NEW YORK — Botox is best-known for its “fountain of youth” effects on an aging face, but scientists have uncovered a new use for the toxin. Researchers at New York University say Botox helps to reveal the inner workings of the brain — which could lead to treatments for Parkinson’s disease.
The botulinum toxin shows brain cells can gauge how much dopamine they need to produce on their own. Scientists had thought they relied on neighboring cells to tell them when to make more or less of the “feel-good hormone,” which is vital for healthy brain processes, including motivation, memory, and movement.
This new research discovers dopamine cells might not need their neighbors’ opinions after all.
The death of dopamine-releasing brain cells is a key factor in Parkinson’s disease. About 60,000 adults are diagnosed with the condition each year in the U.S.
“Our findings provide the first evidence that dopamine neurons regulate themselves in the brain,” says lead author Dr Takuya Hikima in a university release. “Now that we better understand how these cells behave when they are healthy, we can start to unravel why they break down in neurodegenerative disorders like Parkinson’s disease.”
A number of flaws in the “old way of thinking” about how dopamine is released in the brain prompted the researchers to carry out their investigation.
First, for cells to control the dopamine output of others, a large number of connections, known as synapses, would be needed. Yet there were not enough synapses to account for this, the researchers say. Also, given many other hormone producing cells self-regulate, there was no reason dopamine neurons would be any different.
Dopamine neurons were collected from dozens of mice and some were injected with Botox. The toxin blocks nerve cells from sending chemical messages.
“By injecting Botox into single neurons we hoped to show whether any signal to continue or stop dopamine release could only come from outside the paralyzed cell,” says Dr. Hikima. “If the neurons were in fact controlled by neighboring dopamine cells, then dopamine release would remain unaffected because the treated cells would still receive dopamine signals from the untreated cells nearby.”
Cells which had been blocked with Botox produced 75 per ent less dopamine, the study shows. This suggests they were primarily relying on their own discharge to regulate the hormone’s release.
“Since our Botox technique helped us solve the problem of how dopamine neurons regulate their communication, it should also enable us to uncover how other nerve cells interact with each other in the mammalian brain,” says senior author Dr Margaret Rice.
The researchers are planning to examine other areas of dopamine activity, which remain poorly understood. In particular, they’re studying how self-regulation could kill brain cells in Parkinson’s patients and whether it is affected by calcium levels.
The findings are published in the journal Cell Reports.
SWNS writer Tom Campbell contributed to this report.