Scientists unveil shocking new findings on the relationship between cell activity and deep brain blood flow, as well as how salt affects the brain.
When neurons fire, the blood flow to the area increases rapidly. This is called neurovascular coupling, or functional hyperemia, and it happens by dilatation of brain arterioles. Functional magnetic resource imaging (fMRI) uses the notion of neurovascular coupling to identify brain diseases.
However, past research on neurovascular coupling has focused on superficial brain areas (such the cerebral cortex) and how blood flow changes in response to environmental cues (such as visual or auditory stimuli). We don’t know if the same principles apply to deeper brain regions that receive interoceptive cues from the body.
Dr. Javier Stern, a professor of neuroscience at Georgia State University and director of the university’s Center for Neuroinflammation and Cardiometabolic Diseases, led a multidisciplinary team of scientists to devise a novel strategy to studying this association in deep brain areas. As a deep brain region that regulates everything from eating and drinking to body temperature and reproduction, the hypothalamus was a target for researchers.
The research, which was published in the journal Cell Reports, looked at how blood flow to the hypothalamus changed as a result of salt ingestion.
“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,” says 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 accomplishes this in part by activating neurons that cause the production of vasopressin, an antidiuretic hormone that is essential for maintaining a healthy salt balance. The researchers discovered a drop in blood flow when the neurons in the hypothalamus got engaged, in contrast to prior studies that demonstrated a positive connection between neuron activity and increased blood flow.
“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,” adds the researcher.
“Reduced blood flow is normally observed in the cortex in the case of diseases like Alzheimer’s or after a stroke or ischemia.”
The process was named “inverse neurovascular coupling,” or a decrease in blood flow that causes hypoxia, by the researchers. They also noticed the following differences: Vascular responses to stimuli in the cortex are highly localized, and dilation happens quickly. The response in the hypothalamus was widespread and occurred 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 intriguing questions concerning the effects of hypertension on the brain. Between 50 and 60 percent of hypertension is thought to be salt-dependent, meaning it’s caused by eating too much salt. The researchers want to investigate whether this inverse neurovascular coupling mechanism contributes to the pathophysiology of salt-dependent hypertension in animal models. They also intend to apply their method to other brain regions and disorders, such as depression, obesity, and neurodegenerative diseases.
“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,” according to 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.”
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