Limitations to effect of α-MSH on permeability of blood-brain barrier to IV 99mTc-pertechnetate

Kastin, Abba J.; Fabre, L

doi:10.1016/0091-3057(82)90120-4

Cited by 8 publications

(2 citation statements)

References 13 publications

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“…Treatment with α-MSH in physiological concentrations did not modify the basal permeability of the BBB model. Previous studies in rats also found that α-MSH at low concentrations did not alter BBB permeability for albumin ( Sankar, Domer & Kastin, 1981 ) or a small anion ( Kastin & Fabre, 1982 ).…”

Section: Discussionmentioning

confidence: 83%

Protection of cultured brain endothelial cells from cytokine-induced damage by α-melanocyte stimulating hormone

Harazin

Bocsik

Barna

et al. 2018

PeerJ

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The blood–brain barrier (BBB), an interface between the systemic circulation and the nervous system, can be a target of cytokines in inflammatory conditions. Pro-inflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) induce damage in brain endothelial cells and BBB dysfunction which contribute to neuronal injury. The neuroprotective effects of α-melanocyte stimulating hormone (α-MSH) were investigated in experimental models, but there are no data related to the BBB. Based on our recent study, in which α-MSH reduced barrier dysfunction in human intestinal epithelial cells induced by TNF-α and IL-1β, we hypothesized a protective effect of α-MSH on brain endothelial cells. We examined the effect of these two pro-inflammatory cytokines, and the neuropeptide α-MSH on a culture model of the BBB, primary rat brain endothelial cells co-cultured with rat brain pericytes and glial cells. We demonstrated the expression of melanocortin-1 receptor in isolated rat brain microvessels and cultured brain endothelial cells by RT-PCR and immunohistochemistry. TNF-α and IL-1β induced cell damage, measured by impedance and MTT assay, which was attenuated by α-MSH (1 and 10 pM). The peptide inhibited the cytokine-induced increase in brain endothelial permeability, and restored the morphological changes in cellular junctions visualized by immunostaining for claudin-5 and β-catenin. Elevated production of reactive oxygen species and the nuclear translocation of NF-κB were also reduced by α-MSH in brain endothelial cells stimulated by cytokines. We demonstrated for the first time the direct beneficial effect of α-MSH on cultured brain endothelial cells, indicating that this neurohormone may be protective at the BBB.

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Section: Discussionmentioning

confidence: 83%

Protection of cultured brain endothelial cells from cytokine-induced damage by α-melanocyte stimulating hormone

Harazin

Bocsik

Barna

et al. 2018

PeerJ

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“…Intravenous α-MSH is able to change EEG frequency and neurobehavior without affecting blood pressure. It also increases the BBB permeability to the inorganic pertechnetate anion (Kastin and Fabre 1982;Sankar and others 1981) Promotes sleep (Chastrette and Cespuglio 1985b;Panskepp and others 1976), although there is a report of decreased (Opp and others 1988) or ineffective sleep (Chastrette and Cespuglio 1985a) Melanin concentrating hormone (MCH)…”

Section: Circadian Rhythms Of Bbb Functionmentioning

confidence: 99%

The Blood-Brain Barrier

Pan

Kastin

2016

Neuroscientist

Self Cite

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Sleep and its disorders are known to affect the functions of essential organs and systems in the body. However, very little is known about how the blood-brain barrier (BBB) is regulated. A few years ago, we launched a project to determine the impact of sleep fragmentation and chronic sleep restriction on BBB functions, including permeability to fluorescent tracers, tight junction protein expression and distribution, glucose and other solute transporter activities, and mediation of cellular mechanisms. Recent publications and relevant literature allow us to summarize here the sleep-BBB interactions in five sections: (1) the structural basis enabling the BBB to serve as a huge regulatory interface; (2) BBB transport and permeation of substances participating in sleep-wake regulation; (3) the circadian rhythm of BBB function; (4) the effect of experimental sleep disruption maneuvers on BBB activities, including regional heterogeneity, possible threshold effect, and reversibility; and (5) implications of sleep disruption-induced BBB dysfunction in neurodegeneration and CNS autoimmune diseases. After reading the review, the general audience should be convinced that the BBB is an important mediating interface for sleep-wake regulation and a crucial relay station of mind-body crosstalk. The pharmaceutical industry should take into consideration that sleep disruption alters the pharmacokinetics of BBB permeation and CNS drug delivery, being attentive to the chrono timing and activation of co-transporters in subjects with sleep disorders.

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Modulation of immunoactive levels of DSIP and blood‐brain barrier permeability by lighting and diurnal rhythm

Banks

Kastin

Selznick

1985

J of Neuroscience Research

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The brain and plasma levels of immunoactive delta sleep-inducing peptide (DSIP) as well as the permeability of the blood-brain barrier (BBB) to radioiodinated N-Tyr-DSIP (125I-DSIP) were measured at 0400, 0800, 1200, 1600, 2000, and 2400 hr in rats in a normal 12-hr-light/12-hr-dark cycle and at 0800 in rats in constant light or constant dark. Both brain and blood levels of immunoactivity showed statistically significant diurnal changes, whereas the measurement of BBB permeability varied in a regular fashion over time without the changes reaching statistical significance. Immunoactive levels of DSIP in both the plasma and the brain were higher and permeability of the BBB to 125I-DSIP increased in both the constant light and especially the constant dark groups in comparison with the cycled 0800 group. Diurnal variations continued to occur in the blood levels of immunoactive DSIP in the constant dark animals. Studies with radioiodinated serum albumin (RISA) showed that these findings did not result from a change in brain hemodynamics. Immunoactive levels of DSIP in the plasma correlated with brain immunoactive levels and with BBB permeability to 125I-DSIP. The increase in penetration of 125I-DSIP into the brain that occurred with changes in the lighting cycle appeared to be magnified by pre-treatment with aluminum. The results show interrelationships among various aspects of the neuroendocrine axis for DSIP and their modulation by physiological factors.

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Limitations to effect of α-MSH on permeability of blood-brain barrier to IV 99mTc-pertechnetate

Cited by 8 publications

References 13 publications

Protection of cultured brain endothelial cells from cytokine-induced damage by α-melanocyte stimulating hormone

Protection of cultured brain endothelial cells from cytokine-induced damage by α-melanocyte stimulating hormone

The Blood-Brain Barrier

Modulation of immunoactive levels of DSIP and blood‐brain barrier permeability by lighting and diurnal rhythm

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