Editor's note: Science Scan is a roundup of recently published biotechnology-relevant research.

During the just-ended holiday shopping season, boys and girls of all ages were importuned to favor their significant others with romantic perfumes and fragrant aftershaves. Canadian researchers have explored the physiological underpinnings of these olfactory sales pitches.

"Smells are surer than sounds or sights to make your heartstrings crack," wrote Rudyard Kipling over a century ago. Heartstrings correlate with love. A sniffed fragrance travels from nostril to brain in a fraction of a second along nerve cells that reach sensory climax in the cerebral cortex bordering the hippocampus. This convoluted cluster of neurons is thought to be a mission control center for emotions, memory, learning and sex drive.

Science dated Jan. 3, 2003, reports these Canadian findings in an article titled: "Pregnancy-stimulated neurogenesis in the adult female forebrain mediated by prolactin." Its authors are neuroscientists and cell biologists at the University of Calgary, Alberta. Their experiments in mice show that prolactin - a hormone known to surge after orgasm in men and women - can double the number of newly generated neurons in the mouse brain's olfactory bulb.

Prolactin, so named because it triggers lactation in mammals, is abundant in female mice after conception and again after delivery of newborn pups. This enhanced "scents-itivity" presumably helps rodent mothers recognize their mates and nurture their young. The authors suggest that in humans, a similar pattern may help cement relationships during the lengthy waiting period between fertilization and birth.

So if you missed choosing the right fragrance at Christmas, Valentine's Day is only a month off!

Newborn neurons in the brain appear and disappear in response to specific stimuli. Stress and depression, for example, suppress neurogenesis, whereas exercise, interesting environments, sex and antidepression drugs seem to boost those new neurons. They travel smellwise to the olfactory bulb, the brain area that receives sensory information from the nose. The Calgary co-authors propose that pregnancy might boost olfactory neurogenesis. A commentary to the Science paper, titled "Newborn neurons search for meaning," observed, "The team identified prolactin - which increases during pregnancy - as the neurogenesis trigger. They discovered that mice deficient in prolactin have only half the normal surge in neurogenesis during pregnancy. Prolactin increases immediately after sexual activity."

The paper itself leads off by noting, "Neurogenesis occurs in the olfactory system of the adult brain throughout life, in both invertebrates and vertebrates, but its physiological regulation is not understood. We show," it added, "that the production of neural progenitors is stimulated in the forebrain subventricular zone of female mice during pregnancy and that this effect is mediated by the hormone prolactin. Neurogenesis occurs even in females that mate with sterile males, which produces pseudopregnancy."

The authors make the point that prolactin is present in neural tissues where neurogenesis of odor discrimination occurs - from insects and crustaceans (lobsters, crabs, shrimps, barnacles) to rodents and primates. "Taken together," the paper summed up, "our findings indicate that production of new olfactory neurons is a maternal adaptation initiated early in pregnancy and mediated by prolactin. The hormone's effect also extends to mammary gland development, immunomodulation, and - intriguingly - stimulation of maternal pancreatic islet cell proliferation.

"Plasma levels of prolactin," the authors conclude, "increase markedly following orgasm in humans, both males and females. These observations suggest a behavioral relationship to courtship or long-term partnership."

New Role For Rapamycin Tumor Suppressor: Killing Tumors By Angiogenesis, Growth Block

While conducting yeast research on a potential new anticancer drug, scientists at Washington University School of Medicine in St. Louis discovered a mechanism that enables the genome to silence large numbers of genes simultaneously, rather than one gene at a time. Their finding emerged while studying the molecular action of the tumor-suppressor drug rapamycin. It's currently used to suppress the immune system following kidney transplantation, but is also under investigation against cancer.

The team reported its results in the December 2002 issue of the journal Molecular Cell. Its title: "Regulation of subtelomeric silencing during stress response."

Rapamycin stops tumor growth by a unique mechanism. While other immunosuppressants tend to promote the growth of tumor cells, rapamycin blocks their proliferation. Moreover, it inhibits angiogenesis - the proliferation of blood vessels in growing tumors. These features led the paper's co-authors to test rapamycin as a double-whammy inhibitor of angiogenesis and tumor progression.

Earlier in vitro tests by others showed that rapamycin binds to a large, previously unknown cell protein known as TOR, or target of rapamycin. TOR is found ubiquitously in organisms from yeast to humans, suggesting that it may serve an essential purpose in cells. The researchers identified some 300 yeast genes involved in TOR-related functions. One of these gene-encoded products is a protein called Sir3 - "silent information regulator3." Sir3 normally clings to a battery of genes responsible for a stress protein. It thereby keeps the genes inactive and silent.

However, the paper reports, when rapamycin inactivated TOR, Sir3 molecules cut loose from the line of stress-protein genes, thus triggering a stress response. The cells began producing stress proteins and stopped proliferating. Furthermore, when rapamycin inactivated TOR, it also shut down nutrient-processing pathways. This tumor-checking effect prevented yeast cells from using glucose to produce energy, and amino acids to make new proteins. These anticancer actions must now be verified in human cells.