Functional magnetic resource imaging (fMRI) is based on the principle of neurovascular coupling: specialists look for locations of weak blood circulation to detect brain disorders.
A first-of-its-kind study led by scientists at Georgia State reveals surprising new details about the relationship between nerve cell activity and blood flow deep in the brain, as well as how the brain is impacted by salt intake.
When neurons are activated, it generally produces a fast increase of blood flow to the location. This relationship is understood as neurovascular coupling, or practical hyperemia, and it happens through dilation of blood vessels in the brain called arterioles. Functional magnetic resource imaging (fMRI) is based upon the concept of neurovascular coupling: professionals look for locations of weak blood circulation to identify brain conditions.
To study this relationship in deep brain areas, an interdisciplinary group of researchers led by Dr. Javier Stern, professor of neuroscience at Georgia State and director of the universitys Center for Neuroinflammation and Cardiometabolic Diseases, established an unique technique that integrates surgical methods and advanced neuroimaging. The group focused on the hypothalamus, a deep brain area included in critical body functions including drinking, consuming, body temperature level guideline and reproduction. “When you consume salty food, the brain senses it and activates a series of countervailing systems to bring salt levels back down.”
In addition, they hope to use their method to study other brain regions and diseases, consisting of depression, obesity and neurodegenerative conditions.
Nevertheless, previous studies of neurovascular coupling have been limited to superficial locations of the brain (such as the cortex) and scientists have mainly taken a look at how blood flow changes in reaction to sensory stimuli originating from the environment (such as acoustic or visual stimuli). Little is understood about whether the very same concepts use to much deeper brain areas attuned to stimuli produced by the body itself, understood as interoceptive signals.
To study this relationship in deep brain areas, an interdisciplinary team of researchers led by Dr. Javier Stern, teacher of neuroscience at Georgia State and director of the universitys Center for Neuroinflammation and Cardiometabolic Diseases, developed a novel approach that integrates surgical methods and advanced neuroimaging. The group focused on the hypothalamus, a deep brain area involved in vital body functions including drinking, consuming, body temperature level policy and recreation. The study, released in the journal Cell Reports, examined how blood flow to the hypothalamus altered in response to salt consumption.
” We chose salt since the body requires to control salt levels extremely exactly. We even have particular cells that discover how much salt remains in your blood,” stated Stern. “When you ingest salted food, the brain senses it and activates a series of countervailing systems to bring sodium levels back down.”
The body does this in part by triggering nerve cells that trigger the release of vasopressin, an antidiuretic hormonal agent that plays an essential function in keeping the proper concentration of salt. In contrast to previous research studies that have observed a favorable link between neuron activity and increased blood circulation, the scientists discovered a decrease in blood flow as the nerve cells ended up being activated in the hypothalamus.
” The findings took us by surprise due to the fact that we saw vasoconstriction, which is the opposite of what many people explained in the cortex in reaction to a sensory stimulus,” stated Stern. “Reduced blood circulation is usually observed in the cortex when it comes to diseases like Alzheimers or after a stroke or anemia.”
The group called the phenomenon “inverted neurovascular coupling,” or a reduction in blood flow that produces hypoxia. They also observed other differences: In the cortex, vascular actions to stimuli are very localized and the dilation happens quickly. In the hypothalamus, the action was diffuse and took place slowly, over an extended period of time.
” When we consume a lot of salt, our salt levels stay raised for a very long time,” said Stern. “We believe the hypoxia is a mechanism that enhances the neurons ability to react to the sustained salt stimulation, enabling them to remain active for an extended duration.”
The findings raise intriguing concerns about how hypertension may impact the brain. Between 50 and 60 percent of high blood pressure is believed to be salt-dependent– triggered by excess salt intake. The research study group prepares to study this inverted neurovascular coupling system in animal designs to identify whether it contributes to the pathology of salt-dependent hypertension. In addition, they want to use their approach to study other brain regions and diseases, consisting of anxiety, weight problems and neurodegenerative conditions.
” If you chronically consume a lot of salt, youll have hyperactivation of vasopressin nerve cells. This system can then induce excessive hypoxia, which could cause tissue damage in the brain,” said Stern. “If we can better comprehend this procedure, we can create novel targets to stop this hypoxia-dependent activation and perhaps enhance the results of people with salt-dependent hypertension.”
Referral: “Inverse neurovascular coupling adds to favorable feedback excitation of vasopressin neurons throughout a systemic homeostatic difficulty” by Ranjan K. Roy, Ferdinand Althammer, Alexander J. Seymour, Wenting Du, Vinicia C. Biancardi, Jordan P. Hamm, Jessica A. Filosa, Colin H. Brown and Javier E. Stern, 2 November 2021, Cell Reports.DOI: 10.1016/ j.celrep.2021.109925.
The research study authors include Ranjan Roy and Ferdinand Althammer, postdoctoral scientists in the Center for Neuroinflammation and Cardiometabolic Diseases, Jordan Hamm, assistant professor of neuroscience at Georgia State, and coworkers at the University of Otago in New Zealand, Augusta University, and Auburn University. The research was supported by the National Institute of Neurological Disorders and Stroke.
