scholarly journals Ionic lanthanum passage across cerebral endothelium exposed to hyperosmotic arabinose

1983 ◽  
Vol 60 (1-2) ◽  
pp. 49-60 ◽  
Author(s):  
K. Dorovini-Zis ◽  
M. Sato ◽  
G. Goping ◽  
S. Rapoport ◽  
M. Brightman

1975 ◽  
Vol 18 (1) ◽  
pp. 179-197 ◽  
Author(s):  
N.J. Lane ◽  
R.A. Leslie ◽  
L.S. Swales

During incubation in vivo, exogenously applied ionic lanthanum comes to surround the numerous neurosecretory terminals which are found lying within or immediately beneath the acellular neural lamella ensheathing the nerves from fifth instar and adult specimens of Rhodnius prolixus. The lanthanum does not penetrate beyond the cellular perineurium, which completely surrounds the non-neurosecretory axons in these nerves and constitutes a form of ‘blood-brain barrier’. In some cases, however, lanthanum is found in the vicinity of a neurosecretory axon lying beneath the perineurium, where it can be assumed to have leaked in from the neurosecretory terminal lying free in the neural lamella. When nerves are incubated in calcium-free media, regions with an attenuated perineurium become ‘leaky’, in that lanthanum is found lying in those extracellular spaces between axons and glia which lie immediately below the thin part of the perineurial layer. Bathing solutions made slightly hyperosmotic to the haemolymph with sucrose have no apparent disruptive effects on the barrier. When the tissues are incubated in more hypertonic solutions, the perineurial barrier becomes ‘leaky’ throughout, and tracer pervades beyond its cells into all the intercellular spaced between glia and axons. The possible role of the zonulae occludentes in both the maintenance of the perineurial barrier and in the formation of interglial occlusions to local penetration of exogenous substances is considered.



1980 ◽  
pp. 65-79 ◽  
Author(s):  
K. Dorovini-Zis ◽  
J. J. Anders ◽  
M. W. Brightman




2013 ◽  
Vol 71 (6) ◽  
pp. 1055-1066 ◽  
Author(s):  
Nobukazu Miyamoto ◽  
Loc-Duyen D. Pham ◽  
Ji Hae Seo ◽  
Kyu-Won Kim ◽  
Eng H. Lo ◽  
...  
Keyword(s):  


2021 ◽  
pp. 0271678X2110454 ◽  
Author(s):  
Lianne J Trigiani ◽  
Miled Bourourou ◽  
María Lacalle-Aurioles ◽  
Clotilde Lecrux ◽  
Amy Hynes ◽  
...  

A vascular insult occurring early in disease onset may initiate cognitive decline leading to dementia, while pharmacological and lifestyle interventions can prevent this progression. Mice with a selective, tamoxifen-inducible deletion of NF-κB essential modulator (Nemo) in brain endothelial cells were studied as a model of vascular cognitive impairment. Groups included NemoFl controls and three NemobeKO groups: One untreated, and two treated with simvastatin or exercise. Social preference and nesting were impaired in NemobeKO mice and were not countered by treatments. Cerebrovascular function was compromised in NemobeKO groups regardless of treatment, with decreased changes in sensory-evoked cerebral blood flow and total hemoglobin levels, and impaired endothelium-dependent vasodilation. NemobeKO mice had increased string vessel pathology, blood-brain barrier disruption, neuroinflammation, and reduced cortical somatostatin-containing interneurons. These alterations were reversed when endothelial function was recovered. Findings strongly suggest that damage to the cerebral endothelium can trigger pathologies associated with dementia and its functional integrity should be an effective target in future therapeutic efforts.





1985 ◽  
Vol 44 (3) ◽  
pp. 341
Author(s):  
J. J. Olson ◽  
D. W. Beck ◽  
R. J. Linhardt ◽  
N. J. Hays


2012 ◽  
Vol 32 (6) ◽  
pp. 983-988 ◽  
Author(s):  
Changhong Xing ◽  
Tatyana Levchenko ◽  
Shuzhen Guo ◽  
Monique Stins ◽  
Vladimir P Torchilin ◽  
...  

Minocycline has been proposed as a way to blunt neurovascular injury from matrix metalloproteinases (MMPs) during stroke. However, recent clinical trials suggest that high levels of minocycline may have deleterious side-effects. Here, we showed that very high minocycline concentrations damage endothelial cells via calpain/caspase pathways. To alleviate this potential cytotoxicity, we encapsulated minocycline in liposomes. Low concentrations of minocycline could not reduce tumor necrosis factor α (TNF α)-induced MMP-9 release from endothelial cells. But low concentrations of minocycline-loaded liposomes significantly reduced TNF α-induced MMP-9 release. This study provides proof-of-concept that liposomes may be used to deliver lower levels of minocycline for targeting MMPs in cerebral endothelium.



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