New evidence shows that axons do more than just transmit signals between neurons: They can adjust the strength of the transmission, affecting the rate at which information crosses the brain.
Raju Metherate and colleagues at the University of California, Irvine, reached this conclusion by studying the brain-enhancing properties of nicotine. Because stimuli are perceived in the cortex via a central processor—the thalamus—the investigators designed a preparation of mouse brain tissue that included “transmitting” neurons in the thalamus, “receiving” neurons in the cortex, and the entire axon in between. The researchers assumed that nicotine would act on cortical neurons, but efforts to prove as much failed.
“We finally realized that nicotine must be working on the axon itself, which was contrary to scientific dogma,” Metherate says. The team tested their suspicion in a study being published in the September Nature Neuroscience.
The team homed in on the so-called nicotinic acetylcholine receptors in the axon portion of their tissue slice, which was taken from a pathway involved in hearing. Adding nicotine to the tissue preparation doubled the rate at which signals reached the cortex; testing multiple sites proved that nicotine was in fact working at the axon.
When they checked their findings in mice by placing speakers next to the animals’ ears, they found that a drug that blocks the receptor, when applied to the axon, reduced the animals’ ability to hear tones.
Metherate says the fact that axons can respond to neurotransmitters opens up many new possibilities. Researchers are beginning to view some disorders, such as schizophrenia, not just in terms of the brain regions involved but as a disruption in the connections between these regions. “Our study may help to explain this ‘de-synchrony,’ ” Metherate concludes.