A study led by researchers at Georgia State reveals surprising new information about the relationship between neuron activity and blood flow deep in the brain, as well as how the brain is affected by salt consumption.
When neurons are activated, it typically produces a
rapid increase of blood flow to the area. This relationship is known as
neurovascular coupling, or functional hyperemia, and it occurs via dilation of
blood vessels in the brain called arterioles. Functional magnetic resource
imaging (fMRI) is based on the concept of neurovascular coupling: experts look
for areas of weak blood flow to diagnose brain disorders.
However, previous studies of neurovascular coupling
have been limited to superficial areas of the brain (such as the cerebral
cortex) and scientists have mostly examined how blood flow changes in response
to sensory stimuli coming from the environment (such as visual or auditory
stimuli). Little is known about whether the same principles apply to deeper
brain regions attuned to stimuli produced by the body itself, known as
interoceptive signals.
To study this relationship in deep brain regions, an
interdisciplinary team of scientists led by Dr. Javier Stern, professor of
neuroscience at Georgia State and director of the university’s Center for
Neuroinflammation and Cardiometabolic Diseases, developed a novel approach that
combines surgical techniques and state-of-the-art neuroimaging. The team
focused on the hypothalamus, a deep brain region involved in critical body
functions including drinking, eating, body temperature regulation and
reproduction. The study, published in the journal Cell Reports, examined how blood
flow to the hypothalamus changed in response to salt intake.
“We chose salt because the body needs to control
sodium levels very precisely. We even have specific cells that detect how much
salt is in your blood,” said Stern. “When you ingest salty food, the brain
senses it and activates a series of compensatory mechanisms to bring sodium
levels back down.”
The body does this in part by activating neurons that
trigger the release of vasopressin, an antidiuretic hormone that plays a key
role in maintaining the proper concentration of salt. In contrast to previous
studies that have observed a positive link between neuron activity and increased
blood flow, the researchers found a decrease in blood flow as the neurons
became activated in the hypothalamus.
“The findings took us by surprise because we saw
vasoconstriction, which is the opposite of what most people described in the
cortex in response to a sensory stimulus,” said Stern. “Reduced blood flow is
normally observed in the cortex in the case of diseases like Alzheimer’s or
after a stroke or ischemia.”
The team dubbed the phenomenon “inverse neurovascular
coupling,” or a decrease in blood flow that produces hypoxia. They also
observed other differences: In the cortex, vascular responses to stimuli are very
localized and the dilation occurs rapidly. In the hypothalamus, the response
was diffuse and took place slowly, over a long period of time.
“When we eat a lot of salt, our sodium levels stay
elevated for a long time,” said Stern. “We believe the hypoxia is a mechanism
that strengthens the neurons’ ability to respond to the sustained salt
stimulation, allowing them to remain active for a prolonged period.”
The findings raise interesting questions about how
hypertension may affect the brain. Between 50 and 60 percent of hypertension is
believed to be salt-dependent — triggered by excess salt consumption. The
research team plans to study this inverse neurovascular coupling mechanism in
animal models to determine whether it contributes to the pathology of salt-dependent
hypertension. In addition, they hope to use their approach to study other brain
regions and diseases, including depression, obesity and neurodegenerative
conditions.
“If you chronically ingest a lot of salt, you’ll have
hyperactivation of vasopressin neurons. This mechanism can then induce
excessive hypoxia, which could lead to tissue damage in the brain,” said Stern.
“If we can better understand this process, we can devise novel targets to stop
this hypoxia-dependent activation and perhaps improve the outcomes of people
with salt-dependent high blood pressure.”
No comments:
Post a Comment