WASHINGTON : In a breakthrough for smokers who are trying to kick the butt, scientists have identified the brain circuitry responsible for increased anxiety commonly experienced during withdrawal from nicotine addiction.
“We identified a novel circuit in the brain that becomes active during nicotine withdrawal, specifically increasing anxiety,” said principal investigator Andrew Tapper, from the University of Massachusetts Medical School.
“Increased anxiety is a prominent nicotine withdrawal symptom that contributes to relapse in smokers attempting to quit,” said Tapper.
Researchers found that a brain region called the interpeduncular nucleus is activated and appears to cause anxiety during nicotine withdrawal.
The sub region of the interpeduncular nucleus, which is activated and linked to anxiety during withdrawal, is distinct from another sub-region, previously identified by Tapper, where physical nicotine withdrawal symptoms such as headaches, nausea and insomnia originate.
Anxiety is an affective symptom often likely to thwart smokers’ attempts to quit. The newly discovered sub region offers a distinct target for dampening the affective symptoms of nicotine withdrawal, researchers said.
Researchers also found that input from neurons in two other brain regions converge onto the interpeduncular nucleus to stimulate anxiety-provoking neurons.
Surprisingly, the ventral tegmental area, which is traditionally associated with the rewarding or pleasurable effects of abused drugs, activates neuron receptors through corticotropin releasing factor, a protein neurotransmitter released in response to stress.
Neurons in the medial habenula stimulate interpeduncular nucleus neurons by releasing glutamate, the major excitatory neurotransmitter in the brain, an effect that is increased by corticotropin releasing factor receptor activation.
“Both of these inputs are important. We could alleviate anxiety during nicotine withdrawal by either preventing corticotropin releasing factor synthesis in the ventral tegmental area, or by silencing the medial habenula inputs into the interpeduncular nucleus,” said Tapper.
Investigators were able to alleviate anxiety in mice by quieting the activity of those activated neurons, suggesting the same might be possible for humans.
“There are already drugs that block the CRF receptor that contributes to activation of these anxiety-inducing neurons,” Tapper added.
The study was published in the journal Nature Communications. (AGENCIES)
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