Sugar is the key to the nicotine rush according to new research

from Health and Wellbeing (376 articles)

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USC College associate professor Lin Chen, left, and Keck School associate professor Zuo-Zhong Wang worked on the nicotine study with research associate Cosma Dellisanti,

July 27, 2007 Smoking and blood sugar levels are highly interrelated – nicotine causes the body to release satisfying levels of sugar into the bloodstream far faster than eating can, which explains its appetite-inhibiting effects. The results of low blood sugar levels in a quitting nicotine addict are also responsible for some of the most difficult withdrawal symptoms. Now it has been discovered that sugar is also a key element in the chemical reaction that causes a smoker to feel “high”. When nicotine molecules are received by neurotransmitter membranes, it’s sugar molecules that then act as a sort of hinge to open a gate in the cell membrane and send the "nicotine rush" nerve signal onward.

When nicotine binds to a neuron, how does the cell know to send the signal that announces a smoker’s "high"? As with other questions involving good sensations, the answer appears to be sugar.

A USC study appearing with a commentary in Nature Neuroscience online proposes a role for sugar as the hinge that opens a gate in the cell membrane and brings news of nicotine’s arrival.

Structural biologist Raymond Stevens of The Scripps Research Institute, who was not involved in the study, called it “a landmark accomplishment for the fields of structural biology and neuronal cell signaling.”

Besides substance addiction, Stevens pointed to epilepsy, schizophrenia and depression as targets for improved drugs that could result from the study’s findings.

The study provides the first detailed look at part of the mouse nicotinic acetylcholine receptor (nAChR), one in a large and important group of molecules, known as ion channel proteins, that allow signals to pass between neurons.

The results reveal an important role for the sugar molecules in such proteins.

“Our studies fill a major gap in the field and set a new paradigm,” said Lin Chen, associate professor of molecular and computational biology in USC College and co-corresponding author with Zuo-Zhong Wang, associate professor of cell and neurobiology at the Keck School of Medicine of USC.

Many existing theories, which do not consider sugar’s role, are probably incomplete, Chen said.

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