mber of kisspeptin-expressing cells in the brain.

They found hamsters in wintry conditions experienced marked reductions of kisspeptin in a critical brain region important for regulating reproduction and sex behavior compared to hamsters in simulated summer conditions.

Winter hamsters, however, were just as responsive to kisspeptin, elevating a key hormone -- luteinizing hormone -- as much as hamsters in simulated summers. This finding indicates the ability of this hormone to turn on the reproductive switch even in the presence of cues signaling a winter, non-breeding environment.

"What is really striking is the disappearance of kisspeptin in animals experiencing winter-like days, yet the ability to respond to kisspeptin when we provide it," said Timothy Greives, lead author of the study. "These data show that the disappearance of kisspeptin in the brain is likely critical in turning off reproduction during winter."

Recent research by scientists in the U.K. and France have shown human kisspeptin triggers the release of gonadotropin-releasing hormone and luteinizing hormone, both of which are important to puberty and other sex-related functions.

"Studies in humans have shown that individuals with deficits in the receptor for kisspeptin have severe reproductive impairments," Demas said.

Kisspeptin's role in seasonal human reproduction, however, is unknown -- that is, if it even has one. It is interesting to note the CDC reports fertility rates in the United States decrease rapidly in autumn. The phenomenon is particularly clear-cut among Caucasians, believed to have originated in more temperate climes.

KiSS-1 and kisspeptin were not named whimsically. They were originally associated with metastatic tumor suppression (the SS in KiSS-1 stands for "suppressor sequence"). The subsequent connection of KiSS-1 and kisspeptin to reproductive function was entirely fortuitous.

So
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