In the human brain, the cholinergic system is a modulatory neurotransmitter system involved in a variety of brain processes, including learning and memory, attention, and motor processes, among others. Neuroscientist Julie Miwa examines the regulation of this system through the lynx1 gene and its impact on learning.
“There are changes in the brain as we age and lynx 1 turns on, at least in animals, at this transition when we have this robust learning ability to when it becomes less robust,” says Miwa, assistant professor of biological sciences.
Lynx genes are toxin–like proteins that form tight associations with specialized proteins in the brain called nicotinic acetylcholine receptors. Lynx1 acts as a molecular brake over the cholinergic system, limiting cognition and suppressing neural plasticity after a period of vigorous plasticity early in postnatal development. Those receptors can facilitate learning and memory. In adults, however, lynx1 binds to those receptors and clamps or inhibits this neurotransmitter system and inhibits dynamic learning to occur.
Generating genetically engineered mice, Miwa’s research focuses on regulating the cholinergic system to control the plasticity of the brain. Mice lacking the lynx1 gene have improved learning ability. The cholinergic system along a gradient of activation, and within this gradient, there is an optimal window of activation–optimized cholinergic tone — within which it has a variety of pro–cognitive effects. The cholinergic system is increasingly prized as a driving force for neural plasticity as well.
One of the discoverers of the lynx modulators of nicotinic acetylcholine receptors, she has teamed with colleague Amber Rice to study birds to find subtle sequence differences in the gene that might confer better or worse learning potential.
“If we can find these differences and link it to learning, we might be able to use this strategy with humans to see if this gene confers better or worse learning potential. If we devise ways to inhibit lynx1, it may be possible to bring back the youthful learning capability in humans.“ This could be particularly useful for neuropsychiatric disorders in which patients exhibit symptoms as adults, past the age when it is feasible to correct imbalances that happened early in life.
A better understanding of this gene could result in better therapies for people who have learning disabilities, suffer from Alzheimer ’s disease, schizophrenia, or stroke patients.