In a study using rats, Raju Metherate, associate professor of neurobiology and behavior, and colleagues from UC Irvine, showed that nicotine exposure during the equivalent of a human's third trimester led to hearing-related cognitive problems. This is the first time a study has demonstrated this causal link. Further tests then revealed that the probable cause of the deficits was damage to the receptors in the brain that are sensitive to nicotine, which seems to occur when humans or animals are exposed to the substance during development. The study appears this week in the early online issue of the European Journal of Neuroscience.
Children with auditory processing deficits can have a number of hearing-related problems. They may have difficulty understanding speech in a noisy environment, not understand information that is presented verbally, and may not be able to tell the difference between similar sounds.
"This study is significant because it suggests to us precisely what aspect of smoking is so harmful in pregnancy when it comes to cognitive hearing deficits," Metherate said. "Most women who smoke find it difficult to quit during pregnancy. For them, doctors often prescribe a nicotine patch. While that does protect the fetus from the well-known physical under-development related to harmful chemicals in cigarette smoke, exposure to nicotine appears to be enough to cause serious problems on its own, in terms of brain development."
Chemicals known as neurotransmitters act as message carriers between cells and bind with receptors on the cells' surfaces, much like a key fits into the lock. If the receptors are damaged, they can no longer bind properly with the neurotransmitter. Nicotine shares a receptor with the neurotransmitter acetylcholine, which is important for a number of cognitive functions.
Researchers believe that when people are paying attention to something, such as an important sound, acetylcholine is released into the brain. It then interacts with the nicotinic-acetylcholine receptor and, the UCI study showed, thereby enhances sensitivity to that sound. If that receptor is damaged due to prenatal exposure to nicotine, acetylcholine cannot bind with it and increased sensitivity to the important sound is lost.
"While verbal function cannot be measured in an animal, this establishment of a causal relationship between prenatal nicotine exposure and auditory-cognitive deficits is an important step forward in reinforcing these previous findings in humans," Metherate said.
According to the researchers, given the importance of acetylcholine to a number of brain functions, a loss of nicotinic-acetylcholine receptors may have a negative effect on other higher cognitive functions and may also impair vision and other senses.
Nicotine does seem to actually enhance cognitive processing when administered to adults, a finding that has also been shown in previous studies. The researchers found that in this study, nicotine appeared to enhance auditory function in the adult rats, but only if they had not been exposed to the substance during development.
Researchers placed electrodes in the animals' auditory cortex, then exposed them to different frequencies of sound. They found that nicotine made the cortex much more responsive to sound if the rats had not had exposure to nicotine during their early development. In the case of previous exposure, there was no increased sensitivity to sound. According to Metherate, this occurs most likely because the nicotine is mimicking the action of acetylcholine on their shared receptors and increasing responsiveness to sou nd if those receptors had not been previously damaged.