The Blood Brain Barrier Protects The Brain From Neurotoxins
The blood–brain barrier (BBB) is a highly selective permeability barrier that separates the circulating blood from the brain extracellular fluid (BECF) in the central nervous system (CNS). The blood–brain barrier is formed by capillary endothelial cells, which are connected by tight junctions with an extremely high electrical resistivity of at least 0.1 Ω⋅m.
The blood–brain barrier allows the passage of water, some gases, and lipid soluble molecules by passive diffusion, as well as the selective transport of molecules such as glucose and amino acids that are crucial to neural function.
On the other hand, the blood–brain barrier may prevent the entry of lipophilic, potential neurotoxins by way of an active transport mechanism mediated by P-glycoprotein.
From Research Published in Journal of Neuroscience, October 2014
Chronic sleep restriction (CSR) is a common occurrence in modern society, resulting from a variety of factors, such as, longer commuting distances between home and job, increased social pressure, and longer time spent at work and watching media entertainment.
As a regulatory interface, the BBB is susceptible to modulatory changes by hormones, neurotransmitters, and altered states of functional activation (Palmer, 1986). Circadian rhythms of BBB transport have been shown for leptin (Pan and Kastin, 2001) and tumor necrosis factor α (Pan et al., 2002).
Osmotic opening of the BBB by mannitol is well known, and even substances such as alcohol, epinephrine, tobacco, cocaine, and methamphetamine, as well as, morphine withdrawal can increase the paracellular permeability of the BBB (Sharma and Ali, 2006)
We used a CSR paradigm that produced consistent reduction of sleep efficiency as well as percentage of NREM and REM resulting from increased sleep fragmentation and higher total waking time. The pattern of sleep disruption resembles that of patients with severe sleep apnea, the most common disorder seen in a general sleep clinic.
CSR for 6 d was sufficient to cause a series of biochemical changes in enriched cerebral microvessels representing the BBB, and to alter transporter functions as well as levels of protein expression.
Chronic Sleep Restriction Decrease Function of Glucose Transporters and Inhibits Vascular Reactivity
Here we show for the first time that CSR decreased the expression and function of glucose transporters, suppressed vascular reactivity with reduction of iNOS, eNOS and ET-1, increased the vascular inflammatory marker COX-2, and impaired TJ protein expression and BBB transport function.
The results have wide implications for how CSR alters neuroendocrine regulation and could exert long-term consequences on transport across the BBB.