, in this respect."
It was long thought that all brain neurons were formed up to the time of birth, after which production stopped. A paradigm shift occurred when scientists found that nerve cells were being continually formed from stem cells in the mammalian brain, which changed scientific views on the plasticity of the brain and raised hopes of being able to replace neurons lost during some types of neurological disease.
In the adult mammal, new nerve cells are formed in two regions of the brain: the hippocampus and the olfactory bulb. While the former has an important part to play in memory, the latter is essential to the interpretation of smells. However, owing to the difficulty of studying the formation of new neurons in humans, the extent to which this phenomenon also occurs in the human brain has remained unclear. In this present study, researchers at Karolinska Institutet and their Austrian and French colleagues made use of the sharp rise in atmospheric carbon-14 caused by Cold War nuclear tests to find an answer to this question.
Carbon-14 is incorporated in DNA, making it possible to gauge the age of the cells by measuring how much of the isotope they contain. Doing this, the team found that the olfactory bulb neurons in their adult human subjects had carbon-14 levels that matched those at the atmosphere at the time of their birth. This is a strong indication that there is no significant generation of new neurons in this part of the brain, something that sets humans apart from all other mammals.
"Humans are less dependent on their sense of smell for their survival than many other animals, which may be related to the loss of new cell generation in the olfactory bulb, but this is just speculation," continues Professor Frisén.
Professor Frisén and his team now plan to study the extent of neuron generation in the hippocampus, a part of the brain that is important for higher cerebral functions in humans. This present study was made possible by support from the Tobias Foundation, the Swedish Research Council, the Swedish Foundation for Strategic Research (SSF), the American Brain and Behaviour Research Foundation (NARSAD), the Swedish Brain Fund, the Knut and Alice Wallenberg Foundation, AFA Försäkring, the EU and the Stockholm County Council through its ALF agreement with Karolinska Institutet.
Publication: "The age of olfactory bulb neurons in humans", Olaf Bergmann, Jakob Liebl, Samuel Bernard, Kanar Alkass, Maggie S.Y. Yeung, Peter Steier, Walter Kutschera, Lars Johnson, Mikael Landén, Henrik Druid, Kirsty L. Spalding & Jonas Frisén, Neuron, print issue 24 May 2012.
Journal website: http://www.cell.com/neuron/
For further information, please contact:
Jonas Frisén, Professor
Department of Cell and Molecular Biology
Tel: +46 (0)8-524 875 62
Kirsty Spalding, Assistant Professor
Department of Cell and Molecular Biology
Tel: +46 (0)8-524 87464 or +46 (0)70-437 15 42
Contact the press office and download photos: http://ki.se/pressroom
Karolinska Institutet is one of the world's leading medical universities. It accounts for over 40 per cent of the medical academic research conducted in Sweden and offers the country's broadest range of education in medicine and health sciences. Since 1901 the Nobel Assembly at Karolinska Institutet has selected the Nobel laureates in Physiology or Medicine.
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