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Nicotine causes permanent damage in young brains

Nicotine causes permanent damage in young brains

According to research conducted at Amsterdam's VU University, starting to smoke at a young age disrupts normal brain development and leads to permanent changes in the functioning of the prefrontal cortex. This area of the brain is one of the last to mature, and is responsible for higher executive functions, such as long-term planning, decision-making, attention and cognitive control.

Most smokers start at a young age, often during puberty. Smoking at this age is expected to be especially harmful because the brain is still developing; the prefrontal cortex in particular is only fully developed by the age of twenty.

Nicotine has been shown to influence the activity of different types of brain cells in the prefrontal cortex and thereby affect cognitive functioning. Also, previous work on human subjects indicates that smoking during adolescence increases the risk of developing psychological disorders, cognitive impairments, and attention deficit disorders later in life.

Within the limitations of human studies, it is difficult to distinguish cause and effect of nicotine exposure and potential lasting effects on cognitive function. Therefore, Natalia Goriounova, the PhD student who conducted the research, monitored the molecular and cellular effects of nicotine in the brains of "adolescent" rats to investigate the short- and long-term effects of nicotine on the adolescent prefrontal cortical function and cognitive behavior.

Goriounova found that nicotine exposure led to observably impaired concentration as well as a prolonged reduction in the functioning of the inhibitory autoreceptor mGluR2 in the prefrontal cortex. This protein reduces the release of neurotransmitters and prevents overstimulation of nerve cells. Reduction of mGluR2 signalling leads to disinhibition of the prefrontal network, causing reduced synaptic information filtering and reduced attention.

Note that although Goriounova's research was carried out in rats, her results are relevant to humans because neural structures and signal processing in rat brains are similar to those in humans. Therefore, smoking during adolescence may cause similar cognitive deficits to those observed in adolescent rats exposed to nicotine. Her results also indicate that the damaging consequences of adolescent nicotine exposure do not attenuate over time and may persist even after one quits smoking.

This last finding is especially troubling given the close relationship between the Dutch government and the tobacco lobby, and the fact that Dutch smokers have been shown to be less aware of the dangers associated with smoking than citizens of many other countries. Goriounova's results underscore the importance of educating young people about the life-long consequences of smoking.

Gouriounova's entire doctoral thesis can be accessed here.

Carly

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Carly Blair

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