Researchers at the University of Texas Health Science Center at San Antonio have come up with a new technique to measure tiny, rapid-fire secretions in the brains and mouths of fruit flies, which is helping provide insight into the benefits of eating less — information that, surprisingly, could help people suffering from neuromuscular disorders such as Parkinson’s disease.
The researchers say they have uncovered never-before-seen brain chemistry that helps explain why fruit flies genetically manipulated to mimic conditions such as Parkinson’s disease and myasthenia gravis live longer when fed a restricted diet.
Flies on the low-calorie diet showed a 100 percent increase in the release of neurotransmitters in the brain. These chemicals carry signals from one nerve cell to another across gaps called synapses.
The brain has millions of synapses that are believed to be the critical structures required for normal brain function. Diseases such as Parkinson’s harm them irreparably, according to the researchers.
The researchers also noted that the chemicals were secreted at critical locations.
“Diet restriction increased the neurotransmitters released at synapses called neuromuscular junctions,” said senior author Benjamin Eaton, Ph.D., assistant professor of physiology. “These synapses, which form on muscle, transmit nerve impulses from the brain to muscles, resulting in movement.
“If neuromuscular junctions degenerate, resulting in the release of less neurotransmitter, then muscle activity diminishes. This is observed in diseases such as myasthenia gravis and amyotrophic lateral sclerosis (ALS).”
While it has been shown that diet affects the nervous system, the “nuts and bolts of what it is doing to neurons have not been established,” Eaton said. “”We believe we have shown a novel and important effect.”
The researchers genetically engineered a single pair of motor neurons to develop neurodegenerative disease, resulting in a decrease in the fruit flies’ ability to extend the proboscis, which they use to gather food. The team then dissected the head to locate the appropriate muscles on the proboscis and quantified the neurotransmitter activity occurring there, which continues to take place even after death, according to the researchers.
“We went into the very muscles that these motor neurons controlled and analyzed neurotransmission using electrodes,” Eaton said. “We showed diet can rescue proboscis extension by increasing the amount of neurotransmitter released. This suggests that diet could be an important therapy for improving muscle function during motor diseases such as ALS.”
Next up is to define the proteins in neurons that are being altered by diet restriction, he said.