Publications by authors named "K A Stanness"

Article Synopsis
  • The study investigates how adenosine influences excitatory amino acid (EAA) transport across the blood-brain barrier (BBB), which is crucial for maintaining brain EAA balance.
  • At physiological concentrations, adenosine reduces the transport of glutamate and aspartate into the brain without affecting the BBB's permeability to other substances, indicating a selective response.
  • Higher concentrations of adenosine can disrupt BBB integrity, highlighting the need for a precise balance in adenosine levels for optimal neuronal protection and function.
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Blood-brain barrier endothelial cells are characterized by the presence of tight intercellular junctions, the absence of fenestrations, and a paucity of pinocytotic vesicles. The in vitro study of the BBB has progressed rapidly over the past several years as new cell culture techniques and improved technologies to monitor BBB function became available. Studies carried out on viable in vitro models are set to accelerate the design of drugs that selectively and aggressively can target the CNS.

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How the brain meets its continuous high metabolic demand in light of varying plasma glucose levels and a functional blood-brain barrier (BBB) is poorly understood. GLUT-1, found in high density at the BBB appears to maintain the continuous shuttling of glucose across the blood-brain barrier irrespective of the plasma concentration. We examined the process of glucose transport across a quasi-physiological in vitro blood-brain barrier model.

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The blood-brain barrier represents a significant protective barrier for the passage of pathogens and toxicants, but it is difficult to study in vivo. This unit describes an in vitro system that can be used as a model for the blood-brain barrier to study its functions in an accessible format.

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Adenosine is an inhibitory neuromodulator in the central nervous system and has been reported to have neuroprotective properties. Using a dynamic in vitro blood-brain barrier, we investigated the hypothesis that inhibition of adenosine transporters on the lumenal side of the blood-brain barrier may decrease the loss of adenosine from the brain. Our results indicate that lumenal administration of dipyridamole, a nucleoside transport inhibitor, can inhibit adenosine permeation from the extracapillary space into the lumen.

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