US researchers have in a first-of-its-kind study explored the relationship between neuron activity and blood flow deep in the brain, as well as how the brain is affected by salt consumption, resulting in cognitive decline such as Alzheimer's.
The team from the Georgia State University 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 changes in response to salt intake.
According to Javier Stern, professor of neuroscience at the varsity, when people ingest salty food, the brain senses it and activates neurons that trigger the release of vasopressin--an antidiuretic hormone that plays a key role in maintaining the proper concentration of salt in the body.
But, in contrast to previous studies that have observed a positive link between neuron activity and increased blood flow, the new study showed 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.
According to Javier Stern, when people ingest salty food, the brain senses it and activates neurons that trigger the release of vasopressin--an antidiuretic hormone that plays a key role in maintaining the proper concentration of salt in the body"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 --" lack of oxygen. They also observed other differences: In the cortex, vascular responses to stimuli are very localised and the dilation occurs rapidly.
But, 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 per cent of hypertension is believed to be salt-dependent-- triggered by excess salt consumption.
"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," he noted.