Your doctor should be able to translate this into a stroke rehab protocol to make our damaged connections work better.
https://www.technologynetworks.com/neuroscience/news/researchers-make-surprising-discovery-about-how-neurons-talk-to-each-other-291199
Researchers at the University of Pittsburgh have uncovered the
mechanism by which neurons keep up with the demands of repeatedly
sending signals to other neurons. The new findings, made in fruit flies
and mice, challenge the existing dogma about how neurons that release
the chemical signal dopamine communicate, and may have important
implications for many dopamine-related diseases, including
schizophrenia, Parkinson’s disease and addiction.
The research conducted at Pitt and Columbia University was published online today in the journal Neuron.
Neurons
communicate with one another by releasing chemicals called
neurotransmitters, such as dopamine and glutamate, into the small space
between two neurons that is known as a synapse. Inside neurons,
neurotransmitters awaiting release are housed in small sacs called
synaptic vesicles.
“Our findings demonstrate, for the
first time, that neurons can change how much dopamine they release as a
function of their overall activity. When this mechanism doesn’t work
properly, it could lead to profound effects on health,” explained the
study’s senior author Zachary Freyberg, M.D., Ph.D., who recently joined
Pitt as an assistant professor of psychiatry and cell biology. Freyberg
initiated the research while at Columbia University.
When
the researchers triggered the dopamine neurons to fire, the neurons’
vesicles began to release dopamine as expected. But then the team
noticed something surprising: additional content was loaded into the
vesicles before they had the opportunity to empty. Subsequent
experiments showed that this activity-induced vesicle loading was due to
an increase in acidity levels inside the vesicles.
“Our
findings were completely unexpected,” said Freyberg. “They contradict
the existing dogma that a finite amount of chemical signal is loaded
into a vesicle at any given time, and that vesicle acidity is fixed.”
The
team then demonstrated that the increase in acidity was driven by a
transport channel in the cell’s surface, which allowed an influx of
negatively charged glutamate ions to enter the neuron, thus increasing
its acidity. Genetically removing the transporter in fruit flies and
mice made the animals less responsive to amphetamine, a drug that exerts
its effect by stimulating dopamine release from neurons.
“In
this case, glutamate is not acting as a neurotransmitter. Instead it is
functioning primarily as a source of negative charge, which is being
used by these vesicles in a really clever way to manipulate vesicle
acidity and therefore change their dopamine content,” Freyberg said.
“This calls into question the whole textbook model of vesicles as having
fixed amounts of single neurotransmitters. It appears that these
vesicles contain both dopamine and glutamate, and dynamically modify
their content to match the conditions of the cell as needed.”
In
the future, the team plans to look more closely at how increases in
vesicle acidification affect health. A number of brain diseases are
characterized by abnormal dopamine neuron signaling and altered levels
of the neurotransmitter.
“Since we have demonstrated that
the balance between glutamate and dopamine is important for controlling
the amount of dopamine that a neuron releases, it stands to reason that
an imbalance between the two neurotransmitters could be contributing to
symptoms in these diseases,” said Freyberg.
This article has been republished from
materials provided by
UPMC. Note: material may have been edited for length and content. For further information, please contact the cited source.
; Oset-Gasque, M.J.
