Early life exposure to nicotine alters neurons, predisposes brain to addiction later

Neonatal exposure to nicotine alters the reward circuity in the brains of newborn mice, increasing their preference for the drug in later adulthood, report researchers at University of California San Diego School of Medicine in a study published “in press” April 24, 2019 in Biological Psychiatry.

A UC San Diego School of Medicine team of scientists, headed by senior author Davide Dulcis, PhD, associate professor in the Department of Psychiatry, with colleagues at Veterans Affairs San Diego Healthcare System and Michigan State University, found that exposure to nicotine in the first few weeks of life (through maternal lactation) induced a variety of long-term neurological changes in young mice.

Specifically, it caused a form of neuroplasticity that resulted in increased numbers of modified neurons in the ventral tagmental area (VTA) of the brain following nicotine re-exposure as adults. These neurons displayed a different biochemistry than other neurons, including greater receptivity to nicotine and a greater likelihood of subsequent addictive behavior.

Full story at Science Daily

Why might smoking and drinking alcohol raise the risk of osteoporosis?

Recent research has uncovered a cell mechanism that could help explain why smoking, alcohol, and other modifiable factors could raise the risk of developing the bone disease osteoporosis.

The mechanism spurs a cell type in the immune system to turn into osteoclasts, which are a type of cell that resorbs, or dissolves, bone.

It appears that mitochondria, the tiny enclosures that produce energy in cells, send out a signal that triggers this process when under stress.

When this happens in the mitochondria of macrophages, the cells turn into osteoclasts. Macrophages are prolific immune cells that remove cell waste and foreign objects by swallowing and digesting them.

Full story at Medical News Today

Different brain areas linked to smoking and drinking

Academics at the University of Warwick have found that low functional connectivity of the lateral orbitofrontal cortex that is associated with the tendency to smoke is associated with increased impulsiveness — which may contribute to the tendency to smoke. The high connectivity of the reward-related medial orbitofrontal cortex in drinkers may increase the tendency to be attracted to the reward of alcohol consumption.

A new study by Professor Jianfeng Feng, Professor Edmund Rolls from the Department of Computer Science at the University of Warwick, in collaboration with Dr. Wei Cheng from Fudan University, China, examined the neural mechanisms underlying two key types of substance use behavior, smoking and drinking.

In 2000 participants they found that smokers had low functional connectivity in general, and especially in the lateral orbitofrontal cortex, a region of the brain associated with impulsive behavior. This suggests that people who smoke may do so to increase their overall brain connectivity with the stimulating effect of nicotine; and that being impulsive may be a factor leading to smoking.

Full story at Science Daily

Engineered enzyme eliminates nicotine addiction in preclinical tests

Scientists at Scripps Research have successfully tested a potential new smoking-cessation treatment in rodents.

In a study published online in Science Advances on Oct. 17, 2018, the scientists gave nicotine-dependent rats an engineered enzyme that breaks down nicotine in the bloodstream before it can reach the brain. Treatment quickly reduced the animals’ motivation to take nicotine, reversed their signs of nicotine dependence, and kept them from relapsing when they were given access to nicotine again.

“This is a very exciting approach because it can reduce nicotine dependence without inducing cravings and other severe withdrawal symptoms, and it works in the bloodstream, not the brain, so its side effects should be minimal,” says principal investigator Olivier George, PhD, associate professor at Scripps Research.

Full story at Science Daily

One e-cigarette with nicotine leads to adrenaline changes in nonsmokers’ hearts

A new UCLA study found that healthy nonsmokers experienced increased adrenaline levels in their heart after one electronic cigarette (e-cigarette) with nicotine but there were no increased adrenaline levels when the study subjects used an a nicotine-free or empty e-cig.

The findings are published in Journal of the American Heart Association, the Open Access Journal of the American Heart Association/American Stroke Association.

Unlike cigarettes, e-cigs have no combustion or tobacco. Instead, these electronic, handheld devices deliver nicotine with flavoring and other chemicals in a vapor instead of smoke.

Full story at Science Daily