The bloodbrain barrier is playing a vital role in controlling the flow and efflux of biological substances essential for the brain's metabolic activity as well as neuronal function. However, little is known about how the cells that form the barrier affect the nervous system's function.
Delta/Notch signaling in glia maintains motor nerve barrier function and synaptic transmission by controlling matrix metalloproteinase expression, according to a new paper published in the Proceedings of the National Academy of Sciences (PNAS).
The importance of barrier function in establishing a protective, nutrient-rich, and ionically balanced environment for neurons has been appreciated for some time, but little is known about how signaling cues originating in barrier-forming cells contribute to maintaining barrier function and influence synaptic activity, according to the researchers.
Pejmun Haghighi, PhD, a Buck Institute professor, believes that what we know currently about the blood-brain barrier is mainly that we do not know much beyond the basics.
The finding suggests a new approach to looking for therapies that would mitigate the damage caused by neurodegenerative illnesses.
The team used fruit fly larvae as the focus for their investigation. Because of their potential to be critical in interactions between glia and neurons, the team identified a pathway that is called Notch signaling.
We weren't planning on doing a lot of research on Notch, but we discovered that it was the major participant in the maintenance of the blood-brain barrier, according to Haghighi. When the signal is blocked, not only is the barrier function impaired, but also the nervous system's fundamental work is affected, including neurotransmitter release and muscle contractions.
This is a conceptual advancement, according to the author, because no one has ever observed neurons from the barrier themselves influencing neuron activity.
We are still unsure what is the cause or effect, but we may conclude that some patients have a blood-brain barrier that is beyond a correlation, as it is a significant symptom associated with neurodegeneration.
Their findings give us a completely different perspective for the development of novel therapies aimed at preventing damage to barrier function in neurodegenerative diseases.
Haghighi said we are hoping that we may go backward to investigate how the blood-brain barrier interacts with neurodegenerative illnesses. We are looking at all of these signaling pathways to see if we can translate our findings from larval synaptic function to more of a universal age-dependent neurodegeneration model.