In addition to smoothing out wrinkles, researchers have found that the drug Botox can reveal the inner workings of the brain. A new study used it to show that feedback from individual nerve cells controls the release of dopamine, a chemical messenger involved in motivation, memory, and movement.
Such “self-regulation,” the researchers say, stands in
contrast to the widely held view that the release of dopamine — known as the
“feel good” hormone — by any cell relied on messages from nearby cells to
recognize that it is releasing too much of the hormone.
Led by researchers at NYU Grossman School of Medicine,
the new study showed that dopamine-releasing brain cells respond to their own
signals to regulate the hormone’s output. Because the death of
dopamine-releasing brain cells is a key factor in Parkinson’s disease, the new
findings provide insight into why these cells die in the movement disorder, the
researchers say.
“Our findings provide the first evidence that dopamine
neurons regulate themselves in the brain,” says study lead author Takuya
Hikima, PhD. “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,” adds Hikima, an instructor in the
Department of Neurosurgery at NYU Langone Health.
Hikima says their study was prompted by what the
research team saw as flaws in the older way of thinking about how dopamine
works. First, for one cell to control its neighbor with dopamine, a large
number of synapses, or junctions where two cells meet and exchange messages,
would be required. Yet researchers say there were not enough synapses to
account for this.
Second, many types of hormone-producing cells in the body
use a streamlined system that self-regulates further release, so it seemed odd
that dopamine neurons would use a more roundabout process.
For the study, publishing April 6 in the journal Cell
Reports, the research team collected dopamine neurons from dozens
of mice. They injected some of the brain cells with Botox, a toxin that blocks
nerve cells from sending chemical messages to neurons and other cells. The
chemical’s nerve-blocking action accounts for its ability to relax muscles in
migraine and wrinkle treatments.
By injecting Botox into single neurons, says Hikima,
the researchers hoped to show whether any signal to continue or stop dopamine
release could only come from outside the “paralyzed” cell. 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.
Instead, the findings revealed a 75 percent drop in
dopamine outflow, suggesting that dopamine neurons largely rely on their own
discharge to determine release rate of the hormone, according to the
investigators.
“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 study senior author Margaret Rice, PhD.
The research team next plans to explore other areas of
dopamine neuron activity that remain poorly understood, such as the dependence
of dopamine release on calcium from outside the brain cells, says Rice, a
professor in the Departments of Neurosurgery and Neuroscience and Physiology at
NYU Langone. The investigators also intend to examine how self-regulation of
dopamine might contribute to cell death in Parkinson’s disease.
Image & info via NYU Langone
Journal article: https://www.cell.com/cell-reports/fulltext/S2211-1247(21)00265-5
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